The effect of sleep deprivation on the plasma levels of hormones during prolonged physical strain and calorie deficiency

The effect of sleep on the serum levels of hormones during prolonged heavy physical strain and calorie deficiency were investigated in 19 young men participating in a 5 day ranger training course with a calorie consumption of 35,000-50,000 kJ X 24 h-1, and a calorie intake of about 6,000 kJ X 24 h-1. The subjects were divided into two groups: the stress group (8 cadets) were allowed no organized sleep during the course, whereas the sleep group (9 cadets) had 3 h sleep each night. Small but significantly (p less than 0.01) higher serum levels were found in the sleep group compared to the stress group for cortisol, growth hormone and testosterone. No such differences were found for catecholamines, androstendione, dihydrotestosterone, LH, triiodothyronine and thyroxine. Androstendione and dihydrotestosterone decreased in parallel with testosterone (r = 0.5) during the course, changes which directly or indirectly seem to be due to decreased testicular secretion. The changes found during this investigation for the other hormones are similar to changes found during previous courses. LH showed only small variation during the course and cannot explain the decreased secretion from the testis or the difference between the two groups for testosterone. All hormones were normal within 23 days after the end of the course.     

Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 2) Studies during moderate potassium depletion]

We have investigated the relative roles of angiotensin II on the renal function and urinary excretion of some prostanoids in healthy women submitted to different conditions of potassium balance. To this aim we have evaluated the effects of an acute inhibition of angiotensin converting enzyme by enalapril (E). The renal function was explored by clearance (cl.) method during induced hypotonic polyuria (oral water load followed by 5% dextrose solution infusion). During 60 min cl. period the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Each subject received paired studies, in absence and presence of E (10 mg administered per os 1 hour before the water load). Basal values of plasma renin activity (PRA) and urinary aldosterone (excreted during the 24 hours before the water load) were also determined by RIA method. This study protocol was applied in normal potassium balance (n = 6) and induced moderate potassium depletion (n = 6). This paper concerns the group in potassium depletion in both absence (D4) and presence of E (D4.E). Potassium depletion was induced by adaptation to a normal sodium (150 mmol/d) and low potassium (< or = 10 mmol/d) dietary intake combined to natriuretic treatment. The water and NaCl net losses were restored by 0.9% NaCl solution infusion. The cumulative potassium deficit achieved at the end of the depletive treatment was 214 +/- 54 mmol. This treatment induced significant decrease in basal plasma potassium concentration and increase in PRA without affecting urinary aldosterone and plasma sodium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Direct measurement of immunoreactive renin during changes of posture in man.

For several years, it has been possible to determine renin by a direct RIA. In the present study, plasma active renin concentration (PRC) was related to plasma renin activity (PRA) and aldosterone as a function of a standardized posture test. Using PRC, our target was to define the shortest necessary test duration. The three parameters were examined in 10 healthy male subjects (22-34 years old). Salt balance was determined in 24-hour urine, and plasma potassium and sodium were measured. Volunteers were hospitalized for 1 night, and at 8 a.m. the next morning they were subjected to the following postural changes: 3 h active orthostasis and 3 h recumbency. Frequent blood samples were taken. Orthostasis induced a significant rise in PRC, PRA and aldosterone already after 15 min. PRC and PRA reached a maximum level after 90 min of orthostasis and remained relatively stable, while aldosterone reached its highest level already after 30 min and then gradually decreased. Significant correlations were found between PRA and PRC (p < 0.001), between PRC and aldosterone (p < 0.001), and between PRA and aldosterone (p < 0.001). The PRC/PRA ratio changed during the course of the test, especially in supine subjects. When subjects returned to the supine position, all the parameters measured began a continual decrease. There were no significant changes in serum potassium and sodium levels throughout the duration of the test.(ABSTRACT TRUNCATED AT 250 WORDS)     

Daily profiles of aldosterone levels during normal, high and low sodium intake in patients with essential hypertension.

