Comparison of blood pro/antioxidant levels before and after acute exercise in athletes and non-athletes

The aims of our study were to assess the redox state of adolescent athletes and non-athletes both at rest and after acute exposure to physical load and to find relations between parameters of redox state and morphofunctional characteristics of subjects. 58 young handball players and 37 non-athletes were subjected to body composition analysis, measuring of maximal oxygen consumption and blood sampling immediately before and after a maximal progressive exercise test. At rest, athletes had significantly higher superoxide dismutase (SOD) and catalase (CAT) activity, higher levels of glutathione (GSH) and nitric oxide (NO) and lower levels of lipid peroxidation (TBARS) compared with non-athletes. A maximal exercise test induced statistically significant rise of superoxide anion radical (O2-), hydrogen peroxide (H2O2) and NO levels in non-athletes, while TBARS levels decreased. Athletes experienced the fall in NO levels and the fall in CAT activity. After exercise, athletes had significantly lower levels of O2- compared with non-athletes. Two way repeated measures ANOVA showed that the response of O2-, NO and TBARS to the exercise test was dependent on the sports engagement (training experience) of subjects. Significant correlations between morphofunctional and redox parameters were found. These results suggest that physical fitness affects redox homeostasis.     

alpha-Tocopherol transfer protein expression in rat liver exposed to hyperoxia

-Tochopherol transfer protein ( TTP), a 32 kDa protein exclusively expressed in liver cytosol, has a high binding affinity for -tochopherol. The factors that regulate the expression of hepatic TTP are not clearly understood. In this study, we investigated whether or not exposure to hyperoxia (95% O 2 for 48 h) could alter the expression of hepatic TTP. We also examined the association between the expression of antioxidant enzymes (hepatic glutathione peroxidase (GPX) and Mn-superoxide dismutase (Mn-SOD)) and the expression of hepatic TTP. The levels of thiobarbituric acid-reactive substances (TBARS) in both plasma and liver were significantly higher after rats were exposed to hyperoxia for 48 h when compared with the levels in control rats. Northern blotting showed a decrease in the expression of TTP messenger RNA (mRNA) after hyperoxia, although the TTP protein level remained constant. Expression of Mn-SOD mRNA and protein, as well as the expression of GPX mRNA, were stable after hyperoxia. These findings indicate that mRNA for hepatic TTP, rather than Mn-SOD or GPX, may be highly responsive to oxidative stress.     

Adrenergic control of venous capacitance during moderate hypoxia in the rainbow trout (Oncorhynchus mykiss): role of neural and circulating catecholamines

Central venous blood pressure (P(ven)) increases in response to hypoxia in rainbow trout (Oncorhynchus mykiss), but details on the control mechanisms of the venous vasculature during hypoxia have not been studied in fish. Basic cardiovascular variables including P(ven), dorsal aortic blood pressure, cardiac output, and heart rate were monitored in vivo during normoxia and moderate hypoxia (P(W)O(2) = approximately 9 kPa), where P(W)O(2) is water oxygen partial pressure. Venous capacitance curves for normoxia and hypoxia were constructed at 80-100, 90-110, and 100-120% of total blood volume by transiently (8 s) occluding the ventral aorta and measure P(ven) during circulatory arrest to estimate the mean circulatory filling pressure (MCFP). This allowed for estimates of hypoxia-induced changes in unstressed blood volume (USBV) and venous compliance. MCFP increased due to a decreased USBV at all blood volumes during hypoxia. These venous responses were blocked by alpha-adrenoceptor blockade with prazosin (1 mg/kg body mass). MCFP still increased during hypoxia after pretreatment with the adrenergic nerve-blocking agent bretylium (10 mg/kg body mass), but the decrease in USBV only persisted at 80-100% blood volume, whereas vascular capacitance decreased significantly at 90-110% blood volume. In all treatments, hypoxia typically reduced heart rate while cardiac output was maintained through a compensatory increase in stroke volume. Despite the markedly reduced response in venous capacitance after adrenergic blockade, P(ven) always increased in response to hypoxia. This study reveals that venous capacitance in rainbow trout is actively modulated in response to hypoxia by an alpha-adrenergic mechanism with both humoral and neural components.     

