Search PubMed⌕ Search

Biomedical subjects

J Genest

Publications and source records attributed to J Genest.

At least 343 records · Page 19Linked to original sources
PubMed1977

Effects of angiotensin II on steroid metabolism and hepatic blood flow in man.

Metabolic clearance rates (MCR) of aldosterone, cortisol, 11-deoxycorticosterone (DOC), corticosterone, and progesterone were simultaneously measured by constant infusion in eight control subjects before and during angiotensin II infusion in subpressor (3 ng/min per kg) and pressor (22 ng/min per kg) doses. Plasma levels of aldosterone and cortisol, the heat-labile protein-bound fraction of aldosterone, and hepatic blood flow (HBF) (as estimated by the fractional clearance of indocyanine green) were determined concomitantly. Angiotensin II in a subpressor dose produced a significant decrease of the MCR of aldosterone (by 23%), cortisol (by 16%), DOC (by 26%), corticosterone (by 14%) and progesterone (by 33%). The pressor dose further decreased the respective MCR by 37%, 21%, 40%, 28%, and 42% of the baseline value. Plasma aldosterone levels rose by 317% with subpressor and by 434% with pressor doses. HBF decreased by 18% with subpressor and by 33% with pressor doses of angiotensin II. Furthermore, there were significant negative correlations between the MCR of each steroid and the respective values of the fractional clearance of indocyanine green. We conclude that angiotensin II, by its vasoconstrictive action on the splanchnic vascular bed, decreases the MCR of aldosterone, cortisol, DOC, corticosterone, and progesterone. This decrease has to be taken into account when considering the stimulatory effect of angiotensin II on various plasma steroid concentrations.

Adrenal Cortex Hormones↗
PubMed1977

Response of several adrenal steroids to ACTH stimulation in essential hypertension.

Plasma concentrations of progesterone (P), deoxycorticosterone (DOC), 17-hydroxyprogesterone (17-OH P), corticosterone (B), deoxycortisol (S), cortisol (F), and aldosterone were measured in 8 control subjects and in 10 patients with low and normal renin essential hypertension (EH) before and 4 and 8 h after an iv infusion of 25 units of ACTH. Secretion rates of 18-hydroxy-11-deoxycorticosterone (18-OH DOC) were measured for the 24 h prior to and the day of the ACTH infusions. The hypertensive patients had significantly higher plasma levels of aldosterone, DOC and S after ACTH than the controls, whereas plasma B levels were significantly lower. The low renin subgroup considered separately had significantly higher plasma levels of aldosterone and DOC than controls, and higher levels of B and lower levels of F than the normal renin subgroup in response to ACTH. Although not significantly different, the plasma levels of P and the secretion rate of 18-OH DOC tended to be higher, and plasma 17-OH P and F levels lower after ACTH in patients with EH than in controls. The low renin subgroup tended to have the highest plasma S levels and 18-OH DOC secretory rates and lowest F levels. Estimations of adrenal 11beta-hydroxylating efficiency in response to ACTH in patients and controls by plasma steroid ratios revealed significantly lower B/DOC ratios in both low and normal renin patients compared to controls, supported by somewhat lower F/S ratios in these patients, especially those in the low renin subgroup. Altered 17-hydroxylating efficiency seen by significantly lower 17-OH P/P ratios were also found in those with EH, supported by somewhat lower F/B and S/DOC ratios in these patients, agian especially in the low renin subgroup. These data are compatible with a pattern of altered adrenocortical steroid biosynthesis in essential hypertension bearing features similar to adrenal 11beta and 17alpha-hydroxylation deficiencies.

Adrenal Cortex Hormones↗
PubMed1977

Origin of urinary 16 beta-hydroxydehydroepiandrosterone in essential hypertension.

The excretion rates and precursors of the 3-sulfate and glucuronide conjugates of 16 beta-hydroxydehydroepiandrosterone (16 beta-OH DHEA) were measured in normotensive controls and in patients with normal and low renin essential hypertension. The hypertensive subjects, and to the greatest degree those of the low renin subgroup, excreted increased amounts of 16 beta-OH DHEA sulfate and glucuronide and lesser amounts of DHEA sulfate and glucuronide than the controls. The major precursor of the urinary 16 beta-OH DHEA sulfate in the hypertensives was circulating DHEA sulfate, whereas the major precursors of 16 beta-OH DHEA glucuronide were DHEA, DHEA sulfate and 17-OH pregnenolone, as determined from their specific activities. Furthermore, both subgroups of hypertensives had similarly elevated DHEA and DHEA sulfate secretory rates compared to the controls. The stimulus to this increased peripheral conversion of circulating 17-OH pregnenolone, DHEA and DHEA sulfate into 16 beta-OH DHEA conjugates in essential hypertension, especially of the low renin type, is unknown.

17-alpha-Hydroxypregnenolone↗
PubMed1977

Catecholamine excretion in "idiopathic" edema: decreased dopamine excretion, a pathogenic factor?

In 16 women with idiopathic edema, urinary dopamine excretion was decreased when compared to control women (146 +/- 13 SE ng/ml/m2 vs. 212 +/- 32, P less than 0.05 in the supine position and 140 +/- 9 vs. 199 +/- 20, P less than 0.005 combined values of supine and recumbent positions) and was also lower when pooled values for urinary dopamine excretions both before and after furosemide were compared in idiopathic edema patients and in control subjects (270 +/- 30 ng/ml vs. 480 +/- 70, P less than 0.05). These patients have lower basal sodium excretions, decreased tubular rejection fractions of sodium in the upright position and lower urinary sodium excretions following furosemide administration. The urinary sodium and dopamine excretions before and following furosemide are positively correlated in control (P less than 0.05), idiopathic edema patients (P less than 0.02) and in both groups combined (P less than 0.005). Idiopathic edema patients have normal urinary noradrenaline and adrenaline excretions but, as previously observed, elevated: 1) plasma renin activity while either recumbent or upright, and 2) plasma aldosterone concentrations while upright. These results suggest that a decrease in urinary dopamine, a catecholamine recently recognized to have natriuretic action, possibly reflects a suppression of the renal dopaminergic system and may contribute to the excessive sodium retention in idiopathic edema either directly or indirectly through the renin-aldosterone system.

Adult↗
PubMed1977

The role of the adrenal cortex in human essential hypertension: keynote address.

The data presented establish that in early or mild essential hypertension there is a state of inappropriate hypermineralocorticoid activity represented by the sum of aldosterone and 18-hydroxy-11-deoxycorticosterone concentrations in the plasma. This disturbance, associated with a "normal" or excessive salt intake, would produce the arteriolar cationic changes in sodium, potassium, calcium, or magnesium leading to hypersensitivity or hyperresponsiveness of the arteriolar actomyosin to normal levels of circulating norepinephrine or angiotensin. The nature of the cationic changes in the arteriolar cells responsible for the increased tonicity of the arteriolar actomyosin, which is the fundamental cause of essential hypertension, remains to be elucidated.

18-Hydroxydesoxycorticosterone↗