The effect of clonidine on plasma renin activity in human hypertension.
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Biomedical subjects
Publications and source records attributed to F Arzilli.
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We studied the role of alpha-adrenoceptors in controlling renin release by infusing increasing doses of phentolamine into six patients with essential hypertension. Furthermore, in order to evaluate the relative importance of alpha 1- and alpha 2-adrenoceptors, phentolamine infusion was repeated in the same patients after pretreatment with prazosin, a selective alpha 1-blocking agent, and oxprenolol, a nonselective beta-blocker. After placebo, phentolamine infusion did not change mean blood pressure or heart rate and increased plasma renin activity (PRA) in a dose-dependent fashion. This finding suggests that the drug acts directly on the intrarenal renin producing apparatus and seems to confirm the inhibitory role of alpha-adrenoceptors in the control of renin release. After prazosin and oxprenolol pretreatment, PRA was respectively increased and decreased but it was unmodified by phentolamine infusion. This latter finding may indicate that both alpha 1- and alpha 2-adrenoceptors are involved in renin release or that alpha-adrenoceptors cannot be clearly differentiated into alpha 1- and alpha 2-subtypes.
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Treatment of occlusive lesions of renal arteries, defined as renovascular disease (RVD), is aimed both at preventing ischemic renal disease (IRD) and rescuing renal function through revascularization procedures, such as PTRA, endovascular stenting and surgical revascularization, as well as curing or improving hypertension in the presence of renovascular hypertension (RVH), i.e. hypertension caused by these vascular lesions. Preventive treatment of IRD is still an individual decision making process based on the type of renal lesions, degree of renal stenosis and progressive loss of renal mass as well as on immediate and late technical success of revascularization procedures together with their rate of complications. Rescue of renal function and-or prediction of the outcome of renal function after successful revascularization depends not only on the possibility of clarifying whether the decrease in renal function is a functioning-reversible phenomenon linked to renal hypoperfusion but also on the potential risk that the revascularization procedure may induce irreversible kidney damage. The rationale for treating RVH through revascularization procedures derives from the possibility of establishing a pathogenetic link between the occlusive lesions and hypertension, mainly through renal vein renin measurement and captopril renography and possibly their combination. Finally, medical treatment of hypertension is needed in patients who cannot undergo or refuse revascularization and whose blood pressure is not normalized by these procedures.
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