Hydrogen peroxide increases the activities of soxRS regulon enzymes and the levels of oxidized proteins and lipids in Escherichia coli

The effects of hydrogen peroxide treatments on Escherichia coli KS400 and AB1157 cells were assessed by monitoring the accumulation of oxidative damage products, carbonyl proteins and thiobarbituric acid-reactive substances (TBARS), as well as the activities of selected antioxidant enzymes. H(2)O(2) treatment stimulated increases in both TBARS and carbonyl protein levels in dose- and time-dependent manners in KS400 cells. The accumulation of TBARS was much more variable with H(2)O(2) treatment; TBARS content was significantly increased in response to 5 microM H(2)O(2), whereas a significant increase in carbonyl protein content occurred at 100 microM H(2)O(2). Similarly, treatment with 20 microM hydrogen peroxide for different lengths of time resulted in peak TBARS accumulation by 20 min, whereas carbonyl protein levels were significantly elevated only after 60 min. In AB1157 cells, treatment with 20 microM hydrogen peroxide for 20 min led to strong increases in both carbonyl protein and TBARS levels. This treatment also triggered increased activities of enzymes of the oxyR regulon (catalase, peroxidase, and glutathione reductase) in both strains. In the AB1157 strain, H(2)O(2) exposure also increased the activities of two enzymes of the soxRS regulon (superoxide dismutase and glucose-6-phosphate dehydrogenase) by 50-60%. The data show differential variability of lipids versus proteins to oxidative damage induced by H(2)O(2,) as well as strain-specific differences in the accumulation of damage products and the responses by antioxidant enzymes to H(2)O(2) stress.     

Plasma prolactin responses to acute changes in central blood volume in man

The present study examined the relationship between plasma prolactin (PRL) and central blood volume (CBV) in man. 6 adult males lay in a lower body pressure box at a thermoneutral ambient temperature (27 degrees C) on three occasions. On each occasion a 70-min control period was followed by a 20-min exposure to a lower body pressure of either 0 mm Hg, -20 (lower body negative pressure; LBNP), or +10 mm Hg (lower body positive pressure; LBPP), followed by a 60-min recovery period. Blood was drawn and urine collected at 30-min intervals. Blood pressure and heart rate were monitored at 30-min intervals during control and recovery periods and at 10-min intervals during lower body pressure exposure. Neither 0 mm Hg, LBNP, nor LBPP altered plasma osmolality, sodium, or potassium levels. Increasing CBV by LBPP increased systemic blood pressure (p less than 0.01) but had no effect on heart rate, plasma PRL, or urine osmolality. LBNP, in contrast, increased heart rate (p less than 0.05). Half of the subjects undergoing LBNP developed presyncopal symptoms, characteristic of a vasovagal reaction which includes precipitous hypotension. Subjects developing these symptoms tended to exhibit an increase in plasma PRL and an increase in urine osmolality. Asymptomatic subjects demonstrated no change in plasma PRL or urine osmolality. In addition, subjects exhibiting a PRL response to LBNP had a higher control period plasma PRL baseline (231%) than did asymptomatic subjects. These data suggest that while plasma PRL levels are not sensitive to nonhypotensive changes in CBV, they do respond to hypotensive decreases in CBV and/or its associated nausea.(ABSTRACT TRUNCATED AT 250 WORDS)     

Estrogen replacement in middle-aged women: thermoregulatory responses to exercise in the heat.

