Biology and non-preference for oviposition by Bemisia tabaci (Gennadius) biotype B (Hemiptera: Aleyrodidae) on cotton cultivars

The purposes of this work were to evaluate some biological aspects of Bemisia tabaci (Gennadius) biotype B at egg and nymphal stages and to evaluate the non-preference for oviposition and its correlation with the number and type of trichomes on the cotton cultivars BRS Ipê, BRS 186-Precoce 3, BRS Acala, BRS Verde, BRS-200 Marrom, BRS Cedro, BRS Ita 90-2 and BRS Aroeira. The experiments were conducted in climatic chambers at 28 +/- 2 degrees C, 70% RH and photophase of 14h, and in greenhouse. Egg fertility was not affected by the cotton cultivars but survival in egg-adult period was influenced by the host plant. There was no influence of cultivars neither on the duration of egg stage, nymphs at 2nd, 3rd and 4th instars nor on the duration from egg to adult, but nymphs reared on the cultivar BRS Ipê had their 1st instar extended. Low number of eggs was detected on the cultivars BRS Aroeira, BRS Verde and BRS Ita 90-2 in both experiments with and without oviposition choice, indicating a possible mechanism of resistance, but no correlation could be established between trichome densisty and oviposition non-preference.     

Cyclooxygenase inhibition and baroreflex sensitivity in humans

Animal studies suggest that prostanoids (i.e., such as prostacyclin) may sensitize or impair baroreceptor and/or baroreflex responsiveness depending on the site of administration and/or inhibition. We tested the hypothesis that acute inhibition of cyclooxygenase (COX), the rate-limiting enzyme in prostanoid synthesis, impairs baroreflex regulation of cardiac period (R-R interval) and muscle sympathetic nerve activity (MSNA) in humans and augments pressor reactivity. Baroreflex sensitivity (BRS) was determined at baseline (preinfusion) and 60 min after (postinfusion) intravenous infusion of a COX antagonist (ketorolac; 45 mg) (24 +/- 1 yr; n = 12) or saline (25 +/- 1 yr; n = 12). BRS was assessed by using the modified Oxford technique (bolus intravenous infusion of nitroprusside followed by phenylephrine). BRS was quantified as the slope of the linear portion of the 1) R-R interval-systolic blood pressure relation (cardiovagal BRS) and 2) MSNA-diastolic blood pressure relation (sympathetic BRS) during pharmacological changes in arterial blood pressure. Ketorolac did not alter cardiovagal (19.4 +/- 2.1 vs. 18.4 +/- 2.4 ms/mmHg preinfusion and postinfusion, respectively) or sympathetic BRS (-2.9 +/- 0.7 vs. -2.6 +/- 0.4 arbitrary units.beat(-1).mmHg(-1)) but significantly decreased a plasma biomarker of prostanoid generation (plasma thromboxane B2) by 53 +/- 11%. Cardiovagal BRS (21.3 +/- 3.8 vs. 21.2 +/- 3.0 ms/mmHg), sympathetic BRS (-3.4 +/- 0.3 vs. -3.2 +/- 0.2 arbitrary units.beat(-1).mmHg(-1)), and thromboxane B2 (change in -1 +/- 12%) were unchanged in the control (saline infusion) group. Pressor responses to steady-state incremental (0.5, 1.0, and 1.5 microg.kg(-1).min(-1)) infusion (5 min/dose) of phenylephrine were not altered by ketorolac (n = 8). Collectively, these data indicate that acute pharmacological antagonism of the COX enzyme does not impair BRS (cardiovagal or sympathetic) or augment pressor reactivity in healthy young adults.     

