The existence of a vascular renin-angiotensin system and its role in modulating sympathetic activity were evaluated in forearm arterioles of hypertensive individuals. Isoproterenol (0.03, 0.01, 0.3 /ig/100 ml/min for 5 minutes each; n=S) was infused into the brachial artery, and active and inactive renin, angiotensin II, and norepinephrine forearm balance (venous-arterial differences corrected for forearm blood flow by strain-gauge plethysmography) were measured. Isoproterenol caused vasodilation and a dose-dependent active and inactive renin, angiotensin II, and norepinephrine outflow, an effect blunted by propranolol (10 /tg/100 ml/min). To evaluate the role of local angiotensin II on ^-mediated norepinephrine overflow, the experiment was repeated with captopril (2.5 jtg/100 ml/min for 10 minutes; n=5), which abolished angiotensin II release and significantly reduced norepinephrine overflow. To test whether angiotensin II facilitates both prejunctional norepinephrine release and its postjunctional action, we evaluated the effect of exogenous angiotensin II, infused into the brachial artery at low concentrations (0.001 jig/100 ml/min), on forearm vasoconstriction and norepinephrine release induced by endogenous sympathetic activation (application of a lower body negative pressure: -10 and -20 mm Hg for 5 minutes, n=10) and on the vasoconstrictor effect of local norepinephrine (0.0015, 0.005, 0.015, 0.05, 0.15 Aig/100 ml/min for 3 minutes each; n=6). Although angiotensin II increased the vasoconstricting effect and the norepinephrine release induced by lower body negative pressure, it failed to affect norepinephrine-mediated vasoconstriction. Our data indicate the existence in hypertensive individuals of a vascular reninangiotensin system that seems to modulate sympathetic activity through the presynaptic facilitation of norepinephrine release. (Hypertension 1991;18:266-277)

We studied PRL, FSH, and LH response to LRH in 82 anovulatory and 4 normally ovulating women. Ten anovulatory patients who were basally hyperprolactinemic showed no significant change in PRL concentration after LRH. Of the remaining 72 anovulatory patients with basal PRL levels in the normal range, 59 showed no PRL modification after LRH (as in normals) whereas in 13 patients, a prompt and significant rise of PRL concentration above basal levels in response to LRH was observed. In these 13 patients, the basal PRL levels were significantly higher than those of the other 59 normoprolactinemic women. No significant differences in gonadotropin concentrations were detected among the three groups. The unusual rise in PRL levels after LRH in these 13 patients can be interpreted as a paradoxical response of the pituitary to a specific stimulus, as seen in other clinical conditions. It is suggested that this phasic hyperprolactinemia might represent an intermediate phase between true normoprolactinemia and chronic hyperprolactinemia.

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To evaluate the humoral and hemodynamic (both systemic and renal) effects of chronic treatment with celiprolol, six out-patients with mild to moderate uncomplicated essential hypertension received placebo for 1 month and celiprolol (400 mg qid) for 6 months. At the end of placebo and of the first and sixth month of treatment, blood pressure (BP), heart rate (HR), renal plasma flow (RPF), glomerular filtration rate (GFR), plasma renin activity (PRA), aldosterone (ALD) and noradrenaline (NA), urinary enzymes (NAG: N-acetyl-beta glucosaminidase, AAP: alanine aminopeptidase) were measured. Compared to placebo, celiprolol significantly and steadily reduced BP and HR. However, although the systemic hemodynamic effect was constant during the whole period of the study, the reduction of renovascular resistance and of plasma noradrenaline, detectable at the first month of therapy, disappeared at the sixth month. However, PRA, plasma aldosterone, GFR, and urinary enzymes did not change. These findings suggest that the antihypertensive effect of celiprolol is well maintained over the 6-month period; the drug did not exert any adverse effect on the kidney, and chronic celiprolol treatment does not influence renal hemodynamics.

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