Thermoregulatory, cardiovascular, and body fluid responses during exercise in the heat were tested in five middle-aged (48 +/- 2 yr) women before and after 14-23 days of estrogen replacement therapy (ERT). The heat and exercise challenge consisted of a 40-min rest period followed by semirecumbent cycle exercise (approximately 40% maximal O2 uptake) for 60 min. At rest, the ambient temperature was elevated from a thermoneutral (dry bulb temperature 25 degrees C; wet bulb temperature 17.5 degrees C) to a warm humid (dry bulb temperature 36 degrees C; wet bulb temperature 27.5 degrees C) environment. Esophageal (Tes) and rectal (Tre) temperatures were measured to estimate body core temperature while arm blood flow and sweating rate were measured to assess the heat loss response. Mean arterial pressure and heart rate were measured to evaluate the cardiovascular response. Blood samples were analyzed for hematocrit (Hct), hemoglobin ([Hb]), plasma 17 beta-estradiol (E2), progesterone (P4), protein, and electrolyte concentrations. Plasma [E2] was significantly (P < 0.05) elevated by ERT without affecting the plasma [P4] levels. After ERT, Tes and Tre were significantly (P < 0.05) depressed by approximately 0.5 degrees C, and the Tes threshold for the onset of arm blood flow and sweating rate was significantly (P < 0.05) lower during exercise. After ERT, heart rate during exercise was significantly lower (P < 0.05) without notable variation in mean arterial pressure. Isotonic hemodilution occurred with ERT evident by significant (P < 0.05) reductions in Hct and [Hb], whereas plasma tonicity remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intermittent hypoxia modulates nitric oxide-dependent vasodilation and capillary perfusion during ischemia-reperfusion-induced damage

The microvascular function of nitric oxide (NO) during ischemia-reperfusion (I/R) in intermittent hypoxia (IH)-pretreated hamsters was analyzed using 20 mg/kg of the nonselective NO inhibitor N(omega)-nitro-l-arginine methyl ester (l-NAME) and 5 mg/kg of the preferential inducible NO inhibitor S-methylisothiourea sulphate (SMT) injected before I/R. Studies were made in the hamster cheek pouch microcirculation (intravital fluorescence microscopy). IH consisted of 6 min of 8% O(2) breathing followed by 6 min of 21% O(2) for every 8 h for 21 days. Normoxia controls (NCs) were exposed to room air for the same period. The effects were characterized in terms of systemic hemodynamics, diameter, flow, wall shear stress in arterioles, capillary perfusion, and the concentrations of thiobarbituric acid-reactive substances (TBARS) and plasma NO, assessed as nitrite/nitrate (NOx) levels. IH did not change arterial blood pressure and increased hematocrit and shear stress. IH increased NOx and TBARS levels and reduced arterial diameter, blood flow, and capillary perfusion versus the NC. Conversely, TBARS and NOx were lower during I/R in IH-pretreated hamsters, resulting in vasodilation and the increase of capillary perfusion and shear stress. After IH, capillary perfusion was reduced by 24% (2.3%) and enhanced by 115% (1.7%) after I/R (P < 0.05). Both modalities of NO blockade decreased NOx generation and increased TBARS versus IH. l-NAME and SMT induced a significant decrease in arteriolar diameter, blood flow, and capillary perfusion (P < 0.05). l-NAME enhanced TBARS more than SMT and aggravated I/R damage. In conclusion, we demonstrated that preconditioning with IH greatly reduces oxidative stress and stimulates NO-induced vasodilation during I/R injury, thus maintaining capillary perfusion.     

Effects of lethal levels of environmental hypercapnia on cardiovascular and blood-gas status in yellowtail,Seriola quinqueradiata

