Plasma renin system during exercise in normal men

The exercise-related increase in plasma renin activity (PRA) and in the plasma concentration of angiotensin II (ANG II) and aldosterone (Aldo) was studied in 43 healthy volunteers whose 24-h urinary sodium excretion (UVNa) ranged from 10 to 250 mmol. Arterial blood samples were obtained at rest and during bicycle ergometry. Compared with rest, PRA, ANG II, and Aldo rose to a similar extent during light and moderate exercise. However, at peak exercise ANG II increased significantly more (P less than 0.001) than PRA and Aldo. Thus, with increasing intensity of exercise, the slope of the linear regression of ANG II on PRA became significantly (P less than 0.001) steeper, whereas at maximal exercise the Aldo response did not follow the acute rise in ANG II. At rest as well as during exercise, Aldo rose with increasing ANG II, but the stimulatory effect of ANG II on Aldo was attenuated with higher sodium intake, as estimated from UVNa. Finally, independent of the level of physical activity, UVNa was negatively correlated with PRA, ANG II, and Aldo.     

Plasma levels of renin, angiotensin II, and 6-ketoprostaglandin F1 alpha in endurance athletes

Twelve male runners and 12 matched nonathletes performed a prolonged uninterrupted graded exercise test on the bicycle ergometer up to exhaustion to study blood pressure and plasma levels of renin (PRA), vasoconstrictor angiotensin II (ANG II), and 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), a metabolite of the vasodilator prostacyclin. In the athletes work load was increased by 30 W/4 min, and in the control subjects the increments of work load were adjusted to their lower exercise capacity to equalize total exercise duration. Blood was drawn, and blood pressure and O2 uptake (VO2) were measured at rest and at the fourth, eighth, and last steps of exercise. Peak VO2 averaged 60 +/- 1.6 ml . min-1 . kg-1 in the runners and 46.8 +/- 1.5 in the nonathletes. To evaluate differences between athletes and controls, PRA, ANG II, and 6-keto-PGF1 alpha were first adjusted for significant confounding factors, such as age, weight, hematocrit, 24-h urinary sodium excretion, and O2 uptake. PRA was significantly lower in the athletes (F = 11.2; P less than 0.01); ANG II was not different at rest, but its rise with exercise was less steep in the runners (F = 8.2; P less than 0.01), whereas 6-keto-PGF1 alpha was not different between the groups (F = 1.3; NS). Despite the differences in PRA and ANG II, however, blood pressure was similar in athletes and nonathletes (F = 0.0; NS).     

Maximal aerobic power and leg muscle mass and strength related to age in non-athletic males and females

To investigate the relationships between the age-associated decline in peak oxygen uptake (peak VO2), leg muscle mass (LMM) and leg strength (LS) under the modulating effect of gender and level of physical activity (LPA, as assessed by questionnaire), we evaluated 71 sedentary subjects [males(M):females(F), 34:37], aged 20-80 years. Peak VO2 at maximum cycle ergometry was related to LMM (dual energy X-ray absorptiometry) and LS (isokinetic dynamometry) using both standard (y x x(-1)) and power function ratios (allometry). Absolute values of all variables were higher in males and declined with age (P < 0.01). Differences between the genders disappeared after peak VO2 x LS(-1.46(M)or -1.62(F)) adjustment but remained significant between peak VO2 LMM-(-0.51 (M)or -0.45(F)) and LS LMM- (-091(M) or -1.10(F)) corrected values. Allometric correction of peak VO2 and LS by LMM slowed their age-related declines; the flattening effect however, was more evident in the females. Interestingly, while no age-related decrement in peak VO2 LS(-1) was found, power function ratio values also declined with age, and at a slower rate in females. These findings are consistent with those obtained following a multiple regression analysis using LPA as an independent covariate (P < 0.01). We conclude that using adequate scaling methods and controlling by LPA: (1) no gender differences are observed in peak VO2 adjusted for LS, (2) loss of LS and LMM are important determinants of the age-associated reduction in physical fitness in both genders but (3) age per se has an LS- and LMM-independent influence on the functional decline, although this intrinsic effect of senescence is less pronounced in females.     