The episodic secretion of aldosterone depends on the dietary sodium intake, alterations in posture and follows ACTH circadian rhythm. Aldosterone daily profiles have been studied in 23 supine essential hypertensive patients on normal sodium intake. Secretory pulses at a frequency of two to five pulses per 12 hr have occurred, independent of PRA levels. Among 13 patients with normal PRA two lost pulsatility when sodium was loaded (10 g/24 hr) and the same happened with two others on sodium restricted diet (2 g/24 hr). These results suggest a profound effect of dietary sodium intake on the pulsatile pattern of aldosterone secretion, particularly in normal PRA essential hypertension.     

Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 1) Studies during normal sodium and potassium balance]

We have investigated the effective role of angiotensin II on the renal function and urinary excretion of some prostanoids in healthy women submitted to different conditions of potassium balance. To this aim we have evaluated the effects of an acute inhibition of angiotensin converting enzyme by enalapril (E). The renal function was explored by clearance (cl.) method during induced hypotonic polyuria (oral water load followed by 5% dextrose solution infusion). During 60 min cl. period the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Each subject received paired studies, in absence and presence of E (10 mg administered per os 1 hour before the water load). Basal values of plasma renin activity (PRA) and urinary aldosterone (excreted during the 24 hours before the water load) were also determined by RIA method. This study protocol was applied in normal potassium balance (n = 6) and induced moderate potassium depletion (n = 6). This paper concerns the group in normal potassium balance in both absence (N3) and presence of E (N3.E). All subjects were submitted to normal dietary intake of sodium (150 mmol/d) and potassium (50 mmol/d). The basal values of PRA, urinary aldosterone and plasma electrolytes were in the normal range. The only significant effect produced by E was a reduction in mean arterial pressure, without significant changes in creatinine cl., urinary hydro-electrolyte excretions as well as urinary excretions of prostanoids.(ABSTRACT TRUNCATED AT 250 WORDS)     

Regulations of plasma aldosterone in young hyperkalemic patients with stable chronic renal failure.

In a group of four young patients with stable chronic renal failure and hyperkalemia sodium restriction induced a remarkable increase in plasma renin activity (PRA) and plasma aldosterone (PA), a decrease in the elevated serum potassium (SK) and a rise in potassium excretion. During high sodium intake the levels of PRA and PA were lower than those found in the healthy control group suggesting that enhanced suppressibility of the renin-angiotensin-aldosterone system (RAAS) was the main cause of hyperkalemia. During sodium restriction despite a marked increase in PRA and PA levels poor correlations were found between these variables indicating disorganisation within the RAAS and probably a diminished role for renin-angiotensin in the regulation of aldosterone production in three hyperkalemic patients with chronic glomerulonephritis. On the other hand, in the same patients significant correlations were found between fluctuations of SK and PA on constant normal and low sodium diets supporting the concept of an (at least) equal role of potassium and RAAS in the acute regulation of PA. A prominent role for SK was found in an unusual hyperkalemic patient with interstitial nephritis when PRA was suppressed and the elevated SK showed a definite postural rise inducing dramatic increases in PA in the upright posture. Reversion of the postural SK rise masked again the governing role of SK.     

Plasma aldosterone and renal function in runners during a 20-day road race

To evaluate the effects that repeated long-distance running has on plasma aldosterone concentration and urinary excretion of solutes, fifteen male runners were studied during a 20-day, 500-km road race. Venous blood samples were taken on day 1 prior to running, on day 11 after 10 days of running, on day 13 after a 70-h rest, and on day 18 after an additional five days of running. Overnight urine samples were obtained on day 10 before and after running and on days 11, 12, and 13 during the 70-h rest period. Plasma sodium concentrations on days 13 and 18 and plasma potassium concentrations on days 11 and 13 were decreased (P less than 0.05). Plasma aldosterone levels were increased on days 11 and 18 after running and returned to pre-race levels on day 13 after 70 h of rest. Plasma cortisol concentrations were not altered. The urinary excretion rates of sodium were elevated and of aldosterone were decreased after 70 h of rest. Increase in excretion rate of urinary sodium correlated with decrease in concentration of plasma aldosterone. These findings show that plasma aldosterone levels are chronically elevated with repeated long-distance running, resulting in a decrease in urinary excretion rate of sodium.     

