Vascular renin-angiotensin system and sympathetic nervous system activity in human hypertension

Abstract

Experimental data indicate the existence of a vascular tissue renin-angiotensin system in several different vessels from various animal models. Active renin can be locally synthesized into the vessel wall or taken up from circulating plasma to produce vascular angiotensin II. Using the human forearm technique, we produced evidence indicating the release of active and inactive renin and of angiotensin II from the vessels of hypertensive patients. Moreover, the production of vascular angiotensin II seems to be strictly correlated to the circulating renin profile, suggesting the possibility that vascular renin might be at least partially taken up from plasma. To investigate a possible function of the vascular renin-angiotensin system, we studied its interaction with sympathetic neurotransmission in essential hypertensive patients. In line with animal studies, vascular angiotensin II increases the vasoconstriction induced by the stimulation of the sympathetic nervous system through the potentiation of noradrenaline release at a presynaptic level, and this effect seems to be mediated by beta-adrenoceptor activation. This facilitating effect on sympathetic neurotransmission exerted by vascular angiotensin II can be antagonized by both angiotensin II antagonists and angiotensin-converting enzyme inhibitors.