Field testing: assessment of physical fitness of disabled adults

The objectives of this investigation were (i) to develop simple field-test procedures for examining the cardio-respiratory and muscular strength fitness of lower-limb disabled individuals and (ii) to compare fitness levels across disabilities and physical activity levels. Forty-nine disabled adults (42 males and 7 females) were classified according to (i) functional and/or muscular deficit and, (ii) level of habitual physical activity. A forearm ergometer test was used to determine peak oxygen intake (VO2 peak). Sex-specific regression equations developed from the direct test were used in conjunction with a modified Astrand-Ryhming equation to predict VO2 peak from sub-maximal test results. Likewise, an equation was developed to predict isokinetic upper body strength (UBS) from cable tensiometry and hand grip force. The predictive power of the sub-maximal ergometer test was fair (r = 0.67), while the isometric strength measurements were relatively effective in predicting isokinetic total UBS (r = 0.82). Class 1 differed significantly from all other classes with respect to VO2 peak and UBS. The more active individuals also achieved significantly higher scores (p less than 0.05) for both variables. This study shows that an estimate of peak oxygen intake and UBS can be obtained from simple field tests and that active disabled individuals are more fit than their inactive counterparts.     

Influence of endogenous opioids on atrial natriuretic factor release during exercise in man

To evaluate to what extent opioid secretion in exercise induces the release of atrial natriuretic factor (ANF), six healthy male volunteers who were trained subjects, were submitted to two maximal exercise tests with and without (control) opioid receptor blockade by Naltrexone. Blood samples were drawn before (rest) and after exercise (post-exercise) in order to measure human ANF (alpha h ANF), beta-endorphin, plasma aldosterone concentration (PAC) plasma renin activity (PRA) and adreno-cortico trophic hormone (ATCH) by radio-immunological methods. Expired gas was collected during exercise to measure oxygen consumption. On average, the same maximal oxygen consumption (VO2max) during exercise was reached by all subjects with and without treatment. Plasma ANF level at rest slightly decreased after administration of Naltrexone; the response to physical exercise was significantly reduced by Naltrexone. There was no statistical difference between plasma levels of beta-endorphin, PRA and ACTH at rest nor in the post-exercise situation under the influence of Naltrexone. The PAC increased significantly at rest after Naltrexone administration but there was no statistical difference between both values after exercise. These data demonstrate that: (1) ANF secretion during exercise is influenced by the level of beta-endorphin in the plasma; (2) the possible inhibitory role of ANF on aldosterone secretion during exercise is probably over-ruled by the increase in plasma ACTH and PRA.     

Diurnal variation of aldosterone and plasma renin activity: timing relation to melatonin and cortisol and consistency after prolonged bed rest.

Exposure to prolonged bed rest is known to induce changes in the renin-angiotensin-aldosterone system (RAAS) by way of posture, sodium and potassium balance, and stress, which may have serious consequences for patients. We focused on the diurnal variation of the RAAS by investigating changes in the levels of plasma renin activity (PRA) and aldosterone; for comparison to markers of the intrinsic pacemaker and to stress, we measured melatonin and cortisol. PRA, aldosterone, melatonin, and cortisol were measured hourly in 10 normal subjects with standardized sleep patterns, posture, and diet at baseline and after 11 days of prolonged bed rest conducted under a light-dark cycle. Circadian characteristics of hormone secretion patterns were estimated by multiple harmonic regression with excellent goodness-of-fit measures. Variability in the melatonin and cortisol patterns across subjects was minimal. Even for pulsatile hormones, this technique successfully estimated the acrophase, which was the salient feature. Baseline hormone peak times started with melatonin near the middle of the sleep period, followed by PRA, then aldosterone, and then cortisol around wake time. Prolonged bed rest did not induce significant changes in any timing characteristic of the secretion patterns. Baseline and prolonged bed rest peak times for melatonin and cortisol and amplitude characteristics for all hormones were highly correlated, indicating consistency within individuals. These data provide strong evidence that prolonged bed rest of 11 days' duration does not disrupt either the timing characteristics of the RAAS or the intrinsic pacemaker.     