The cardiorespiratory responses were examined in yellowtail, Seriola quinqueradiata exposed to two levels of hypercapnia (seawater equilibrated with a gas mixture containing 1% CO(2) (water PCO(2) = 7 mmHg) or 5% CO(2) (38 mmHg)) for 72 hr at 20 degrees C. Mortality was 100% within 8 hr at 5% CO(2), while no fish died at 1% CO(2). No cardiovascular variables (cardiac output, Q; heart rate, HR; stroke volume, SV and arterial blood pressure, BP) significantly changed from pre-exposure values during exposure to 1% CO(2). Arterial CO(2) partial pressure (PaCO(2)) significantly increased (P < 0.05), reaching a new steady-state level after 3 hr. Arterial blood pH (pHa) decreased initially (P < 0.05), but was subsequently restored by elevation of plasma bicarbonate ([HCO(3)(-)]). Arterial O(2) partial pressure (PaO(2)), oxygen content (CaO(2)), and hematocrit (Hct) were maintained throughout the exposure period. In contrast, exposure to 5% CO(2) dramatically reduced Q (P < 0.05) through decreasing SV (P < 0.05), although HR did not change. BP was transiently elevated (P < 0.05), followed by a precipitous fall before death. The pHa was restored incompletely despite a significant increase in [HCO(3)(-)]. PaO(2) decreased only shortly before death, whereas CaO(2) kept elevated due to a large increase in Hct (P < 0.05). We tentatively conclude that cardiac failure is a primary physiological disorder that would lead to death of fish subjected to high environmental CO(2) pressures.     

α-Tocopherol Transfer Protein Expression in Rat Liver Exposed to Hyperoxia

&#102 -Tochopherol transfer protein ( &#102 TTP), a 32 kDa protein exclusively expressed in liver cytosol, has a high binding affinity for &#102 -tochopherol. The factors that regulate the expression of hepatic &#102 TTP are not clearly understood. In this study, we investigated whether or not exposure to hyperoxia (>95% O 2 for 48 h) could alter the expression of hepatic &#102 TTP. We also examined the association between the expression of antioxidant enzymes (hepatic glutathione peroxidase (GPX) and Mn-superoxide dismutase (Mn-SOD)) and the expression of hepatic &#102 TTP. The levels of thiobarbituric acid-reactive substances (TBARS) in both plasma and liver were significantly higher after rats were exposed to hyperoxia for 48 h when compared with the levels in control rats. Northern blotting showed a decrease in the expression of &#102 TTP messenger RNA (mRNA) after hyperoxia, although the &#102 TTP protein level remained constant. Expression of Mn-SOD mRNA and protein, as well as the expression of GPX mRNA, were stable after hyperoxia. These findings indicate that mRNA for hepatic &#102 TTP, rather than Mn-SOD or GPX, may be highly responsive to oxidative stress.     

Dynamic changes in parameters of redox balance after mild heat stress in aged laying hens (Gallus gallus domesticus)

In order to evaluate the metabolic responses of laying hens induced by high temperature at later laying stage, nine 60-wk-old laying hens (Gallus gallus domesticus) were employed in the present study. The hens were exposed to 32 degrees C for 21 d and blood samples were obtained before and at 1, 7, 14 and 21 d of heat exposure. The reactive oxygen species (ROS) formed in blood during heat exposure were estimated by the ex vivo spin-trapping method. Body temperature and plasma concentrations of glucose, urate, creatine kinase (CK), triiodothyronine (T(3)), thyroxine (T(4)), corticosterone (CORT), thiobarbituric acid reacting substances (TBARS), ferric/reducing antioxidant power (FRAP) and superoxide dismutase (SOD) activity were measured. Plasma levels of glucose, CK and CORT were not significantly influenced by heat exposure at any time point. The circulating concentrations of T(3) were decreased while plasma T(4) levels changed in the opposite way. The formation of ROS was significantly augmented by heat exposure in laying hens though the body temperature was not significantly altered. The enhanced enzymatic and non-enzymatic antioxidant systems acted in concert to alleviate the heat stress evoked oxidative damage.     

mRNA expression of antioxidant enzymes (SOD, CAT and GSH-Px) and lipid peroxidative stress in liver of Atlantic salmon (Salmo salar) exposed to hyperoxic water during smoltification