Aldosterone impairs baroreflex sensitivity in healthy adults

Animal studies suggest that acute and chronic aldosterone administration impairs baroreceptor/baroreflex responses. We tested the hypothesis that aldosterone impairs baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA, sympathetic BRS) in humans. Twenty-six young (25 +/- 1 yr old, mean +/- SE) adults were examined in this study. BRS was determined by using the modified Oxford technique (bolus infusion of nitroprusside, followed 60 s later by bolus infusion of phenylephrine) in triplicate before (Pre) and 30-min after (Post) beginning aldosterone (experimental, 12 pmol.kg(-1).min(-1); n = 10 subjects) or saline infusion (control; n = 10). BRS was quantified from the R-R interval-systolic blood pressure (BP) (cardiovagal BRS) and MSNA-diastolic BP (sympathetic BRS) relations. Aldosterone infusion increased serum aldosterone levels approximately fourfold (P < 0.05) and decreased (P < 0.05) cardiovagal (19.0 +/- 2.3 vs. 15.6 +/- 1.7 ms/mmHg Pre and Post, respectively) and sympathetic BRS [-4.4 +/- 0.4 vs. -3.0 +/- 0.4 arbitrary units (AU).beat(-1).mmHg(-1)]. In contrast, neither cardiovagal (19.3 +/- 3.3 vs. 20.2 +/- 3.3 ms/mmHg) nor sympathetic BRS (-3.8 +/- 0.5 vs. -3.6 +/- 0.5 AU.beat(-1).mmHg(-1)) were altered (Pre vs. Post) in the control group. BP, heart rate, and MSNA at rest were similar in experimental and control subjects before and after the intervention. Additionally, neural and cardiovascular responses to a cold pressor test and isometric handgrip to fatigue were unaffected by aldosterone infusion (n = 6 subjects). These data provide direct experimental support for the concept that aldosterone impairs baroreflex function (cardiovagal and sympathetic BRS) in humans. Therefore, aldosterone may be an important determinant/modulator of baroreflex function in humans.     

Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats

This study compared the baroreflex control of lumbar and renal sympathetic nerve activity (SNA) in conscious rats. Arterial pressure (AP) and lumbar and renal SNA were simultaneously recorded in six freely behaving rats. Pharmacological estimates of lumbar and renal sympathetic baroreflex sensitivity (BRS) were obtained by means of the sequential intravenous administration of sodium nitroprusside and phenylephrine. Sympathetic BRS was significantly (P < 0.05) lower for lumbar [3.0 +/- 0.4 normalized units (NU)/mmHg] than for renal (7.6 +/- 0.6 NU/mmHg) SNA. During a 219-min baseline period, spontaneous lumbar and renal BRS were continuously assessed by computing the gain of the transfer function relating AP and SNA at heart rate frequency over consecutive 61.4-s periods. The transfer gain was considered only when coherence between AP and SNA significantly differed from zero, which was verified in 99 +/- 1 and 96 +/- 3% of cases for lumbar and renal SNA, respectively. When averaged over the entire baseline period, spontaneous BRS was significantly (P < 0.05) lower for lumbar (1.3 +/- 0.2 NU/mmHg) than for renal (2.3 +/- 0.3 NU/mmHg) SNA. For both SNAs, spontaneous BRS showed marked fluctuations (variation coefficients were 26 +/- 2 and 28 +/- 2% for lumbar and renal SNA, respectively). These fluctuations were positively correlated in five of six rats (R = 0.44 +/- 0.06; n = 204 +/- 8; P < 0.0001). We conclude that in conscious rats, the baroreflex control of lumbar and renal SNA shows quantitative differences but is modulated in a mostly coordinated way.     

Central actions of angiotensin II on spontaneous baroreflex sensitivity in the trout Onc orhynchus mykiss

The goal of the present study was to investigate the central action of native angiotensin II (ANG II) on the spontaneous baroreflex sensitivity (BRS) in unanesthetized trout. The animals were equipped with two subcutaneous electrocardiographic (ECG) electrodes, a dorsal aorta catheter and an intracerebroventricular (ICV) cannula which was inserted within the third ventricle of the brain. The ECG and the systolic blood pressure (SBP) signals were recorded during a pre-injection period of 5 min and during five post-injection periods of 5 min. All injections were made at the fifth minute of the test. The time-series were processed with a sequence technique in order to detect the sequences of three or more consecutive increases in the SBP pulse, or three or more decreases in the SBP pulse correlated respectively with one delay beat increase of the RR interval of the ECG signal or shortening of this interval. The slope of the average regression line between the SBP and the RR intervals for each type of sequence was taken as a measure of the spontaneous BRS. Compared with pre-injection values, the ICV injection of vehicle (0.5 microl) had no effect on heart rate (HR), SBP, the total number of positive or negative sequences or on the spontaneous BRS during the post-injection periods. By contrast, ANG II at doses of 5 and 50 pmol increased HR but only 50 pmol ANG II elevated SBP. For all doses, ANG II depressed the spontaneous BRS, but the peptide had no effect upon the number of each baroreflex sequences. Intra-arterial injections of atropine dramatically reduced the number of positive and negative baroreflex sequences and decreased the sensitivity of the few remaining sequences, suggesting that the autonomic control of the cardiac BRS was solely due to vagal parasympathetic control. In atropinized trout the ICV injection of 5 pmol ANG II had no effect upon HR, SBP and the baroreflex parameters. This study determines for the first time the spontaneous BRS in a non-mammalian species and demonstrates an inhibitory action of ICV injection of ANG II upon this variable through a probable control of the vagal parasympathetic activity.     

