Three pressor system, and arginine vasopressin (AVP). In this study we determined the ability of each system to support MAP in the conscious rat when the other two systems were inactivated. After administration of the converting-enzyme inhibitor teprotide (CEI) and the α-adrenergic receptor antagonist phenoxybenzamine (POB), MAP decreased 40% as a result of a 45% decrease in peripheral vascular resistance (PVR). Despite hypotension, plasma AVP levels were not increased, and an AVP pressure antagonist (AVP-A) did not result in a further decrease in MAP. Thus the profound hypotension after POB plus CEI was the result of inhibition of all three systems. POB, rather than CEI, prevented AVP release since following hypotensive hemorrhage, plasma levels reached 51 ± 13 pg/ml with CEI but only 4.7 ± 0.8 pg/ml with POB. To study the pressor effect of AVP alone, AVP was infused in POB plus CEI-treated rats. AVP increased MAP (from 68 ± 4 to 92 ± 5 mmHg; P <0.005) and plasma AVP (to 13.8 ± 1.9 pg/ml). Since POB inhibited both the AVP and the α-adrenergic system, the role of ANG II alone was determined in POB-treated rats. In the presence of ANG II MAP was 97 ± 1 mmHg. To study the α-adrenergic system, MAP was determined in CEI plus AVP-A-treated rats. In the presence of an intact α-adrenergic system MAP was 101 ± 1 mmHg. We conclude that PVR and MAP are profoundly decreased in the absence of all three pressor systems. In contrast, MAP is well maintained as long as a single pressor system remains intact.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1984|