Plasma hormonal responses at graded hypohydration levels during exercise-heat stress

1985 ◽  
Vol 59 (6) ◽  
pp. 1855-1860 ◽  
Author(s):  
R. P. Francesconi ◽  
M. N. Sawka ◽  
K. B. Pandolf ◽  
R. W. Hubbard ◽  
A. J. Young ◽  
...  

The effects of graded levels of hypohydration (3, 5, and 7% of body weight) on hormonal responses to exercise in the heat were examined in six heat-acclimated male volunteers. On the day following dehydration, subjects performed light (approximately 25% maximal O2 consumption, 1.03 1 X min-1) exercise in a hot (49 degrees C, 20% relative humidity) environment for four consecutive 25-min intervals interspaced by 10-min rests; blood was obtained before exercise and at approximately 10 min before completion of each exercise period. During euhydration, plasma cortisol (PC) levels manifested significant decrements over time (e.g., time 0, 14.2 micrograms X 100 ml-1 vs. time 2, 8.9 micrograms X 100 ml-1), probably related to its diurnal periodicity. However, during hypohydration, levels of PC were increased and correlated with hypohydration intensity (e.g., time 0, 0, 3, 5, and 7% hypohydration, 14.2, 16.5, 19.8, and 36.2 micrograms X 100 ml-1, respectively). Plasma renin activity (PRA) was increased significantly by hypohydration (e.g., time 0, euhydrated vs. 3%, 3.7 vs. 6.2 units) but was unaffected by exercise in the heat. Plasma aldosterone (ALD) levels were generally increased by exercise in the heat (e.g., time 0 vs. time 4, 3% hypohydration, 12.1 vs. 18.7 ng X 100 ml-1). Regression analysis illustrated that graded intensities of hypohydration were correlated with incremented PRA and ALD through 5% hypohydration. Conversely, PC was incrementally elevated through 7% hypohydration.

1977 ◽  
Vol 43 (3) ◽  
pp. 421-424 ◽  
Author(s):  
J. R. Sutton ◽  
G. W. Viol ◽  
G. W. Gray ◽  
M. McFadden ◽  
P. M. Keane

Responses of plasma renin activity, plasma aldosterone, plasma cortisol, and plasma electrolyte concentration and urinary electrolyte and aldosterone excretion were studied in four men during hypoxic decompression to a stimulated altitude of 4,760 m in a pressure chamber. Three of the four subjects developed significant acute mountain sickness. Plasma sodium and potassium concentrations were unchanged. No significant change in plasma renin activity was observed, but values tended to fall. Plasma aldosterone concentration was depressed while plasma cortisol was elevated and diurnal variation lost. Urinary sodium excretion was unchanged, but urinary potassium and aldosterone excretion were decreased. The decrease in plasma and urinary aldosterone and urinary potassium in the absence of change in plasma renin activity or plasma potassium is of uncertain origin. It is unlikely to be due to a decrease in adrenocorticotropin secretion since plasma cortisol rose during the same time. None of the changes could be causally implicated in the development of acute mountain sickness although the increase in plasma cortisol was greatest in the most ill.


1989 ◽  
Vol 256 (6) ◽  
pp. R1171-R1175 ◽  
Author(s):  
G. A. Sagnella ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
M. A. Miller ◽  
D. R. Singer ◽  
...  

The effects of gradual (50 mmol/day) increases in dietary sodium intake from 10 to 350 mmol/day on plasma atrial natriuretic peptide (ANP), aldosterone, and plasma renin activity (PRA) were studied in six normal subjects. With the increases in sodium intake there was a progressive increase in urinary sodium from 12.2 +/- 4.4 to 314.8 +/- 31.4 mmol/24 h; plasma ANP increased gradually from 9.9 +/- 1.1 to 23.3 +/- 2.2 pg/ml, with the increases being closely associated with the changes in cumulative sodium balance. Plasma aldosterone decreased significantly from 2,519.7 +/- 147.4 pmol/l on the 10 mmol/day to 1,393.3 +/- 125.4 pmol/l when the sodium intake was increased to 50 mmol/day and decreased further to 251.6 +/- 78.7 pmol/l by the end of the study. The changes in PRA paralleled those in plasma aldosterone with the exception of no significant change in plasma PRA within 24 h of the initial increase in sodium intake. This marked sensitivity in the responses of both the ANP and the renin-aldosterone system to small increases in sodium intake clearly points to their importance in the renal adaptations to alterations in dietary sodium intake.