The mRNA levels of three antioxidant genes, Cu/Zn superoxide dismutase (SOD), catalase (CAT) and phospholipid hydroperoxide glutathione peroxidase (GSH-Px), were quantified with real-time qRT-PCR in liver of Atlantic salmon Salmo salar exposed to 80% (normoxia), 105% and 130% O2 saturation for 54 days. The salmon were then translocated and exposed to 90% and 130% O2 saturation for additional 72 days during smoltification. TBARS and vitamin E levels in liver and the levels of oxidized glutathione (GSSG), total glutathione (GSH) and the resulting oxidative stress index (OSI) in blood were quantified as traditional oxidative stress markers. No significant mean normalized expression (MNE) differences of SOD, CAT or GSH-Px were found in liver after hyperoxia exposure at the two sampling times. Significantly decreased OSI was found in smolt exposed to 130% O2 saturation after 126 days (n = 18, P < 0.0001), indicating hyperoxia-induced oxidative stress. No effects were seen on growth, or on the levels of thiobarbituric reactive substances (TBARS) and vitamin E in liver after the exposure experiment. Overall, the mRNA expression of SOD, CAT and GSH-Px in liver related poorly with the hyperoxic exposure regimes, and more knowledge are needed before the expressed levels of these antioxidant genes can be applied as biomarkers of hyperoxia in Atlantic salmon.     

Oxygen consumption, blood lactate and inter-individual variation in the gulf killifish, Fundulus grandis, during hypoxia and recovery

Rates of oxygen consumption (M(O(2))) for Fundulus grandis, the gulf killifish, were measured in air-saturated water, at four progressively lower levels of oxygen and upon normoxic recovery. The pattern of M(O(2)) versus oxygen partial pressure (P(w)O(2)) was that of an oxygen regulator, with a critical oxygen pressure (P(c)) of 34 torr (1 torr=133.3 Pa). Below this value, M(O(2)) decreased and the concentration of blood lactate increased, indicating anaerobic metabolism during hypoxia. Recovery was characterized by elevated M(O(2)) compared to the initial normoxic exposure, coupled with the rapid clearance of blood lactate. Variation in M(O(2)) among the individual fish was appreciable and, in general, it was greater at higher levels of P(w)O(2). This inter-individual variation was significantly larger than the variation between replicate measures of M(O(2)) for a given individual, i.e. it cannot be attributed solely to random error. Furthermore, values for M(O(2)) during normoxia were found to be repeatable when the same fish were used in multiple experimental trials. The observation of significant, repeatable inter-individual variation in M(O(2)) suggests that such variation is a real and potentially important feature of fish metabolism.     

Impact of α-lipoic acid on liver peroxisome proliferator-activated receptor-α, vascular remodeling, and oxidative stress in insulin-resistant rats

This study sought to determine the impact of α-lipoic acid (LA) on superoxide anion (O(2)(?-)) production and peroxisome proliferator-activated receptor-α (PPARα) expression in liver tissue, plasma free fatty acids (FFA), and aortic remodeling in a rat model of insulin resistance. Sprague-Dawley rats (50-75 g) were given either tap water or a drinking solution containing 10% D-glucose for 14 weeks, combined with a diet with or without LA supplement. O(2)(?-) production was measured by lucigenin chemiluminescence, and PPAR-α expression by Western blotting. Cross-sectional area (CSA) of the aortic media and lumen and number of smooth muscle cells (SMC) were determined histologically. Glucose increased systolic blood pressure (SBP), plasma levels of glucose and insulin, and insulin resistance (HOMA index). All of these effects were attenuated by LA. Whereas glucose had no effect on liver PPAR-α protein level, it decreased plasma FFA. LA decreased the aortic and liver O(2)(?-) production, body weight, and plasma FFA levels in control and glucose-treated rats. Liver PPAR-α protein levels were increased by LA, and negatively correlated with plasma FFA. Medial CSA was reduced in all glucose-treated rats, and positively correlated with plasma FFA but not with SBP or aortic O(2)(?-) production. Glucose also reduced aortic lumen area, so that the media-to-lumen ratio remained unchanged. The ability of LA to lower plasma FFA appears to be mediated, in part, by increased hepatic PPAR-α expression, which may positively affect insulin resistance. Glucose-fed rats may serve as a unique model of aortic atrophic remodeling in hypertension and early metabolic syndrome.     