Effects of two different experimental situations of hypothyroidism on serum aldosterone concentration and plasma renin in rats

When hypothyroidism is induced surgically in early steps of development in the rat, an increase in serum aldosterone concentration (AC), in absence of changes in plasma renin activity (PRA), is observed. In contrast, in propylthiouracil (PTU) induced hypothyroidism, in adult animals, both AC and PRA decrease. Potassium iodide (KI) or triiodo-L-thyronine (T3) administration to thyroidectomized rats restores AC to normal levels, increasing PRA during the latter treatment. A close relationship between AC and plasma renin concentration (PRC) is observed in these experimental situations. The decrease in urinary aldosterone concentration (ACu), and the relation found between AC/ACu ratio and T3 concentration, suggest that metabolic clearance of aldosterone might be related to peripheric T3 levels in thyroidectomized animals, treated with KI or T3. These observations support the hypothesis, previously reported, which suggests different mechanisms involved in the control of aldosterone and renin release during the two different types of hypothyroidism.     

Influence of insulin on plasma concentration and renal excretion of sodium and potassium in normal, electrolytes depleted and aldosterone treated dogs

Effects of insulin on plasma concentration and renal excretion of sodium and potassium were compared in conscious dogs 1) maintained in water and electrolytes balance (Series 1, 10 dogs), 2) depleted of electrolytes by repeated i.v. loading with 20% mannitol (Series 2, 10 dogs), and 3) aldosterone treated (0.8 micrograms.kg-1.h-1 i.v., Series 3, 10 dogs). In each Series intravenous infusion of insulin at a rate of 0.05 U.kg-1.h-1 elicited transient increase in plasma sodium concentration and prolonged hypokalemia. Repeated loading with mannitol in Series 2 elicited significant elevation of plasma sodium, ADH and aldosterone concentrations, as well as decrease in extracellular fluid volume. Infusion of insulin in this Series elicited smaller decrease in plasma potassium concentration and longer lasting hypernatremia than in dogs in water-electrolytes balance. Aldosterone infusion in Series 3 did not change hypokalemic effect of insulin but attenuated hypernatremia. Infusion of insulin in Series 1 elicited increase of sodium excretion and decrease in potassium excretion. These effects were absent in Series 2 and 3. The results indicate that depletion of electrolytes and blood aldosterone elevation modify the effects of insulin on plasma concentration and renal excretion of sodium and potassium.     

The effect of magnesium deficiency on serum aldosterone in rats fed two levels of sodium.

Rats were fed 47 (deficient) and 606 ppm (adequate) magnesium with either 2,100 or 14,000 ppm sodium. Serum corticosterone and aldosterone levels were determined by randoimmunoassay in six rats from each treatment group killed on days 7, 14, and 28 of consumption of the experimental diets. Serum corticosterone levels were moderately, but not significantly, decreased in magnesium deficient animals. Serum aldosterone levels increased over time in the rats fed the lower sodium diet with adequate magnesium and were further elevated in magnesium deficient animals. In sodium loaded rats the increase in aldosterone levels in magnesium deficiency was less and occurred later. Retention and urinary excretion of sodium and potassium did not appear to be affected by magnesium status or the serum concentration of aldosterone. Possible mechanisms underlying the changes in aldosterone levels of magnesium depleted animals are discussed with reference to the known effects of magnesium deficiency on physiological functions.     

Water and electrolyte excretion during the oestrous cycle in sheep.

Electrolyte excretion was observed during 24 oestrous cycles in housed sheep, together with mixed salivary Na/K ratio during 10 additional cycles. 1. The sharp fall in food and fluid intake at oestrus accompanied a peak of sodium excretion which changed to peak retention 3 days later, both in faeces and urine. 2. Potassium excretion declined with food intake at oestrus but subsequently failed to recover to pre-oestrous levels dispite full recovery of dietary intake. 3. Curiously, water intake also recovered completely whereas urinary and faecal water retention continued; faecal loss actually exceeded renal excretion on these liberal water intakes. 4. Changes in salivary, urinary and faecal Na/K indicated an aldosterone peak neither during the luteal phase nor at oestrus but three days later. The data raise questions concerning the regulation of water and electrolyte balance within the normal cycle. They also provide a baseline for the investigation of renal effects of gonadal steroids. Possible roles for aldosterone, ADH and progesterone in maintaining fluid and electrolyte balance are discussed, emphasising problems confronting species which have evolved with heavy obligatory potassium excretion but undependable supplies of sodium and water.     

