Human umbilical artery was perfused with Krebs-Ringer bicarbonate-glucose medium at 37 C and pH 7.4. An increase in transmural pressure elicited a vasoconstriction. The artery wall contained no significant amount of norepinephrine, which supports the anatomic evidence of absence of nerve supply. Thus, the response to stretch is due to a smooth muscle cell-borne positive feedback mechanism. The myogenic reflex could still be elicited at 44 C but was reversibly abolished by cooling to 4 C. It was reversibly abolished in the absence of calcium. K2SO4-Ringer solution (50 mm in K) markedly increased the tone of the artery after an initial vasodilatation and induced rhythmicity when the perfusion pressure was increased. Bradykinin, 5-hydroxytryptamine, and angiotensin caused vasoconstriction when the artery no longer responded to stretch. Stretch could induce vasoconstriction when angiotensin no longer elicited a response because of tachyphylaxis. The stretch reflex was not blocked by phenoxybenzamine which suppressed the response to 5-hydroxytryptamine. Tachyphylaxis was not observed with bradykinin; the effect of bradykinin was not blocked by phenoxybenzamine.
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Davignon et al. (1965) studied this question.