1975 ◽  
Vol 80 (1) ◽  
pp. 95-103 ◽  
Author(s):  
Helmut Armbruster ◽  
Wilhelm Vetter ◽  
Rainer Beckerhoff ◽  
Jürg Nussberger ◽  
Hans Vetter ◽  
...  

ABSTRACT In order to investigate the role of renin secretion and of ACTH on the circadian rhythm of plasma aldosterone (PA), plasma renin activity (PRA), plasma cortisol (PC) and PA were determined at short-time intervals in 10 normal supine men. Six subjects were studied under a normal sodium intake and 4 under sodium restriction. In 4 subjects the secretion of ACTH was suppressed by dexamethasone. Under normal sodium intake changes in PA seemed to be more in parallel with changes in PC than by those in PRA as indicated by a higher significant correlation between PA and PC than between PA and PRA in 3 of the 4 subjects. In 1 subject no correlation was observed between PA and PC despite visual synchronism between the plasma concentrations of both hormones. Under dexamethasone medication fluctuations in PA were followed by those in PRA while PC was less than 2 μg/100 ml. In the sodium restricted state, changes in PA were closely paralleled and significantly correlated to PRA while no correlation was seen between PA and PC. Under dexamethasone medication the significant correlation between PA and PRA persisted. Our results indicate that in normal supine man the influence of ACTH and renin on PA may vary with different sodium intakes. Under normal sodium intake ACTH seems to be the dominant factor controlling PA, whereas under sodium restriction changes in PA are mediated through the renin angiotensin system. When the secretion of ACTH is suppressed by dexamethasone, renin controls PA both under normal and low sodium intake.


1977 ◽  
Vol 42 (4) ◽  
pp. 554-558 ◽  
Author(s):  
J. P. Finberg ◽  
G. M. Berlyne

Plasma renin activity (PRA) and aldosterone concentration (PA) increased in eight men following a brief (30--40 min) heat exposure (50 degrees C dry bulb, 25 degrees C wet bulb) with light work. Sweat loss was less than 1% body weight. Plasma cortisol concentration was unchanged or decreased. In four subjects, a standard heat test was repeated in winter and summer (natural acclimatization). The increase in PRA and PA following heat exposure was less in summer than in winter. Four other subjects were artificially acclimated by daily work periods of 90 min at 50 degrees C for 7 days (artificial acclimation). Heat-induced elevation in PRA was considerably reduced by artificial acclimation, although postheat PA was reduced in only two of the four subjects. The small degree of sweat loss under the conditions of these experiments shows that circulating renin and aldosterone levels are increased in the heat even when a significant sodium deficit is not incurred.


1975 ◽  
Vol 79 (2) ◽  
pp. 295-300 ◽  
Author(s):  
Fred H. Katz ◽  
Peggy Romfh ◽  
Judith A. Smith ◽  
Ellen F. Roper ◽  
John S. Barnes

ABSTRACT A post-ovulatory peak of fasting supine plasma aldosterone (PA) preceded or accompanied by an increase in plasma renin activity (PRA) was previously reported. These studies have now been extended in 4 additional normal menstruating women and 4 women taking oestrogen-progestogen oral contraceptive pills (OCP), all studied daily for an entire cycle. Distinct luteal phase increases in PRA were seen in the 4 normals, with 2 also demonstrating a rise in PA. Plasma renin substrate (PRS) was usually unvarying throughout the control cycles. The women taking OCP, on the other hand, all had PA and PRA peaks that were apparent by the fourth or fifth day of taking "the pill". All 4 of the treated women had elevated PRS levels but only one woman showed an increase which preceded the elevation of PRA and PA. Plasma cortisol levels were usually above the normal range in the women taking OCP. This study thus indicates that factors other than oestrogen-induced increased substrate production may be responsible for the PRA and PA rise during OCP treatment Such factors might be the natri-uretic effects of oestrogens and progestogens or a direct effect on renin secretion by one of these steroids.