Sleep deprivation induces excess diuresis and natriuresis in healthy children

Urine production is reduced at night, allowing undisturbed sleep. This study was undertaken to show the effect of sleep deprivation (SD) on urine production in healthy children. Special focus was on gender and children at an age where enuresis is still prominent. Twenty healthy children (10 girls) underwent two 24-h studies, randomly assigned to either sleep or SD on the first study night. Diet and fluid intake were standardized. Blood samples were drawn every 4 h during daytime and every 2 h at night. Urine was fractionally collected. Blood pressure and heart rate were noninvasively monitored. Blood was analyzed for plasma antidiuretic hormone (AVP), atrial natriuretic peptide (ANP), angiotensin II, aldosterone, and renin. Urine was analyzed for aquaporin-2 and PGE(2). Successful SD was achieved in all participants with a minimum of 4 h 50 min, and full-night SD was obtained in 50% of the participants. During SD, both boys and girls produced markedly larger amounts of urine than during normal sleep (477 ± 145 vs. 291 ± 86 ml, P < 0.01). SD increased urinary excretion of sodium (0.17 ± 0.05 vs. 0.10 ± 0.03 mmol·kg(-1)·h(-1)) whereas solute-free water reabsorption remained unchanged. SD induced a significant fall in nighttime plasma AVP (P < 0.01), renin (P < 0.05), angiotensin II (P < 0.001), and aldosterone (P < 0.05) whereas plasma ANP levels remained uninfluenced (P = 0.807). Nighttime blood pressure and heart rate were significantly higher during SD (mean arterial pressure: 78.5 ± 8.0 vs. 74.7 ± 8.7 mmHg, P < 0.001). SD leads to natriuresis and excess diuresis in healthy children. The underlying mechanism could be a reduced nighttime dip in blood pressure and a decrease in renin-angiotensin-aldosterone system levels during sleep deprivation.     

Potassium loading effect on potassium balance in athletes during prolonged restriction of muscular activity

Negative potassium balance during hypokinesia (decreased number of kilometers taken/day) is not based on the potassium shortage in the diet, but on the impossibility of the body to retain potassium. To assess this hypothesis, we study the effect of potassium loading on athletes during prolonged hypokinesia (HK). Studies were done during 30 d of a pre-HK period and during 364 d of an HK period. Forty male athletes aged 23–26 yr were chosen as subjects. They were divided equally into four groups: unloaded ambulatory control subjects (UACS), unloaded hypokinetic subjects (UHKS), loaded hypokinetic subjects (LHKS), and loaded ambulatory control subjects (LACS). For the simulation of the hypokinetic effect, the LHKS and UHKS groups were kept under an average running distance of 1.7 km/d. In the LACS and LHKS groups, potassium loading tests were done by administering 95.35 mg KC1 per kg body weight. During the pre-HK and HK periods and after KC1 loading tests, fecal and urinary potassium excretion, sodium and chloride excretion, plasma potassium, sodium and chloride concentration, and potassium balance were measured. Plasma renin activity (PRA) and plasma aldosterone concentration was also measured. Negative potassium balance increased significantly (p < -0.01) in the UHKS and LHKS groups when compared with the UACS and LACS groups. Plasma electrolyte concentration, urinary electrolyte excretion, fecal potassium excretion, PRA, and PA concentration increased significantly (p ≤ 0.01) in the LHKS and UHKS groups when compared with LACS and UACS groups. Urinary and fecal potassium excretion increased much more and much faster in the LHKS group than in the UHKS group. By contrast, the corresponding parameters change insignificantly in the UACS and LACS groups when compared with the base line control values. It was concluded that urinary and fecal potassium excretion increased significantly despite the presence of negative potassium balance; thus, negative potassium balance may not be based on potassium shortage in the diet because of the impossibility of the body to retain potassium during HK.     