Gender difference in baroreflex-mediated bradycardia in young rats: role of cardiac sympathetic and parasympathetic components.

In a previous clinical study we have demonstrated a significantly lower baroreflex-mediated bradycardic response in young women compared with men. The present study determined whether sexual dimorphism in baroreflex sensitivity in young rats also covers the reflex tachycardic response. The study was then extended to test the hypothesis that an attenuated cardiac cholinergic component of the baroreflex heart rate response in females may account for the gender difference. Baroreflex sensitivity (BRS) was expressed as the regression coefficient of the reciprocal relationship between evoked changes in blood pressure and heart rate. BRS measured in conscious rats with phenylephrine (BRS(PE)) and nitroprusside (BRS(NP)) represented the reflex bradycardic and tachycardic responses, respectively. Female rats exhibited significantly lower BRS(PE) compared with male rats (-1.53+/-0.1 vs. -2.36+/-0.13 beats x min(-1) x mmHg(-1); p < 0.05) but similar BRS(NP) (-2.60+/-0.20 vs. -2.29+/-0.17 beats x min(-1) x mmHg(-1)). Blockade of cardiac muscarinic receptors with atropine methyl bromide elicited greater attenuation of BRS(PE) in male than in female rats (72+/-4.6 vs. 53+/-6.7% inhibition; p < 0.01) and abolished the gender difference. In male rats cardiac muscarinic blockade attenuated BRS(PE) significantly more than did cardiac beta-adrenergic receptor blockade with propranolol (72+/-4.6 vs. 43+/-2.7; p < 0.01), which suggests greater dependence of BRS(PE) on the parasympathetic component. In females, muscarinic and beta-adrenergic blockade elicited similar attenuation of BRS(PE). The findings suggest that (i) BRS is differentially influenced by gender; female rats exhibit substantially lower BRS(PE) but similar BRS(NP) compared with age-matched male rats and (ii) the sexual dimorphism in BRS(PE) results, at least partly, from a smaller increase in vagal outflow to the heart in response to baroreceptor activation.     

Altered hemodynamic regulation and reflex control during exercise and recovery in obese boys

The aims of the present study were to assess in obese and lean boys 1) the hemodynamic responses and baroreflex sensitivity (BRS) to isometric handgrip exercise (HG) and recovery and 2) the muscle metaboreflex-induced blood pressure response and the variables that determine this response. Twenty-seven boys (14 obese and 13 lean boys, body mass index: 29.2 ± 0.9 vs. 18.9 ± 0.3 kg/m(2), respectively) participated. The testing protocol involved 3 min of baseline, 3 min of HG (30% maximum voluntary contraction), 3 min of circulatory occlusion, and 3 min of recovery. The same protocol was repeated without occlusion. At baseline, no differences were detected between groups in beat-to-beat arterial pressure (AP), heart rate (HR), and BRS; however, obese boys had higher stroke volume and lower total peripheral resistance than lean boys (P < 0.05). During HG, lean boys exhibited higher HR and lower BRS compared with their obese counterparts. In lean boys, BRS decreased during HG compared with baseline, whereas in obese boys, it was not significantly modified. In lean boys, TPR was elevated during HG and declined after exercise, whereas in obese boys, TPR did not significantly decrease after exercise cessation. In the postexercise period, BRS in lean boys returned to baseline, whereas an overshoot was observed in obese boys. Postexercise BRS was correlated with body mass index (R = 0.56, P < 0.05). Although the metaboreflex-induced increase in AP was similar between obese and lean children, it was achieved via different mechanisms: in lean children, total peripheral resistance was the main contributor to AP maintenance during the metaboreflex, whereas in obese children, stroke volume significantly contributed to AP maintenance during the metaboreflex. In conclusion, obese normotensive children demonstrated altered cardiovascular hemodynamics and reflex control during exercise and recovery.     

Characterization of bovine respiratory syncytial virus proteins and mRNAs and generation of cDNA clones to the viral mRNAs.

