Search

Adrenomedullin (ADM) infusion increases salt excretion in the rat. However, there is no evidence that this substance is related to changes in salt intake in humans. In this study we sought whether the urinary excretion rate of this autacoid is related to salt intake and by the expected changes in arterial pressure in patients with mild essential hypertension. The influence of salt intake on the renal excretion of ADM was investigated in 55 hypertensive patients in a double blind, randomized and crossover study comparing a 2-week 50 mmol/day salt intake period with a 150 mmol/day salt intake period. Twenty-four-hour ADM and endothelin-1 (ET-1) excretion rate were measured by radioimmunoassay on preextracted urinary samples (intraassay confidence variable

BACKGROUND: Established hypertension is associated with abnormal exercise hemodynamics and reduced exercise capacity through mechanisms that may include contributions from arterial stiffness and endothelial vasomotor dysfunction. Phosphodiesterase type 5 (PDE5) inhibitors prolong nitric oxide-mediated cyclic guanosine monophosphate (cGMP) signaling in vascular smooth muscle, and have beneficial effects on exercise tolerance in pulmonary hypertension and heart failure. Recent studies suggest they may also be useful antihypertensive agents. We hypothesized they would reduce arterial stiffness and increase exercise capacity in hypertensive men. METHODS: In a 3-way, randomized, placebo-controlled study, 15 untreated hypertensive and 15 matched normotensive male subjects received 50mg sildenafil (PDE5 inhibitor), 25mg hydralazine (control, cGMP-independent vasodilator) or placebo, 3 times daily for 1 week, and the effects on exercise blood pressure (during modest and maximal exercise), peak oxygen uptake, and arterial stiffness were investigated. RESULTS: Peak oxygen uptake was significantly lower in hypertensive than normotensive subjects (analysis of variance [ANOVA] P < 0.0001), but not affected by sildenafil in either group. However, while pulse wave velocity, as a measure of arterial stiffness, increased after exercise in hypertensive men following placebo, sildenafil reversed these changes, significantly reducing pulse wave velocity compared with both placebo and hydralazine (ANOVA P = 0.0001). CONCLUSIONS: PDE5 inhibition with sildenafil did not improve exercise capacity in hypertensive men. Nevertheless, our findings suggest that sildenafil may reduce arterial stiffness in the recovery period after exercise.