Acute exercise stimulates the renin-angiotensin-aldosterone axis: adaptive changes in runners

The plasma concentrations of aldosterone and its known regulators, plasma renin, potassium and ACTH, were examined during graded intensities of treadmill exercise (50, 70 and 90% of maximal oxygen uptake, VO2max). Sedentary men (n = 7) and two groups of runners of different training status (moderately trained, 15-25 miles/week, n = 7; highly trained, greater than 45 miles/week, n = 7) were studied in an attempt to define whether physical training causes changes in aldosterone homeostasis. Acute exercise was associated with elevations in plasma aldosterone, renin activity, potassium and ACTH in all three groups of subjects at exercise intensities of 70 and 90% VO2max. There were no differences in any of the responses among the three groups except for a blunted response of PRA at 90% VO2max in highly trained athletes. The exercise-induced rise of plasma aldosterone concentration did not correlate with changes in the concentration of its regulatory substances. We conclude that exercise stimulates the renin-angiotensin-aldosterone axis in an intensity-dependent fashion. With increased physical training identical hormonal and metabolic responses result at increased absolute workloads.     

Effects of 3-day bed rest on physiological responses to graded exercise in athletes and sedentary men.

To test the hypotheses that short-term bed-rest (BR) deconditioning influences metabolic, cardiorespiratory, and neurohormonal responses to exercise and that these effects depend on the subjects' training status, 12 sedentary men and 10 endurance- and 10 strength-trained athletes were submitted to 3-day BR. Before and after BR they performed incremental exercise test until volitional exhaustion. Respiratory gas exchange and heart rate (HR) were recorded continuously, and stroke volume (SV) was measured at submaximal loads. Blood was taken for lactate concentration ([LA]), epinephrine concentration ([Epi]), norepinephrine concentration ([NE]), plasma renin activity (PRA), human growth hormone concentration ([hGH]), testosterone, and cortisol determination. Reduction of peak oxygen uptake (VO(2 peak)) after BR was greater in the endurance athletes than in the remaining groups (17 vs. 10%). Decrements in VO(2 peak) correlated positively with the initial values (r = 0.73, P < 0.001). Resting and exercise respiratory exchange ratios were increased in athletes. Cardiac output was unchanged by BR in all groups, but exercise HR was increased and SV diminished in the sedentary subjects. The submaximal [LA] and [LA] thresholds were decreased in the endurance athletes from 71 to 60% VO(2 peak) (P < 0.001); they also had an earlier increase in [NE], an attenuated increase in [hGH], and accentuated PRA and cortisol elevations during exercise. These effects were insignificant in the remaining subjects. In conclusion, reduction of exercise performance and modifications in neurohormonal response to exercise after BR depend on the previous level and mode of physical training, being the most pronounced in the endurance athletes.     

Ageing and isokinetic plantar flexion

Isokinetic torques (Cybex II) of the plantar flexors in 25 healthy men were compared at 5 angular velocities (30, 60, 90, 120 and 180 degrees X s-1). The purposes were to compare plantar flexion torques in young and old subjects, and to determine whether the expected decrease was significantly associated with age, physical activity, or aerobic fitness. Four groups were studied: young (21.7 +/- 2.0 years) and older (63.3 +/- 2.8 years), active and sedentary. Measurements of height, weight, % body fat, VO2max, and daily leisure energy expenditure (questionnaire) were determined for each subject. Statistical measures of analysis of variance were used to determine significant differences among groups; product moment correlation and stepwise regression analysis were used to describe the degree of association between the dependent variable of plantar flexion torque and the independent variables at each velocity. A decline in torque was observed as the isokinetic velocity of angular motion increased. Age alone was a significant determinant of plantar flexion torque, whereas at the slowest speed, when VO2max was used as an explanatory variable, age was not a significant determinant of torque. At 30 degrees X s-1 47% of the variance in torque was explained by VO2max while at 180 degrees X s-1 49% of the variance was explained by age.     

