V1 receptor activation induced by hemorrhage and sympathoinhibition in the mesentery and hindquarters of spontaneously hypertensive rats.

ABSTRACT

The aim of this study was to determine the effects of vasopressin V1 receptor antagonism on regional hemodynamics in spontaneously hypertensive rats (SHR/Izm). Changes in blood flow in the superior mesenteric artery or terminal aorta were measured in rats with a chronically implanted electromagnetic flowmeter. The combination of a non-hypotensive hemorrhage (0.3 ml/100 g weight) and ganglionic blockade with hexamethonium bromide (C6; 25 mg/kg weight) had no effect on mesenteric resistance. On the other hand, subsequent intravenous administration of a peptide vasopressin V1 receptor antagonist (V1A; 10 microg/kg[d(CH2)5(1)-O Methyl-Tyr(2)-Arg8]-vasopressin) significantly reduced mesenteric resistance in SHR/Izm but had no effect on hindquarter resistance. Furthermore, the infusion of C6 (after pretreatment with hemorrhage plus V1A) induced a marked reduction of blood pressure and a significant decrease in superior mesenteric resistance only in SHR/Izm. Thus, we showed an altered reactivity to V1A in the superior mesenteric and/or hindquarter vascular regions of SHR/Izm, suggesting that maintenance of elevated resistance in the mesenteric vascular bed mainly relates to a potential vasopressin-mediated vasoconstriction and that a new sympathetic vasoconstrictor tone is generated within the superior mesenteric vascular bed to compensate for hypotensive intervention (minor hemorrhage plus V1A) in conscious SHR/Izm.