We have characterized the proteins and mRNAs of bovine respiratory syncytial (BRS) virus strain 391-2 and constructed cDNA clones corresponding to 9 of the 10 BRS virus mRNAs. The proteins of BRS virus-infected cells were compared with the proteins from human respiratory syncytial (HRS) virus-infected cells. Nine proteins specific to BRS virus-infected cells, corresponding to nine HRS virus proteins, were identified. Only a BRS virus polymerase protein remains to be identified. The BRS virus G glycoprotein showed major antigenic differences from the HRS virus G glycoprotein by immunoprecipitation and Western (immuno-) blot analysis, whereas the BRS virus F, N, M, and P proteins showed antigenic cross-reactivity with their HRS virus counterparts. Analysis of RNAs from BRS virus-infected cells showed virus-specific RNAs which had electrophoretic mobilities similar to those of mRNAs of HRS virus but which hybridized poorly or not at all with HRS virus-specific probes in Northern (RNA) blot analysis. To analyze the BRS virus RNAs further, cDNA clones to the BRS virus mRNAs were generated. Nine separate groups of clones were identified and shown to correspond to nine BRS virus mRNAs by Northern blot analysis. A 10th BRS virus large mRNA was identified by analogy with the HRS virus polymerase mRNA. These data show that like HRS virus, BRS virus has 10 genes coding for 10 mRNAs.     

Determination of baroreflex sensitivity during the modified Oxford maneuver by trigonometric regressive spectral analysis

Background

Differences in spontaneous and drug-induced baroreflex sensitivity (BRS) have been attributed to its different operating ranges. The current study attempted to compare BRS estimates during cardiovascular steady-state and pharmacologically stimulation using an innovative algorithm for dynamic determination of baroreflex gain.

Methodology/Principal Findings

Forty-five volunteers underwent the modified Oxford maneuver in supine and 60° tilted position with blood pressure and heart rate being continuously recorded. Drug-induced BRS-estimates were calculated from data obtained by bolus injections of nitroprusside and phenylephrine. Spontaneous indices were derived from data obtained during rest (stationary) and under pharmacological stimulation (non-stationary) using the algorithm of trigonometric regressive spectral analysis (TRS). Spontaneous and drug-induced BRS values were significantly correlated and display directionally similar changes under different situations. Using the Bland-Altman method, systematic differences between spontaneous and drug-induced estimates were found and revealed that the discrepancy can be as large as the gain itself. Fixed bias was not evident with ordinary least products regression. The correlation and agreement between the estimates increased significantly when BRS was calculated by TRS in non-stationary mode during the drug injection period. TRS-BRS significantly increased during phenylephrine and decreased under nitroprusside.

Conclusions/Significance

The TRS analysis provides a reliable, non-invasive assessment of human BRS not only under static steady state conditions, but also during pharmacological perturbation of the cardiovascular system.     

Drought tolerance in two oil palm hybrids as related to adjustments in carbon metabolism and vegetative growth

Drought tolerance was examined in two oil palm hybrids (BRS Manicoré and BRS C 2501) grown in large pots and subjected to long-term drought (57 days) and rehydration. Regardless of hybrids, predawn water potential (Ψ _pd), net photosynthesis rates, and stomatal conductance decreased similarly upon drought imposition, but the absolute values of these variables were lower in BRS C 2501 than in BRS Manicoré. Overall, drought-induced decreases in activities of key enzymes associated with carbon metabolism, including Rubisco, ADP-glucose pyrophosphorylase, and sucrose-phosphate synthase, were stronger in BRS C 2501 than in BRS Manicoré. Our data suggest that synthesis of starch (and possibly sucrose) was fundamentally limited by a lower substrate availability rather than by enzymatic constraints, particularly until day 34 after suspending watering. Drought stress provoked similar decreases in biomass accumulation in either hybrid; however, BRS Manicoré plants displayed higher total leaf area and root length coupled with greater relative decreases in dry matter of above-ground parts than of roots as compared to BRS C 2501, thereby leading to an increased root-to-above ground ratio in the former. Upon resuming irrigation, the slow recovery of Ψ _pd preceded the recovery of stomatal conductance and photosynthesis irrespective of hybrid. BRS Manicoré was better able to recover enzyme activities and carbohydrate status than BRS C 2501. In conclusion, both hybrids could tolerate (or survive) the severe drought conditions, but, overall, BRS Manicoré plants were better able to adjust its physiological, morphological, and biochemical traits to cope with drought than did BRS C 2501.     