Circadian variations in plasma renin activity, catecholamines and aldosterone during exercise in women

Four women were studied at 0400 h and 1600 h to determine if their hormonal and hemodynamic responses to exercise varied with the circadian cycle. Esophageal temperature was measured during rest and exercise (60% peak VO2; 30 min) in a warm room (Ta = 35 degrees C; PH2O = 1.7 kPa). Venous blood samples were drawn during rest and exercise and hemoglobin concentration (Hb), hematocrit (Hct), plasma osmolality (Posm), plasma protein concentration (Pp), colloid osmotic pressure (COP), plasma renin activity (PRA), cortisol, aldosterone, norepinephrine (NE) and epinephrine (E) were determined. Changes in plasma volume (PV) were estimated from changes in Hb and Hct. The relative hemoconcentration (-11.2%) was similar at 0400 h and 1600 h, but the absolute PV was smaller at 1600 h than at 0400 h (p = 0.03). The responses of Posm, Pp and COP to exercise were unaffected by time of day. Although PRA was not different at the two times of day, PRA was 244% greater during exercise at 1600 h, but only 103% greater during exercise at 0400 h. The normal circadian rhythms in plasma aldosterone (p = 0.043) and plasma cortisol (p = 0.004) were observed. Plasma aldosterone was 57% greater during exercise, while plasma cortisol did not change. The change in E and NE was greater at 0400 h, but this was due to the lower resting values of the catecholamines at 0400 h. These data indicate that time of day generally did not affect the hormonal or hemodynamic responses to exercise, with the exception that PRA was markedly higher during exercise at 1600 h compared to 0400 h.     

Plasma volume restoration with salt tablets and water after bed rest prevents orthostatic hypotension and changes in supine hemodynamic and endocrine variables

Head-down bed rest changes the values of many cardiovascular and endocrine variables and also elicits significant hypovolemia. Because previous studies had not controlled for hypovolemia, it is unknown whether the reported changes were primary effects of bed rest or secondary effects of bed rest-induced hypovolemia. We hypothesized that restoring plasma volume with salt tablets and water after 12 days of head-down bed rest would result in an absence of hemodynamic and endocrine changes and a reduced incidence of orthostatic hypotension. In 10 men, we measured changes from pre-bed-rest to post-bed-rest in venous and arterial pressures; heart rate; stroke volume; cardiac output; vascular resistance; plasma norepinephrine, epinephrine, vasopressin, renin activity (PRA), and aldosterone responses to different tilt levels (0 degrees, -10 degrees, 20 degrees, 30 degrees, and 70 degrees); and plasma volume and platelet alpha2- and lymphocyte beta2-adrenoreceptor densities and affinities (0 degrees tilt only). Fluid loading at the end of bed rest restored plasma volume and resulted in the absence of post-bed-rest orthostatic hypotension and changes in supine hemodynamic and endocrine variables. Fluid loading did not prevent post-bed-rest increases in beta2-adrenoreceptor density or decreases in the aldosterone-to-PRA ratio (P = 0.05 for each). Heart rate, epinephrine, and PRA responses to upright tilt after bed rest were increased (P < 0.05), despite the fluid load. These results suggest that incidents of orthostatic hypotension and many of the changes in supine hemodynamic and endocrine variables in volume-depleted bed-rested subjects occur secondarily to the hypovolemia. Despite normovolemia after bed rest, beta2-adrenoreceptors were upregulated, and heart rate, epinephrine, and PRA responses to tilt were augmented, indicating that these changes are independent of volume depletion.     

