[Effects of muscular effort on urinary excretion of adrenal gland hormones in normal humans].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to M Follenius.
Explore the source record for details and available documents.
In previous studies, we established a strong concordance between nocturnal oscillations in plasma renin activity (PRA) and REM-NREM sleep cycles. To determine whether this relation persists in the case of moderate essential hypertension and if it is influenced by antihypertensive therapies affecting renin release, six normal subjects and six hypertensive patients were studied. The normal subjects underwent one control night. The hypertensive patients were studied during a first night when a placebo was given. Four of them underwent a second night following a single dose of an angiotensin-converting enzyme (ACE) inhibitor, perindopril; and a third night, 45 days later, with the antihypertensive treatment. In addition, two of the patients underwent two night-studies, after a single and repeated doses of a beta-blocker, atenolol, to see whether preventing renin release modified the sleep structure. The relationship between the nocturnal PRA oscillations and the sleep stage patterns persisted in hypertensive patients receiving placebo. In patients who had low PRA levels, the increases associated with NREM sleep were small. However, the mean relative amplitude of the oscillations, expressed as a percentage of the nocturnal mean, was about 60%, which was similar to that in normotensive subjects. Active renin and PRA oscillations were closely coupled. ACE activity profiles displayed damped fluctuations and no systematic relationship with sleep stages.(ABSTRACT TRUNCATED AT 250 WORDS)
To assess the role of the renin-angiotensin system in the control of aldosterone reease in response to heat exposure, 6 sodium restricted subjects were studied on three random experimental days: a control day and two heat exposure days (46C, 35 mbar, 90 min) with and without propranolol. Plasma aldosterone, renin activity, ACTH and K+ were determined from plasma samples taken every 20 min from 08:00 to 14:00. After propranolol administration, plasma aldosterone responsiveness to heat exposure increased, though plasma renin activity was depressed. Concurrently, propranolol reduced heat tolerance, leading to an increased ACTH and cortisol release in 3 of the subjects. Plasma levels of K+ were not significantly different during both heat exposure days. The enhanced response of plasma aldosterone may in part be related to the concurrent rises in ACTH, but a similar sustained aldosterone response was observed in subjects without ACTH release. Except for a significantly lower heart rate, propranolol induced no changes in hemodynamic and thermal response to heat. Plasma volume, blood pressure, sodium excretion, mean skin and rectal temperature rises and body weight losses were not modified by prior administration of the drug. The dissociation between aldosterone and renin activity after propranolol administration suggests that the aldosterone response to heat exposure is not primarily mediated by changes in activity of the renin-angiotensin system. Propranolol may lead to a reduced metabolic clearance rate of aldosterone or increase the sensitivity of the adrenal cortex to concomitant changes in the known stimuli, but the involvement of an additional factor in aldosterone regulation during heat exposure cannot be excluded.
To determine anterior pituitary response to mild hyperthermia, plasma GH, ACTH, PRL and TSH were measured every 10 min in five subjects exposed to hot air (120 min, 50 C, 20 mbar) in a climatic chamber. Mean rectal temperatures increases of 0,8 C and mean sweat losses of 760 g were observed. GH levels increased from 4.4 +/- 0.4 ng/ml to 22.0 +/- 7.0 ng/ml (mean +/- SE) and reached maximum 80 min after the beginning of heat exposure and then declined before the end of the heat stress. These peak levels varied widely with the individual, whereas no significant changes in ACTH, PRL and TSH levels were observed during the exposure period. These results suggest that the mechanisms regulating GH secretion are more sensitive to an acute heat exposure than those of the other pituitary hormones studied.
Explore the source record for details and available documents.