1991 ◽  
Vol 124 (3) ◽  
pp. 267-270 ◽  
Author(s):  
Yo Kageyama ◽  
Hiromichi Suzuki ◽  
Takao Saruta

Abstract. Changes in plasma aldosterone, plasma renin activity, plasma cortisol, serum sodium and potassium concentrations were studied in 9 patients with thromboembolic diseases treated with heparin. Heparin was administered at doses of 700-1000 units/h for 7-10 days. Plasma aldosterone decreased from 239±33 to 114±25 pmol/l during heparin therapy and returned to basal levels after discontinuation of the therapy. In addition, responses to a low sodium intake (3 g/day) and ACTH were examined in 5 patients during and 2 weeks after heparin therapy. The increase in plasma aldosterone caused by low sodium intake was significantly attenuated during heparin therapy (124±5% increase from baseline) as compared with that 2 weeks after heparin therapy (148±7%, p<0.05). On the other hand, ACTH stimulated plasma aldosterone similarly during and at 2 weeks after heparin therapy (increase from baseline: 190±20% vs 193±9%). These results suggest that heparin decreased plasma aldosterone owing to attenuation of the angiotensin Il-induced aldosterone production.


1984 ◽  
Vol 247 (3) ◽  
pp. E336-E342
Author(s):  
T. Eguchi ◽  
E. L. Bravo

The mechanism(s) by which intracerebroventricularly administered angiotensin II (ANG II) regulates aldosterone production was investigated in dogs with chronically implanted cannula into a lateral cerebroventricle. In salt-replete and salt-depleted dogs, artificial cerebrospinal fluid (CSF) with or without ANG II (1, 10, 100 ng X kg-1 X min-1) was infused intracerebroventricularly for 2 h under pentobarbital anesthesia. Artificial CSF produced no significant humoral changes. Intracerebroventricular ANG II decreased plasma renin activity and increased both ACTH and plasma cortisol in both groups but decreased plasma aldosterone (PA) only in salt-depleted dogs. Dexamethasone pretreatment during intracerebroventricular ANG II decreased PA further in salt-replete but not in salt-depleted dogs. Moreover, the fall in PA during intracerebroventricular ANG II in salt-depleted dogs was prevented when intravenous infusion of ANG II (10 ng X kg-1 X min-1) was given simultaneously to maintain circulating ANG II levels. We conclude that PA response to intracerebroventricular ANG II is mediated primarily through the renin-angiotensin system in the salt-depleted state; however, in the salt-replete state, ACTH assumes a more important role.


1982 ◽  
Vol 62 (6) ◽  
pp. 595-604 ◽  
Author(s):  
J. S. Milledge ◽  
E. I. Bryson ◽  
D. M. Catley ◽  
R. Hesp ◽  
N. Luff ◽  
...  

