Dysfunction of central angiotensinergic aminopeptidase activity in spontaneously hypertensive rats.

Alert spontaneously hypertensive (SH) rats, prepared with indwelling carotid artery catheters, demonstrated heightened and prolonged blood pressure (BP) responses to intracerebroventricular (i.c.v.) injections of 10 and 100 pmol angiotensin II and III (AII and AIII) as compared with Wistar-Kyoto (WKY) and Sprague-Dawley normotensive animals. Pretreatment with the aminopeptidase B inhibitor bestatin (10 nmol, i.c.v.) potentiated and prolonged the heightened pressor response to AIII (100 pmol, i.c.v.) in SH rats. These results suggest that dysfunction of angiotensin peptidase activity may be contributing to the progressive and sustained elevations in blood pressure noted to occur in the SH rat model of human essential hypertension.