Hemodynamic responses to heat stress in the resting and exercising human leg: insight into the effect of temperature on skeletal muscle blood flow

Heat stress increases limb blood flow and cardiac output (Q) in humans, presumably in sole response to an augmented thermoregulatory demand of the skin circulation. Here we tested the hypothesis that local hyperthermia also increases skeletal muscle blood flow at rest and during exercise. Hemodynamics, blood and tissue oxygenation, and muscle, skin, and core temperatures were measured at rest and during exercise in 11 males across four conditions of progressive whole body heat stress and at rest during isolated leg heat stress. During whole body heat stress, leg blood flow (LBF), Q, and leg (LVC) and systemic vascular conductance increased gradually with elevations in muscle temperature both at rest and during exercise (r(2) = 0.86-0.99; P < 0.05). Enhanced LBF and LVC were accompanied by reductions in leg arteriovenous oxygen (a-vO(2)) difference and increases in deep femoral venous O(2) content and quadriceps tissue oxygenation, reflecting elevations in muscle and skin perfusion. The increase in LVC occurred despite an augmented plasma norepinephrine (P < 0.05) and was associated with elevations in muscle temperature (r(2) = 0.85; P = 0.001) and arterial plasma ATP (r(2) = 0.87; P < 0.001). Isolated leg heat stress accounted for one-half of the increase in LBF with severe whole body heat stress. Our findings suggest that local hyperthermia also induces vasodilatation of the skeletal muscle microvasculature, thereby contributing to heat stress and exercise hyperemia. The increased limb muscle vasodilatation in these conditions of elevated muscle sympathetic vasoconstrictor activity is closely related to the rise in arterial plasma ATP and local tissue temperature.     

Hypoxemia raises muscle sympathetic activity but not norepinephrine in resting humans

The experimental objective was to determine whether moderate to severe hypoxemia increases skeletal muscle sympathetic nervous activity (MSNA) in resting humans without increasing venous plasma concentrations of norepinephrine (NE) and epinephrine (E). In nine healthy subjects (20-34 yr), we measured MSNA (peroneal nerve), venous plasma levels of NE and E, arterial blood pressure, heart rate, and end-tidal O2 and CO2 before (control) and during breathing of 1) 12% O2 for 20 min, 2) 10% O2 for 20 min, and 3) 8% O2 for 10 min--in random order. MSNA increased above control in five, six, and all nine subjects during 12, 10, and 8% O2, respectively (P less than 0.01), but only after delays of 12 (12% O2) and 4 min (8 and 10% O2). MSNA (total activity) rose 83 +/- 20, 260 +/- 146, and 298 +/- 109% (SE) above control by the final minute of breathing 12, 10, and 8% O2, respectively. NE did not rise above control at any level of hypoxemia; E rose slightly (P less than 0.05) at one time only with both 10 and 8% O2. Individual changes in MSNA during hypoxemia were unrelated to elevations in heart rate or decrements in blood pressure and end-tidal CO2--neither of which always fell. We conclude that in contrast to some other sympathoexcitatory stimuli such as exercise or cold stress, moderate to severe hypoxemia increases leg MSNA without raising plasma NE in resting humans.     

Energy Metabolites,Lipid Variables and Lactation Performance of Periparturient Murrah Buffaloes (Bubalus bubalis) Fed on Diet Supplemented with Inorganic Chromium

