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Role of endothelial cells in responses of spontaneously hypertensive rat mesenteric arteries to norepinephrine and angiotensins.

The role of endothelial cells in the constrictor and dilator responses of mesenteric arteries to infused drugs was evaluated. Fifteen- to seventeen-week-old spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were used. Periarterial sympathetic nerve stimulation (PNS, 6 Hz, 30 sec) elicited greater pressor responses in SHR than WKY. Acetylcholine (ACh, 1.0 microM) lowered the perfusion pressure elevated by norepinephrine (NE, 0.1 microM) significantly more in SHR than WKY. Angiotensin I and II (AI and AII, 1.0 nM) markedly potentiated the PNS-induced constriction in both animals. Collagenase perfusion (Type 1A, 2 mg/ml, 5 ml/min intermittently, for 23 min) significantly diminished the ACh-induced dilation, indicative of endothelium destruction. However, it greatly increased the constrictor effect of NE and AI and AII in SHR and the potentiating effects of AI and AII on PNS-evoked construction in both SHR and WKY, especially in SHR. These results suggest that, while endothelial cells mediate the dilator response to ACh, they are unnecessary for the constrictor and potentiating effects of NE, AI and AII and, in fact, counteract the latter two effects, particularly in the hypertensive rats. Furthermore, the endothelial cell functions promoting the effect of ACh or countering those of NE, AI and AII are in general greater in SHR than WKY.