Mechanism of suppressed renin-angiotensin system in spontaneously hypertensive rat (SHR)

Plasma renin concentration (PRC) of SHR decreased with the elevation of blood pressure. In addition in vitro study of basal renin release from kidney slices obtained from SHR produced similar results. However kidney renin activity and total renin content in kidney of SHR were not less than those of Wistar rats. These results indicate that the decreased renin release from kidney might be responsible for the suppression of renin-angiotensin system of SHR after the development of hypertension. Administration of fusaric acid, a dopamine-beta-hydroxylase inhibitor markedly decreased urinary excretion of catecholamine and prostaglandin E in both SHR and Wistar rat and abolished the development of hypertension in SHR. PRC of SHR which became normotensive by fusaric acid administration (normotensive SHR), increased up to the level of control Wistar rats. Therefore suppressed renin-angiotensin system was not observed in normotensive SHR. Nevertheless basal renin release from kidney slices obtained from normotensive SHR was still less than that from control Wistar rats. As urinary catecholamine and prostaglandin E excretion were decreased by fusaric acid administration, these well-known renin stimulators could not be responsible for the reversal of suppressed renin-angiotensin system in normotensive SHR. Rather decreased arterial blood pressure in normotensive SHR lowered renal perfusion pressure, and led to the stimulation of renin release up to the levels of control Wistar rats by the activation of renal arteriolar baroreceptors.