The aim of this study was to elucidate the effects of chromium (Cr) supplementation as inorganic Cr (CrCl₃?·?6H₂O) on energy balance, lipid peroxidation, and lactation performance in periparturient Murrah buffaloes. Twenty-four multiparous Murrah buffaloes according to lactation, parity, body mass, and expected calving date were divided equally. Experimental buffaloes were randomly assigned to four treatment diets: a control diet and three diets with an inorganic Cr supplementation at 0.5, 1.0, and 1.5 mg of Cr/kg dry matter (DM), respectively from 60 days before expected calving date until 60 days of lactation. Milk productions of buffaloes were recorded every day until 60 days in milk. Blood samples were collected at days ?60, ?45, ?30,?21, ?15, ?7, ?3, 0, 7, 15, 21, 30, 45, and 60 days relative to actual calving for determination of plasma glucose, nonesterified fatty acid (NEFA), thiobarbituric acid reactive substance (TBARS), total cholesterol, total protein, albumin, blood urea nitrogen (BUN), and minerals. Adding inorganic Cr to the diet of Murrah buffaloes increased milk yield. Percentage of fat and total solid yield increased significantly through the experiment in the Cr-supplemented group. At the day of calving, buffaloes showed a decrease in dry matter intake (DMI), plasma glucose, and zinc (Zn) and Cr concentrations. In contrast, plasma NEFA, TBARS, and copper (Cu) levels were found highest at the day of calving among all groups. Cr supplementation increased peripheral blood glucose concentration while decreased level of NEFA and TBARS was recorded in Cr-fed buffaloes. Supplemental Cr had no effect on plasma cholesterol, total protein, albumin, and BUN in periparturient period. Dietary Cr supplementation had positive effect on plasma Cr concentration, but the plasma concentration of Cu, Zn, and iron (Fe) was not affected by different dietary Cr level supplementation. The results suggest that dietary inorganic Cr supplementation improved milk yield by reducing negative energy balance and lipid peroxidation in buffaloes during periparturient period.     

Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

We investigated the effect of the intravenous infusion of atrial natriuretic peptide (ANP) on the response of plasma arginine vasopressin (AVP) levels to intravenous infusion of angiotensin II (ANG II) in healthy individuals. Intravenous infusion of ANP (10 ng·kg(-1)·min(-1)) slightly but significantly decreased plasma AVP levels, while intravenous infusion of ANG II (10 ng·kg(-1)·min(-1)) resulted in slightly increased plasma AVP levels. ANG II infused significant elevations in arterial blood pressure and central venous pressure (CVP). Because the elevation in blood pressure could have potentially inhibited AVP secretion via baroreceptor reflexes, the effect of ANG II on blood pressure was attenuated by the simultaneous infusion of nitroprusside. ANG II alone produced a remarkable increase in plasma AVP levels when infused with nitroprusside, whereas the simultaneous ANP intravenous infusion (10 ng·kg(-1)·min(-1)) abolished the increase in plasma AVP levels induced by ANG II when blood pressure elevation was attenuated by nitroprusside. Thus, ANG II increased AVP secretion and ANP inhibited not only basal AVP secretion but also ANG II-stimulated AVP secretion in humans. These findings support the hypothesis that circulating ANP modulates AVP secretion, in part, by antagonizing the action of circulating ANG II.     

Age-dependent metabolic effects of repeated hypoxemia in piglets

The aim of this study was to determine whether repeated exposure to hypoxemia would modify the response to hypoxemia during maturation. We exposed piglets to three 1-h cycles of hypoxemia (PaO2 = 30 to 35 mmHg; 1 mmHg = 133.3 Pa) at 1 week (n = 9), 2-3 weeks (n = 10), and 4-5 weeks of age (n = 10). O2 consumption (V(O2)) and CO2 production (V(CO2)) were measured, and alveolar ventilation (V(A)) was derived from V(CO2) and PaCO2. Levels of lactic acid (lactate) and serum catecholamines were also measured. With hypoxemia, time had a significant effect on V(O2) and body temperature in an age-dependent fashion: that is, whereas the 1 week group and the 4-5 week group showed both variables decreasing over time, the 2-3 week group showed no drop in V(O2) and a small increase in body temperature over time. Lactate levels increased with hypoxemia in all animals during the first exposure. However, with repeated exposures to hypoxemia, only the 2-3 week group continued to increase its lactate levels. Furthermore, the changes in lactate levels paralleled the changes in epinephrine levels with hypoxemia. We found, too, that although V(A) increased significantly with hypoxemia in all animals, this change was not modified by age or repeated exposures. No significant effects of age or repeated exposures were found in the cardiovascular response to hypoxemia. We concluded that, from a metabolic viewpoint, after repeated exposures to hypoxemia the 2-3 week animals responded differently.     