Autonomic control of the respiratory-hemodynamic system in 8-to 11-year-old children with different baroreflex sensitivities

The efficiency of baroreflex control depends on the baroreflex sensitivity (BRS), which is defined as the ratio of the change in the heart rate (HR) to the change in the blood pressure (BP). The BRS value may be used for assessing the autonomic control of the cardiovascular system and the degree of autonomic dysfunction. Until recently, the baroreflex had not been assessed in a large population of healthy subjects. In this study, the BRS was estimated by the ratio of the low-frequency component of the HR spectrum and the low-frequency component of the rhythm of the systolic BP. For assessing the arterial baroreflex in children, the BRSs for spontaneous and induced baroreflexes were compared. Sex-and age-related differences in BRS were found in 8-to-11-year-old children, and correlations between BRS and some spectral components of HR variability (HRV) and BP rhythm variability were determined. Cluster analysis of the BRS calculated for the spontaneous baroreflex at rest was used to distinguish three clusters of subjects (with high, medium, and low BRSs). These clusters differed in the variability of the basic parameter and size and showed sex-related differences.     

Overweight and decreased baroreflex sensitivity as independent risk factors for hypertension in children, adolescents, and young adults

We studied the relationship between blood pressure (BP), body mass index (BMI, kg/m(2)) and baroreflex sensitivity (BRS, ms/mmHg) in adolescents. We examined 34 subjects aged 16.2+/-2.4 years who had repeatedly high causal BP (H) and 52 controls (C) aged 16.4+/-2.2 years. Forty-four C and 22 H were of normal weight (BMI between 19-23.9), and 8 C and 12 H were overweight (BMI between 24-30). Systolic BP was recorded beat-to-beat for 5 min (Finapres, controlled breathing 0.33 Hz). BRS was determined by the cross-spectral method. The predicting power of BMI and BRS for hypertension was evaluated by sensitivity, specificity, and receiver operating curve (ROC - plot of sensitivity versus specificity). H compared with C had lower BRS (p<0.01) and higher BMI (p<0.05). Multiple logistic regression analysis (p<0.001) revealed that a decreased BRS (p<0.05) and an increased BMI (p<0.01) were independently associated with an increased risk of hypertension. No correlation between BMI and BRS was found either in H or in C. Following optimal critical values by ROC, the sensitivity, specificity and area under ROC were determined for: BMI - 22.2 kg/m(2), 61.8 %, 69.2 %, 66.0 %; BRS - 7.1 ms/mmHg, 67.7 %, 69.2 %, 70.0 %; BMI and BRS - 0.439 a.u., 73.5 %, 82.7 %, and 77.3 %. Decreased BRS and overweight were found to be independent risk factors for hypertension.     

Reduced baroreflex sensitivity in alcoholic cirrhosis: relations to hemodynamics and humoral systems

In cirrhosis, arterial vasodilatation leads to central hypovolemia and activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. As the liver disease and circulatory dysfunction may affect baroreflex sensitivity (BRS), we assessed BRS in a large group of patients with cirrhosis and in controls who were all supine and some after 60 degrees passive head-up and 30 degrees head-down tilting in relation to central hemodynamics and activity of the sympathetic nervous and renin-angiotensin-aldosterone systems. One-hundred and five patients (Child classes A/B/C: 21/55/29) and 25 (n=11 + 14) controls underwent a full hemodynamic investigation. BRS was assessed by cross-spectral analysis of variabilities between blood pressure and heart rate time series. The median BRS was significantly lower in the supine cirrhotic patients, 3.7 (range 0.3-30.7) ms/mmHg than in matched controls (n=11): 14.3 (6.1-23.6) ms/mmHg, P<0.001. A stepwise multiple-regression analysis revealed that serum sodium (P=0.044), heart rate (P=0.027), and central circulation time (P=0.034) independently correlated with BRS. Head-down tilting had no effects on BRS, but, after head-up tilting, BRS was similar in the patients (n=23) and controls (n=14). In conclusion, BRS is reduced in cirrhosis in the supine position and relates to various aspects of cardiovascular dysfunction, but no further reduction was observed in parallel with the amelioration of the hyperdynamic circulation after head-up tilting. The results indicate that liver dysfunction and compensatory mechanisms to vasodilatation may be involved in the low BRS, which may contribute to poor cardiovascular adaptation in cirrhosis.     

