Blackwell Publishing Journal Backfiles 1879-2005
〈list xml:id="l1" style="custom"〉1There is considerable in vitro evidence that, at high concentrations, atrial natriuretic peptide (ANP) acts directly on pre-constricted blood vessels to cause vasorelaxation. Previously, we have seen vasoconstriction rather than vasodilatation in conscious dogs at physiological levels of the peptide. It is possible that the low resting vascular tone in our conscious, unstressed animals prevented the manifestation of the relaxant properties of ANP in vivo.2In the present study in conscious, instrumented dogs, we studied the mesenteric vascular responses to 10 min infusions of ANP (10, 25, 50 and 100ng/kg per min, i.v.) when resting vascular tone was enhanced with a continuous infusion of AVP (75 pg/kg per min, i.v.) and compared these with responses in the normal condition (no added AVP).3Mesenteric vascular resistance was increased by ANP (10, 25, 50 and 100ng/kg per min) by 9±2, 20±6, 29±7 and 32±9%, respectively. Increased resting vascular tone did not alter the mesenteric vasoconstrictor response to ANP. Thus, the discrepancy between in vitro (vasorelaxation) and in vivo (vasoconstriction) findings may be the result of the widely different concentrations of ANP used, rather than the state of resting vascular tone.
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