Decreased plasma levels of nitric oxide metabolites, angiotensin II, and aldosterone in spontaneously hypertensive rats exposed to 5 mT static magnetic field

Previously, we found that whole body exposure to static magnetic fields (SMF) at 10 mT (B(max)) and 25 mT (B(max)) for 2-9 weeks suppressed and delayed blood pressure (BP) elevation in young, stroke resistant, spontaneously hypertensive rats (SHR). In this study, we investigated the interrelated antipressor effects of lower field strengths and nitric oxide (NO) metabolites (NO(x) = NO(2)(-) + NO(3)(-)) in SHR. Seven-week-old male rats were exposed to two different ranges of SMF intensity, 0.3-1.0 mT or 1.5-5.0 mT, for 12 weeks. Three experimental groups of 20 animals each were examined: (1) no exposure with intraperitoneal (ip) saline injection (sham-exposed control); (2) 1 mT SMF exposure with ip saline injection (1 mT); (3) 5 mT SMF exposure with ip saline injection (5 mT). Arterial BP, heart rate (HR), skin blood flow (SBF), plasma NO metabolites (NO(x)), and plasma catecholamine levels were monitored. SMF at 5 mT, but not 1 mT, significantly suppressed and retarded the early stage development of hypertension for several weeks, compared with the age matched, unexposed (sham exposed) control. Exposure to 5 mT resulted in reduced plasma NO(x) concentrations together with lower levels of angiotensin II and aldosterone in SHR. These results suggest that SMF may suppress and delay BP elevation via the NO pathways and hormonal regulatory systems.     

Circulating catecholamines and cardiorespiratory responses in hypoxic lungfish (Protopterus dolloi): a comparison of aquatic and aerial hypoxia

Circulating catecholamine levels and a variety of cardiorespiratory variables were monitored in cannulated bimodally breathing African lungfish (Protopterus dolloi) exposed to aquatic or aerial hypoxia. Owing to the purported absence of external branchial chemoreceptors in lungfish and the minor role played by the gill in O2 uptake, it was hypothesized that plasma catecholamine levels would increase only during exposure of fish to aerial hypoxia. The rapid induction of aquatic hypoxia (final PWo2 = 25.9+/-1.6 mmHg) did not affect the levels of adrenaline (A) or noradrenaline (NA) within the plasma. Similarly, none of the measured cardiorespiratory variables--including heart rate (fH), blood pressure, air-breathing frequency (fV), O2 consumption (Mo2), CO2 excretion (Mco2), or blood gases--were influenced by acute aquatic hypoxia. In contrast, however, the rapid induction of aerial hypoxia (inspired Po2=46.6+/-3.3 mmHg) caused a marked increase in the circulating levels of A (from 7.9+/-2.0 to 18.8+/-6.1 nmol L(-1)) and NA (from 7.7+/-2.2 to 19.7+/-6.3 nmol L(-1)) that was accompanied by significant decreases in Mo2, arterial Po2 (Pao2), and arterial O2 concentration (Cao2). Air-breathing frequency was increased (by approximately five breaths per hour) during aerial hypoxia and presumably contributed to the observed doubling of pulmonary Mco2 (from 0.25+/-0.04 to 0.49+/-0.07 mmol kg(-1) h(-1)); fH and blood pressure were unaffected by aerial hypoxia. An in situ perfused heart preparation was used to test the possibility that catecholamine secretion from cardiac chromaffin cells was being activated by a direct localized effect of hypoxia. Catecholamine secretion from the chromaffin cells of the heart, while clearly responsive to a depolarizing concentration of KCl (60 mmol L(-1)), was unaffected by the O2 status of the perfusion fluid. The results of this study demonstrate that P. dolloi is able to mobilize stored catecholamines and increase f(V) during exposure to aerial hypoxia while remaining unresponsive to aquatic hypoxia. Thus, unlike in exclusively water-breathing teleosts, P. dolloi would appear to rely solely on internal/airway O2 chemoreceptors for initiating catecholamine secretion and cardiorespiratory responses.