Cardiorespiratory fitness predicts changes in adiposity in overweight Hispanic boys

We have previously shown that cardiorespiratory fitness predicts increasing fat mass during growth in white and African-American youth, but limited data are available examining this issue in Hispanic youth. Study participants were 160 (53% boys) overweight (BMI>or=85th percentile for age and gender) Hispanic children (mean+/-s.d. age at baseline=11.2+/-1.7 years). Cardiorespiratory fitness, assessed by VO2max, was measured through a maximal effort treadmill test at baseline. Body composition through dual-energy X-ray absorptiometry and Tanner stage through clinical exam were measured at baseline and annually thereafter for up to 4 years. Linear mixed models were used to examine the gender-specific relationship between VO2max and increases in adiposity (change in fat mass independent of change in lean tissue mass) over 4 years. The analysis was adjusted for changes in Tanner stage, age, and lean tissue mass. In boys, higher VO2max at baseline was inversely associated with the rate of increase in adiposity (beta=-0.001, P=0.03); this effect translates to a 15% higher VO2max at baseline resulting in a 1.38 kg lower fat mass gain over 4 years. However, VO2max was not significantly associated with changes in fat mass in girls (beta=0.0002, P=0.31). In overweight Hispanic boys, greater cardiorespiratory fitness at baseline was protective against increasing adiposity. In girls however initial cardiorespiratory fitness was not significantly associated with longitudinal changes in adiposity. These results suggest that cardiorespiratory fitness may be an important determinant of changes in adiposity in overweight Hispanic boys but not in girls.     

Plasma vasopressin, neurophysin, renin and aldosterone during a 4-day head-down bed rest with and without exercise

The purpose of this study was to investigate the main renal and hormonal responses to head-down bed rest, which is currently considered a reliable experimental model for the simulation of weightlessness. Urinary output and electrolytes, plasma renin activity (PRA), aldosterone (PA), antidiuretic hormone (ADH) and immunoreactive neurophysin-I (Np) were measured in eight adult volunteers submitted to a 4-day head-down bed rest (-6 degrees) after a 24-h control period in the horizontal position (day 0). Four of the eight subjects were submitted to two 1-h periods of controlled muscular exercise (50% VO2max) from day 1 to day 4. Throughout the head-down bed rest period, urinary output remained stable, although lower than in the control period (day 0), but the urinary Na/K ratio decreased. Plasma electrolytes and osmolality, and creatinine clearance remained unchanged. There was no significant difference between exercising and non-exercising subjects. At the hormonal level, PRA and PA increased during the head-down bed rest. This increase was more pronounced in the group with exercise. At the end of the tilt period, PRA and PA were about 3 times higher than on day 1. No significant changes could be observed for ADH and Np. It is concluded that a 4-day head-down bed rest results in no apparent changes in neurohypophyseal secretory activity, and in a progressive secondary hyperaldosteronism.     

Impact of heart failure and exercise capacity on sympathetic response to handgrip exercise

Peak oxygen uptake (VO(2 peak)) in patients with heart failure (HF) is inversely related to muscle sympathetic nerve activity (MSNA) at rest. We hypothesized that the MSNA response to handgrip exercise is augmented in HF patients and is greatest in those with low VO(2 peak). We studied 14 HF patients and 10 age-matched normal subjects during isometric [30% of maximal voluntary contraction (MVC)] and isotonic (10%, 30%, and 50% MVC) handgrip exercise that was followed by 2 min of posthandgrip ischemia (PHGI). MSNA was significantly increased during exercise in HF but not normal subjects. Both MSNA and HF levels remained significantly elevated during PHGI after 30% isometric and 50% isotonic handgrip in HF but not normal subjects. HF patients with lower VO(2 peak) (<56% predicted; n = 8) had significantly higher MSNA during rest and exercise than patients with VO(2 peak) > 56% predicted (n = 6) and normal subjects. The muscle metaboreflex contributes to the greater reflex increase in MSNA during ischemic or intense nonischemic exercise in HF. This occurs at a lower threshold than normal and is a function of VO(2 peak).     

