Low dihydrotestosterone and weight loss in the AIDS wasting syndrome.

24 consecutive AIDS patients with wasting, and who had never received anabolic therapies, were evaluated to determine their profile of sex hormones and whether transformation of testosterone (T) to the nuclear androgen, dihydrotestosterone (DHT), was impaired. Eleven (46%) patients had normal testosterone and DHT (group I), 10 (42%) had normal testosterone but low DHT (group II), and 3 (12%) had low testosterone and low DHT (group III). Age, prior opportunistic complications, symptoms, serum albumin, hemoglobin levels, and CD4 lymphocyte counts were similar in the groups.

Magnesium modulates ouabain action on angiotensin II-induced aldosterone synthesis in vitro.

Ouabain can block the action of angiotensin II (AII on aldosterone secretion in both rat and human adrenal tissue although its action is much more potent on human zona glomerulosa cells (ZG). Since magnesium can antagonize digitalis action in vivo, we have examined the interaction of both agents on aldosterone secretion in both rat and human adrenal cells. Ouabain itself at high concentration (10(-5) M) in Mg++ buffer blocks AII action on aldosterone secretion on rat ZG cells and at 1000-fold lower concentrations inhibits AII-action in human cells as previously reported by us.

Ouabain is a potent inhibitor of aldosterone secretion and angiotensin action in the human adrenal.

Digitalis glycosides and a putative ouabain-like substance act by inhibiting Na,K-adenosine triphosphatases and could regulate aldosterone secretion. We studied the effects of ouabain on basal and angiotensin II (AII)-induced aldosterone in rat and human adrenal glomerulosa cells. In the rat, ouabain at doses as high as 10(-4) mol/L had no effect on basal aldosterone secretion, but caused a dose-related inhibition of AII and ACTH secretion.

A 12-lipoxygenase product, 12-hydroxyeicosatetraenoic acid, is increased in diabetics with incipient and early renal disease.

Earlier studies in diabetic animal models or ex vivo from diabetics suggest a deficiency in prostacyclin (PGI2) production and an increase in an alternate arachidonic acid metabolite, 12-hydroxyeicosatetraenoic acid (12-HETE), which stimulates angiogenesis, mitogenesis, and inhibits renin secretion. We studied the urinary excretion rate of 6-keto-PGF1 alpha (a stable metabolite of PGI2) and 12-HETE in controls and 42 noninsulin-dependent diabetes mellitus (NIDDM) patients with normal renal function and those with micro- or macroalbuminuria/hyporeninemic hypoaldosteronism (HH). The 2 eicosanoids were measured in urine using previously described high pressure liquid chromatography and RIA methods.

Renin response to 12-hydroxyeicosatetraenoic acid is increased in diabetic rats.

Eicosanoids (prostaglandins) can alter renin secretion and angiotensin (ANG) II action. We have studied the effects of both prostacyclin and a lipoxygenase (LO) product, 12-hydroxyeicosatetraenoic acid (12-HETE), on renin in normal and streptozotocin-induced diabetic rats. 12-HETE is not only a potent inhibitor of basal renin secretion but also a key mediator of ANG II-induced renin inhibition.