Indirect evidence for an endothelium-derived contracting factor released in arterioles of deoxycorticosterone acetate salt hypertensive rats.

In order to investigate if endothelium-derived contracting factor (EDCF) is involved in the altered reactivity of microvessels of deoxycorticosterone acetate (DOCA)-salt hypertensive rats, mesenteric arterioles, either perfused in vitro or studied in vivo in situ, were used. The responses to norepinephrine, acetylcholine, sodium nitroprusside and papaverine were studied in animals treated with indomethacin. Norepinephrine was equally effective in evoking a constrictor response in the in vitro perfused arteriolar bed of DOCA-salt hypertensive and control rats. A potentiation to this agent was, however, observed in preparations tested in vivo in situ. A decreased response to acetylcholine, an endothelium-dependent vasodilator, was observed in perfused in vitro and in vivo in situ preparations. The responses to sodium nitroprusside, an endothelium-independent agent, in microvessel preparations of hypertensive rats, and the response to papaverine, an agent partially dependent on endothelium, were unaltered. Indomethacin treatment did not correct the altered response to norepinephrine in mesenteric preparations studied in vivo in situ. Thus, the involvement of an EDCF which is sensitive to indomethacin blockade could be discarded. Since indomethacin treatment corrected the decreased response to acetylcholine observed in both mesenteric arterioles perfused in vitro or tested in vivo in situ, it is suggested that in arterioles of DOCA-salt hypertensive rats, an EDCF is involved in the decreased response to acetylcholine. Smooth muscle vasodilating capability appears to be unaltered.