Pre- and postsynaptic effects of angiotensins in the femoral artery of spontaneously @entity101 and @entity35 -Kyoto XXXX .

@entity129 @entity3160 @entity4689 @entity101 @entity3045 @entity1808 @entity3371 @entity3044 @entity3774 @entity35 @entity1063
The effects of @entity4689 (AI) and @entity1808 ( @entity1808 ) on ring segments of femoral arteries from spontaneously @entity101 @entity35 (SHR) and normotensive @entity35 -Kyoto @entity35 (WKY) were studied. AI and @entity1808 elicited significantly greater direct contractile response in arteries from SHR than those from WKY. These peptides also potentiated the contractile response to @entity129 ( @entity129 ) in both preparations, but to a greater extent in those of WKY than SHR, without potentiating the contractile response to exogenous @entity1063 (NE). The potentiation of the @entity129 response and direct contraction caused by AI were markedly attenuated by @entity3371 , an AI-converting enzyme inhibitor. Destruction of endothelium failed to alter the contractile response to AI in both WKY and SHR but augmented that to @entity1808 in WKY. @entity3044 and @entity3045 produced significant potentiation of @entity129 response only in arteries of SHR. @entity3160 and @entity3774 alpha potentiated @entity129 response to a similar extent in arteries of WKY and SHR. These results suggest that @entity1808 locally generated from AI can act postsynaptically to cause contraction and presynaptically to promote adrenergic neurotransmission in the isolated @entity35 femoral artery. The AI to @entity1808 conversion appears to take place mainly at sites other than endothelial cells. The postsynaptic effect of @entity1808 is greater in SHR than WKY, but its presynaptic effect is diminished in SHR unlike some other agents which facilitate adrenergic neurotransmission, and unlike that in mesenteric arteries of SHR.