Intraspecific relationships between resting and activity metabolism in anuran amphibians: influence of ecology and behavior

The aerobic capacity model, as well as other models for the evolution of aerobic metabolism and the origin of endothermy, requires a mechanistic link between rates of resting and activity oxygen consumption (VO2rest and VO2act). The existence of such link is still controversial, but studies with anuran amphibians support a correlation between VO2rest and VO2act at both the intraspecific and interspecific levels. Because results at the intraspecific level are based only on a few species, we test for the generality of a link between these two metabolic variables in anurans by studying the intraspecific correlational patterns between mass-independent VO2rest and VO2act in anurans. We focus on 21 Neotropical species from different geographical areas that include remarkable diversity in behavior and thermal ecology. Although uncorrelated, VO2rest and VO2act seem to be consistent among individuals. Diverse intraspecific phenotypic correlational trends were detected, indicating that the intraspecific relationships between VO2rest and VO2act might be very diverse in anurans. The three possible trends (positive, negative, and absent correlations) were observed and appeared to be predictable from ecological and behavioral variables that relate to evolutionary physiological shifts in anurans. Positive correlations between VO2rest and VO2act were more common in species with active lifestyles (e.g., intense vocal activity) and in species that call at low temperatures (e.g., winter or high-elevation specialists).     

Effects of physical exercise and anti-G suit inflation on atrial natriuretic factor plasma level

The purpose of this study was to measure the effect of enhanced venous return on atrial natriuretic factor (ANF) secretion during exercise and upright posture and the consequences on renin angiotensin aldosterone system (RAAS) activity. Six healthy male subjects were submitted to four different procedures. All procedures were performed in the same position, i.e. riding on a support with legs hanging. Two procedures were performed at rest: the subjects were studied after a 25-min rest in this position, with and without the lower limb fitted with an anti-G suit inflated to 60 mmHg. Two procedures were carried out with physical exercise; arm-cranking was performed in the same position with and without the anti-G suit inflated to 60 mmHg. Venous blood was collected before and after each procedure in order to measure plasma ANF, plasma aldosterone concentration (PAC), plasma renin activity (PRA), corticotrophin (ACTH) and catecholamine level. The data mean +/- SEM showed that the ANF plasma level decreased significantly (p less than 0.05) from 32.5 +/- 4 to 28 +/- 6 pg.ml-1 after a 20-min rest in the upright posture, whereas this effect was absolished with anti-G suit inflation. Physical exercise with and without the anti-G suit increased the ANF level above control values (60 +/- 13.6 pg.ml-1 and 53 +/- 13 pg.ml-1): anti-G suit inflation had no significant effect. PRA increased after rest in an upright posture and during physical exercise; anti-G suit inflation abolished this increase in both conditions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolonged exercise following diuretic-induced hypohydration effects on fluid and electrolyte hormones.

To investigate the hypothesis that a reduction in plasma volume (PV) induced by diuretic administration would result in an increase in the fluid and electrolyte hormonal response to exercise, ten untrained males (VO(2) peak = 3.96 +/- 0.14 l/min) performed 60 min of cycle ergometry at 61 % VO(2) peak twice. The test was carried out once under control conditions (CON) (placebo) and once after 4 days of diuretic administration (DIU) (Novotriamazide; 100 mg triamterene and 50 mg hydrochlorothiazide). Calculated resting PV decreased by 14.6 +/- 3.3 % (p < 0.05) with DIU. No difference in plasma osmolality was observed between conditions. For the hormones measured, differences (p < 0.05) between conditions at rest were noted for plasma renin activity (PRA) (0.62 +/- 0.09 vs. 5.61 +/- 0.94 ng/ml/h), angiotensin I (ANG 1) (0.26 +/- 0.03 vs. 0.56 +/- 0.08 ng/ml), aldosterone (ALD) (143 +/- 14 vs. 1603 +/- 302 pg/ml), arginine vasopressin (AVP) (4.13 +/- 1.1 vs. 9.58 +/- 1.6 pg/ml) and atrial natriuretic peptide (alpha-ANP) (11.5 +/- 2.8 vs. 6.33 +/- 1.0 pg/ml). The exercise resulted in increases (p < 0.05) in PRA, ANG I, ALD, AVP, alpha-ANP. DIU led to higher levels of PRA, ANG I, and ALD (p < 0.05) and lower levels of alpha-ANP (p < 0.05) compared to CON. Arginine vasopressin was not affected by the loss of PV. For the catecholamines--norepinephrine (NE) and epinephrine (EPI)--only NE was higher during exercise with DIU compared to CON (p < 0.05). For PRA and ALD, the higher levels observed during exercise with DIU could be explained both by higher resting levels and a greater increase during exercise itself. For ANG I and NE, the effect of DIU only manifested itself during exercise. In contrast, the lower alpha-ANP observed during exercise with DIU was due to the lower resting levels. These results support the hypotheses that hypohydration leads to alterations in the secretion of all of the fluid and electrolyte hormones with the exception of AVP. The specific mechanisms of these alterations remain unclear, but appear to be related directly to the decrease in PV.     