Amplification of nocturnal oscillations in PRA and aldosterone during continuous heat exposure

To assess the effect of continuous heat exposure on the nocturnal patterns of renin, aldosterone, adrenocorticotropic hormone (ACTH), and cortisol, six young men were exposed to thermoneutral environment for 5 days, followed by a 5-day acclimation period in a hot dry environment (35 degrees C). Blood was collected at 10-min intervals during the second night at thermoneutrality (N0) and during the first (N1) and the last (N5) nights of heat exposure. Polygraphic recordings of sleep were scored according to established criteria. Continuous heat exposure led to progressive decreases in the 24-h urinary volume and in Na excretion, whereas urinary osmolality increased. After 5 days of uninterrupted heat, significant increases were found in plasma volume (P less than 0.05), osmolality (P less than 0.01), plasma Na (P less than 0.01), and protein levels (P less than 0.05). Sweat gland output increased during the first 3 days and then declined without any concomitant increases in body temperature. Compared with N0, there were no differences in plasma renin activity (PRA) and aldosterone (PA) profiles during N1 at 35 degrees C. However, during N5 the mean PRA and PA levels were significantly (P less than 0.05) enhanced, and their nocturnal oscillations were amplified (P less than 0.05). This amplification occurred mainly in the second part of the night when regular rapid-eye-movement and non-rapid-eye-movement sleep cycles were observed, leading to a general upward trend in the nocturnal profiles. The relationship between the nocturnal PRA oscillations and the sleep cycles was not modified. ACTH and cortisol patterns were not affected by continuous heat exposure.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Plasma renin activity, aldosterone and catecholamine levels when swimming and running

The purpose of this study was to determine the response of plasma renin activity (PRA), plasma aldosterone concentration (PAC) and catecholamines to two graded exercises differing by posture. Seven male subjects (19-25 years) performed successively a running rest on a treadmill and a swimming test in a 50-m swimming pool. Each exercise was increased in severity in 5-min steps with intervals of 1 min. Oxygen consumption, heart rate and blood lactate, measured every 5 min, showed a similar progression in energy expenditure until exhaustion, but there was a shorter time to exhaustion in the last step of the running test. PRA, PAC and catecholamines were increased after both types of exercise. The PRA increase was higher after the running test (20.9 ng AngI X ml-1 X h-1) than after swimming (8.66 ng AngI X ml-1 X h-1). The PAC increase was slightly greater after running (123 pg X ml-1) than swimming (102 pg X ml-1), buth the difference was not significant. Plasma catecholamine was higher after the swimming test. These results suggest that the volume shift induced by the supine position and water pressure during swimming decreased the PRA response. The association after swimming compared to running of a decreased PRA and an enhanced catecholamine response rule out a strict dependence of renin release under the effect of plasma catecholamines and is evidence of the major role of neural pathways for renin secretion during physical exercise.     

Chronic low-sodium diet in rats: responses to severe heat exposure

To determine the effects of sodium (Na+) deficiency on the responses to severe heat stress (35.5 degrees C), immature (mean wt 150.4 g) male rats (n = 21) were fed a low-Na+ diet for 71 days. Rates of weight gain and food consumption were significantly (P less than 0.001) reduced in the low-Na+ group, whereas water consumption was unaffected. Prior to heat exposure circulating Na+ levels were unaffected by dietary Na+ restriction, but both circulating potassium (K+) and hematocrit levels were significantly (P less than 0.001) increased. After 24-h exposure to severe heat stress, circulating Na+ levels did manifest a significant (P less than 0.001) decrement in the low-Na+ group. K+ levels increased significantly (P less than 0.01) in the control group after 6 h of heat exposure but remained depressed in comparison with the low-Na+ group after 48 and 72 h. Although plasma renin activity (PRA) was not increased by chronic consumption of the low-Na+ diet or by severe heat exposure in the control group, severe heat stress in the low-Na+ group did elicit significant (P less than 0.005) increments in PRA after 24 h of exposure. Alternatively, plasma aldosterone levels were significantly (P less than 0.001) elevated by both the low-Na+ diet and heat stress. We concluded from these studies that chronic consumption of the low-Na+ diet had severe effects on hematologic, endocrinological, and thermoregulatory variables as well as thermal sensitivity to prolonged and sedentary exposure to severe heat stress.     