1. The effect of 5 consecutive days of hill walking on electrolyte balance, fluid homeostasis, plasma renin activity and plasma aldosterone concentration was studied in five male subjects. 2. The 5-day exercise period was preceded by a 4-day control period and followed by a 4-day recovery period. Throughout the 13-day study subjects ate a fixed diet. 3. After 5 days of exercise subjects had retained a mean of 264 mmol (sd 85) of sodium. Plasma sodium concentration remained constant at 142.0 mmol/l (sd 5.4). This indicates an expansion of the extracellular space by 1.84 litres. 4. By the end of the exercise period there was a positive water balance of about 0.9 litre. Thus there was a net movement of 0.94 litre of fluid from the intracellular to the extracellular space. 5. Packed cell volume decreased from a mean of 43.5% to 37.9% after 5 days of exercise, indicating that about 0.9 litre of the extracellular fluid entered the vascular compartment. The remaining fluid may be responsible for the significant increase in lower leg volume. 6. During the exercise period plasma aldosterone concentration and plasma renin activity rose, and there was a highly significant correlation between these values and the sodium retention. There was also a significant correlation between sodium retention and the increase in leg volume, which suggests that oedema may be the result of prolonged exercise of this type.


1982 ◽  
Vol 100 (4) ◽  
pp. 573-580 ◽  
Author(s):  
Wolfgang Oelkers ◽  
Angelika Köhler ◽  
Lutz Belkien ◽  
Regina Fuchs-Hammoser ◽  
Mahamane Maiga ◽  
...  

Abstract. Ten IU of ACTH (1–24) per day was infused for 34 h (starting at 7 a.m.) into 8 normal men on a constant diet containing 135 mm Na+ per day. All subjects retained between 152 and 181 mm of sodium. Potassium balance was negative. Plasma renin activity (PRA) and plasmaangiotensin II (P-A II) started to rise in most subjects after 6 to 8 h of infusion, reached a maximum after 24 h and then tended to decline. As shown previously, the rise in PRA is not due to a rise in plasma renin substrate concentration. Systolic, but not diastolic blood pressure increased significantly on the second day of ACTH-infusion. Plasma cortisol (P-F) was continuously stimulated by ACTH. Plasma aldosterone (P-aldo) increased rapidly 1 h after ACTH administration, then tended to fall, and increased again in most subjects, roughly in parallel with PRA. No significant changes in electrolyte balance, PRA, P-A II, P-F and P-aldo occurred in 3 subjects receiving 'sham'-infusions. Additional experiments in subjects treated with propranolol or indomethacin allowed the conclusion that the effect of ACTH on PRA and P-A II is not mediated by renal beta-adrenergic receptors, but perhaps (partially?) by prostaglandins. Since the infusion rate of ACTH was not much higher than the secretion rate of ACTH in the early morning hours, it is possible that ACTH is physiologically involved in the regulation of renin secretion.


1985 ◽  
Vol 110 (2) ◽  
pp. 207-213 ◽  
Author(s):  
Kazuhiro Iitake ◽  
Tokihisa Kimura ◽  
Kuniaki Matsui ◽  
Kozo Ota ◽  
Masaru Shoji ◽  
...  

Abstract. Changes in plasma ADH levels and plasma aldosterone levels (PA) were studied in patients with end-stage renal disease (N = 40). The patients were divided into two groups according to their plasma renin activity (PRA) into a low renin (LR, n = 9) and a high renin group (HR, n = 31). The metabolic clearance rate (MCR) of plasma ADH was also investigated in 4 patients and 5 normal volunteers. Additionally, it was examined whether plasma ADH, aldosterone and renin were permeable through the dialysis membrane. Pre- and post-dialysis plasma ADH levels in LR were similar to those in the HR group. However, pre- and post-dialysis PA in the HR group were significantly greater than those in the LR group. Post-dialysis PRA was significantly increased in HR compared to pre-dialysis, but not in LR. Pre- and post-dialysis plasma osmolality was increased in both groups, but effective plasma osmolality (EPosm) was within the normal range. There was a significant correlation between EPosm and plasma ADH level both before and after haemodialysis, but the majority of the abnormally high values of ADH compared to the normal values was found within the normal range of EPosm. The patients exhibited high blood pressure and a rise in body weight, and haemodialysis caused a significant fall in body weight and blood pressure in both groups. MCR of ADH was significantly lower in the patients than that in normal subjects. Plasma ADH proved to be permeable through the dialysis membrane in all cases, but aldosterone in only a few cases. Renin was not permeable.


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