Nucleotide sequence analysis and expression from recombinant vectors demonstrate that the attachment protein G of bovine respiratory syncytial virus is distinct from that of human respiratory syncytial virus

Bovine respiratory syncytial (BRS) virus causes a severe lower respiratory tract disease in calves similar to the disease in children caused by human respiratory syncytial (HRS) virus. While there is antigenic cross-reactivity among the other major viral structural proteins, the major glycoprotein, G, of BRS virus and that of HRS virus are antigenically distinct. The G glycoprotein has been implicated as the attachment protein for HRS virus. We have carried out a molecular comparison of the glycoprotein G of BRS virus with the HRS virus counterparts. cDNA clones corresponding to the BRS virus G glycoprotein mRNA were isolated and analyzed by dideoxynucleotide sequencing. The BRS virus G mRNA contained 838 nucleotides exclusive of poly(A) and had a major open reading frame coding for a polypeptide of 257 amino acid residues. The deduced amino acid sequence of the BRS virus G polypeptide showed only 29 to 30% amino acid identity with the G protein of either the subgroup A or B HRS virus. However, despite this low level of identity, there were strong similarities in the predicted hydropathy profiles of the BRS virus and HRS virus G proteins. A cDNA molecule containing the complete BRS virus G major open reading frame was inserted into the thymidine kinase gene of vaccinia virus by homologous recombination, and a recombinant virus containing the BRS virus G protein gene was isolated. This recombinant virus expressed the BRS virus G protein, as demonstrated by Western immunoblot analysis and immunofluorescence of infected cells. The BRS virus G protein expressed from the recombinant vector was transported to and expressed on the surface of infected cells. Antisera to the BRS virus G protein made by using the recombinant vector to immunize animals recognized the BRS virus attachment protein but not the HRS virus G protein and vice versa, confirming the lack of antigenic cross-reactivity between the BRS and HRS virus attachment proteins. On the basis of the data presented here, we conclude that BRS virus should be classified within the genus Pneumovirus in a group separate from HRS virus and that it is no more closely related to HRS virus subgroup A than it is to HRS virus subgroup B.     

A dampening effect of pulse interval variability on blood pressure variations with respect to primary variability in blood pressure during exercise

The correlation between baroreflex sensitivity (BRS) and the spectrum component at a frequency of 0.1 Hz of pulse intervals (PI) and systolic blood pressure (SBP) was studied. SBP and PI of 51 subjects were recorded beat-to-beat at rest (3 min), during exercise (0.5 W/kg of body weight, 9 min), and at rest (6 min) after exercise. BRS was determined by a spectral method (a modified alpha index technique). The subjects were divided into groups according to the spectral amplitude of SBP at a frequency of 0.1 Hz. The following limits of amplitude (in mm Hg) were used: very high > 5.4 (VH); high 5.4 > H > 3 (H); medium 3 > M > 2 (M), low < 2 (L). We analyzed the relationships between 0.1 Hz variability in PI and BRS at rest, during the exercise and during recovery in subgroups VH, H, M, L. The 0.1 Hz variability of PI increased significantly with increasing BRS in each of the groups with identical 0.1 Hz variability in SBP. This relationship was shifted to the lower values of PI variability at the same BRS with a decrease in SBP variability. The primary SBP variability increased during exercise. The interrelationship between the variability of SBP, PI and BRS was identical at rest and during exercise. A causal interrelationship between the 0.1 Hz variability of SBP and PI, and BRS was shown. During exercise, the increasing primary variability in SBP due to sympathetic activation was present, but it did not change the relationship between variability in pulse intervals and BRS.     

Can we detect the development of baroreflex sensitivity in humans between 11 and 20 years of age?

The aim of the study was to determine changes of baroreflex sensitivity in humans between 11 and 20 years of age. Continuous 5 min blood pressure recordings using a Finapres were taken in 415 healthy subjects while in a sitting, resting position (breathing at a frequency of 0.33 Hz). Beat-by-beat values of interbeat intervals (IBI) or heart rate, and systolic and diastolic blood pressures were measured. Baroreflex sensitivity in ms/mmHg (BRS) and in mHz/mmHg (BRSf) was determined at an average frequency of 0.1 Hz by spectral analysis. BRS did not correlate with age, but BRSf significantly decreased with age (p < 0.001). BRS correlated with mean IBI (p < 0.001) in all subjects and also in the particular subgroups, but BRSf was IBI-independent. Results of multiregression equations were BRS = 1.37 - 0.56 x age (years) + 0.02 x IBI (ms) (p < 0.001 for BRS vs. age and for BRS vs. IBI); BRSf = 34.74 - 0.97 x age (years) - 0.001 x IBI (ms) (p < 0.001 only for BRS vs. age), where age was measured in years and IBI was measured in ms. The limits of BRS were estimated for the total group: 5th percentile, 3.9; 50th percentile, 9.1; and 95th percentile, 18.7 ms/mmHg; and limits for BRSf were 5th percentile, 8.5; 50th percentile, 16.4; and 95th percentile, 33.6 mHz/mmHg. We conclude that IBI-dependent BRS was unchanged in the particular age groups, but the standardization of BRS on IBI decreased with age. BRSf was IBI-independent and better reflected the development of the BRS.     

