V1 Receptor Activation Induced by Hemorrhage and Sympathoinhibition in the Mesentery and Hindquarters of Spontaneously Hypertensive Rats

The aim of this study was to determine the effects of vasopressin V 1 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 μg/kg:[d(CH2)5 1-O Methyl-Tyr2-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 V 1A) 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 V 1A) in conscious SHR/Izm.