Pharmacological evidence for involvement of the sympathetic nervous system in the increase in renin secretion produced by a low sodium diet in rats

To determine the degree to which increased sympathetic activity contributes to the increase in renin secretion produced by a low sodium diet, the beta-adrenergic blocking drug propranolol or saline vehicle was injected through indwelling jugular cannulas in rats fed a normal diet and rats fed a low sodium diet for 9 days. Plasma renin activity (PRA) and plasma renin concentration (PRC) were elevated by the low sodium diet, and these values were reduced 42-45% by propranolol, although they were still higher than in the normal diet controls. Plasma corticosterone was moderately elevated in cannulated rats on regular diet, compared to decapitated controls, but corticosterone did not differ between cannulated and decapitated rats on low salt diet; propranolol reduced plasma corticosterone. However, PRA and PRC were comparable in cannulated rats and decapitated controls on both the normal and the low sodium diets, and propranolol did not produce a significant reduction in PRA and PRC in rats fed the normal diet. This indicates that the effects of propranolol on PRA and PRC in the low sodium rats were not simply due to reduction of a stress-induced increase in renin secretion. The results indicate that increased sympathetic activity makes a substantial contribution to the increase in renin secretion produced by 9 days of dietary sodium restriction.     

The effects of TRH on prolactin, plasma renin activity, water and electrolyte excretion in normal males.

The effect of TRH induced secretion of TSH and prolactin (hPrl) on plasma renin activity (PRA), water and electrolyte excretion, was studied in 7 normal males before and after an intravenous injection of 2 ml normal saline or 200 microgram TRH. Plasma hPrl and TSH rose significantly (p less than 0.01) in all 7 subjects after TRH but not after saline injection. No significant differences in the hourly excretion of sodium, potassium and free water clearance were noted before and after either saline or TRH injection. Mean PRA values of the 7 subjects were similar after either the 2 ml saline of TRH injection. Our results indicate that despite a correlation between basal hPrl and sodium excretion as well as free water clearance, acute TRH induced elevation of hPrl is not associated with changes of urinary sodium and potassium excretion, free water clearance and PRA in normal males. These findings provide some evidence against a direct osmoregulatory role of hPrl in man.     

Plasma renin activity and aldosterone concentration in children.

Using semi-micro methods, plasma renin activity (PRA) and plasma aldosterone concentration (PA) were measured concurrently in 79 healthy children aged 1 month to 15 years to establish a reference range. PRA and PA varied inversely with age. Eleven children with renal hypertension had higher PRA and PA than age-matched controls. In contrast, PRA was much greater in 38 saline-depleted children. PA was not uniformly increased in this group and was within the normal range in children with adrenal diseases compared with the high values seen in other salt-wasting states. The findings emphasise the need to relate data from patients to age-matched control values before attempting interpretation and suggest that sodium depletion is a more potent stimulator of renin-aldosterone release than renovascular disease or renal scarring in children. Plasma renin-aldosterone profiles were also valuable in discriminating between renal and adrenal causes of salt loss in childhood.