Attenuation of sympathetic baroreflex sensitivity during the onset of acute mental stress in humans

Mental stress consistently induces a pressor response that is often accompanied by a paradoxical increase of muscle sympathetic nerve activity (MSNA). The purpose of the present study was to evaluate sympathetic baroreflex sensitivity (BRS) by examining the relations between spontaneous fluctuations of diastolic arterial pressure (DAP) and MSNA. We hypothesized that sympathetic BRS would be attenuated during mental stress. DAP and MSNA were recorded during 5 min of supine baseline, 5 min of mental stress, and 5 min of recovery in 32 young healthy adults. Burst incidence and area were determined for each cardiac cycle and placed into 3-mmHg DAP bins; the slopes between DAP and MSNA provided an index of sympathetic BRS. Correlations between DAP and MSNA were strong (> 0.5) during baseline in 31 of 32 subjects, but we evaluated the change in slope only for those subjects maintaining a strong correlation during mental stress (16 subjects). During baseline, the relation between DAP and MSNA was negative when expressed as either burst incidence [slope = -1.95 ± 0.18 bursts·(100 beats)?1)·mmHg?1; r = -0.86 ± 0.03] or total MSNA [slope = -438 ± 91 units·(beat)?1 mmHg?1; r = -0.76 ± 0.06]. During mental stress, the slope between burst incidence and DAP was significantly reduced [slope = -1.14 ± 0.12 bursts·(100 beats)?1·mmHg?1; r = -0.72 ± 0.03; P < 0.01], indicating attenuation of sympathetic BRS. A more detailed analysis revealed an attenuation of sympathetic BRS during the first 2 min of mental stress (P < 0.01) but no change during the final 3 min of mental stress (P = 0.25). The present study demonstrates that acute mental stress attenuates sympathetic BRS, which may partially contribute to sympathoexcitation during the mental stress-pressor response. However, this attenuation appears to be isolated to the onset of mental stress. Moreover, variable MSNA responses to mental stress do not appear to be directly related to sympathetic BRS.     

Increased sympathetic and decreased parasympathetic cardiovascular modulation in normal humans with acute sleep deprivation.

Cardiovascular autonomic modulation during 36 h of total sleep deprivation (SD) was assessed in 18 normal subjects (16 men, 2 women, 26.0 +/- 4.6 yr old). ECG and continuous blood pressure (BP) from radial artery tonometry were obtained at 2100 on the first study night (baseline) and every subsequent 12 h of SD. Each measurement period included resting supine, seated, and seated performing computerized tasks and measured vigilance and executive function. Subjects were not supine in the periods between measurements. Spectral analysis of heart rate variability (HRV) and BP variability (BPV) was computed for cardiac parasympathetic modulation [high-frequency power (HF)], sympathetic modulation [low-frequency power (LF)], sympathovagal balance (LF/HF power of R-R variability), and BPV sympathetic modulation (at LF). All spectral data were expressed in normalized units [(total power of the components/total power-very LF) x 100]. Spontaneous baroreflex sensitivity (BRS), based on systolic BP and pulse interval powers, was also measured. Supine and sitting, BPV LF was significantly increased from baseline at 12, 24, and 36 h of SD. Sitting, HRV LF was increased at 12 and 24 h of SD, HRV HF was decreased at 12 h SD, and HRV LF/HF power of R-R variability was increased at 12 h of SD. BRS was decreased at 24 h of SD supine and seated. During the simple reaction time task (vigilance testing), the significantly increased sympathetic and decreased parasympathetic cardiac modulation and BRS extended through 36 h of SD. In summary, acute SD was associated with increased sympathetic and decreased parasympathetic cardiovascular modulation and decreased BRS, most consistently in the seated position and during simple reaction-time testing.     