Some Effects of a Low Sodium Diet High in Potassium on the Renin-Angiotensin System and Plasma Electrolyte Concentrations in Normal Dogs

Eight normal male Beagle dogs received 0.7 mmol Na+/kg/day for 5 weeks and 4.0 mmol Na+/kg/day in one 3 week control period preceding and another similar period following the low sodium period. The dogs received 6.8 mmol K+/kg/day throughout the study. The median plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were higher in the low sodium period than in the following control period (0.67 versus 0.28 ng/ml/h, p < 0.0001) and (204 versus 31 pg/ml, p < 0.0001). PRA and PAC quickly stabilized on a new steady level in response to altered intake of sodium chloride. The angiotensin-converting enzyme (ACE) activity was not changed by the altered intake of sodium chloride. The plasma concentrations of sodium and chloride were increased during the low sodium period. This could be due to an indirect effect of the high potassium intake of the dogs. Potassium leads to an increased secretion of aldosterone and thereby to an increased retention of sodium and chloride in the kidney. The possible implications of a high potassium content in a low sodium diet are discussed.     

Secretin—a new stress hormone?

The plasma concentration of secretin was measured during a 5-day military training course comprising prolonged physical exercise (35% of max O₂ uptake), severe caloric deficiency (approx. 35700 kJ/24 h) and sleep deprivation (only 2 h of sleep as a total during 5 days). 24 subjects were divided into 3 groups, one group was compensated for the caloric deficiency and another group was partly compensated for the sleep deprivation. The results showed that the fasting plasma secretin increased 3–6-fold (from 1.8–3.7 to 13.3–19.1 pmol/l) during the course with small differences in increase between the groups. Ingestion of a mixed meal reduced the fasting plasma secretin by about 40% during the course, while oral glucose reduced the plasma secretin to the concentrations found in the control experiment.The study shows that plasma secretin is increased when man is exposed to prolonged multifactorial stress. Additional food or sleep appears to have small influence on the fasting plasma secretin, but after giving a meal or oral glucose solution the plasma secretin decreases rapidly.     

Plasma aldosterone, renin activity, and cortisol responses to heat exposure in sodium depleted and repeleted subjects.

The effect of 90-min heat exposure (46 degrees C, 35 mbar) on plasma aldosterone (PA) patterns was studied and the respective roles of plasma renin activity (PRA), adrenocorticotropin (ACTH), Na+ and K+ concentrations in the control of PA response were in investigated in eight subjects on a low sodium diet and in five subjects on a high sodium diet. In all subjects, transitory PA increases of varying importance were observed, which were not related to sweat losses (less than 1% bodyweight) or to rectal temperature rise. In sodium-repleted subjects, basal PA and PRA levels as well as heat-induced rises were low (mean PA peak level = 12.62 +/- 1.15 ng/100 ml). They were enhanced by sodium depletion and PA reached a mean peak level of 34.07 +/- 2.73 ng/100 ml. But, in both conditions, the heat-induced PA peaks were 3-times higher than the initial levels. PA correlated with PRA in all but one of the sodium-repleted subjects and in 6 of the 8 sodium-depleted subjects. ACTH release, as measured by plasma cortisol (PC) levels, occurred in those subjects who noted an increased feeling of annoyance and discomfort. Thus, PA correlated positively with PC in 4 sodium-depleted subjects. A high sodium intake improved heat-tolerance. Plasma K+ and Na+ concentrations were not significantly modified by exposure to heat. PA increases can occur without concomitant changes in PRA, PC, K+ or Na+, which suggests that an additional factor may play a role in aldosterone regulation during acute heat exposure.