Bradykinin-induced relaxation of renal and pulmonary arteries is dependent upon intact endothelial cells.

When most arteries are removed from mammals and man, the in vitro response to kinins, particularly of helically-cut vascular strips, is usually one of contraction; and often no response is observed. This is in sharp contrast to the in situ arterial vasodilator action of kinins. The reason(s) for this transformation is not known. The present in vitro experiments demonstrate that bradykinin can produce potent relaxation of canine isolated intrapulmonary arteries (threshold concentration = 7.5 +/- 2.7 x 10(-10) M) and renal arteries (threshold concentration = 3.2 +/- 1.6 x 10(-10) M) contracted by phenylephrine, provided the endothelium is left intact. Selective, mechanical destruction of the endothelium transforms the vasodilator activity of bradykinin to either contraction or to no response at all. Our results probably explain why previous investigators have found that bradykinin usually induced contraction, rather than relaxation, of excised peripheral arteries.