Age-dependent relationship between the carotid intima-media thickness, baroreflex sensitivity, and the inter-beat interval in normotensive and hypertensive subjects

The interrelationship between baroreflex sensitivity expressed in ms/mm Hg (BRS) or in Hz/mm Hg (BRSf), carotid wall thickness (IMT), and age was investigated in hypertensive and normotensive subjects with respect to the mean inter-beat interval (IBI) and blood pressure (BP). BP monitoring was performed in 25 treated hypertensives (Hy; 47.4+/-9.2 years of age) and 23 normotensives (Norm; 44.5+/-8.1 years). IMT was measured by ultrasonography. BRS and BRSf were determined by the spectral method (five-minute non-invasive beat-to-beat recording of BP and IBI, Finapres, controlled breathing at a frequency of 0.33 Hz). Significant differences between Hy and Norm were detected in IMT (Hy: 0.624+/-0.183, Norm: 0.522+/-0.070 mm; p<0.01), BRS (Hy: 3.5+/-1.6, Norm: 5.7+/-2.3 ms/mm Hg; p<0.01), BRSf (Hy: 0.005+/-0.002, Norm: 0.009+/-0.004 Hz/mm Hg; p<0.01), systolic BP (Hy: 131+/-21, Norm: 116+/-17 mm Hg; p<0.01) and diastolic BP (Hy: 77+/-16, Norm: 64+/-12 mm Hg; p<0.01). A significant correlation was found between age and IMT (Norm: 0.523, p<0.05; Hy+Norm: 0.419, p<0.01), age and BRS (Norm: -0.596, p< 0.01; Hy+Norm: -0.496, p<0.01), age and BRSf (Norm: -0.555, p<0.01; Hy: -0.540, p <0.01; Hy+Norm: -0.627, p<0.01), age and IBI (Hy: 0.478, p<0.05), age and diastolic BP (Hy: -0.454, p<0.05), BRS and IMT (Hy+Norm: -0.327, p<0.05) and BRSf and IMT (Hy+Norm: -0.358, p<0.05). Hypertensive patients have increased IMT and decreased BRS and BRSf. The positive correlation between age and IMT and the negative correlation between age and BRS and BRSf are in agreement with the hypothesis that the age-dependent decrease of baroreflex sensitivity corresponds to the age-related structural changes of the carotid wall. Using two indices of baroreflex sensitivity, BRS and BRSf, we could show that baroreflex sensitivity in hypertensives is lower not only due to thickening of the carotid wall, but also due to aging.     

Effect of acute hyperlipidemia on autonomic and cardiovascular control in humans.

Blood lipids may detrimentally affect autonomic and circulatory control. We tested the hypotheses that acute elevations in free fatty acids and triglycerides (acute hyperlipidemia) impair baroreflex control of cardiac period [cardiovagal baroreflex sensitivity (BRS)] and muscle sympathetic nerve activity (MSNA: sympathetic BRS), increase MSNA at rest, and augment physiological responses to exercise. Eighteen young adults were examined in this randomized, double-blinded, and placebo-controlled study. BRS was determined using the modified Oxford technique before (pre) and 60 min (post) after initiating infusion of Intralipid (0.8 ml x m(-2) x min(-1)) and heparin (1,000 U/h) (experimental; n = 12) to induce acute hyperlipidemia, or saline (0.8 ml x m(-2) x min(-1)) and heparin (1,000 U/h) (control; n = 6). Responses to isometric handgrip to fatigue (IHG) were also determined. Blood pressure increased more (P < 0.05) in experimental than control subjects during the infusion. MSNA at rest (14 +/- 2 vs. 11 +/- 1 bursts/min), cardiovagal (19.8 +/- 1.8 vs. 19.1 +/- 2.4 ms/mmHg pre and post, respectively) and sympathetic BRS (-5.5 +/- 0.6 vs. -5.2 +/- 0.4 au x beat(-1) x mmHg(-1)), and the neural and cardiovascular responses to IHG were unchanged by acute hyperlipidemia (pre vs. post) in experimental subjects. Similarly, MSNA at rest (10 +/- 2 vs. 12 +/- 2 bursts/min), cardiovagal (22.1 +/- 4.0 vs. 21.0 +/- 4.6 ms/mmHg) and sympathetic BRS (-5.8 +/- 0.5 vs. -5.5 +/- 0.5 au x beat(-1) x mmHg(-1)), and the neural and cardiovascular responses to IHG were unchanged by the infusion in control subjects. These data do not provide experimental support for the concept that acute hyperlipidemia impairs reflex cardiovagal or sympathetic regulation in humans.