Are sodium-dependent V1 receptors and sympathetic nerve activations involved in regulation of blood pressure in borderline-hypertensive Hiroshima rats?

Abstract

Sympathetic nerve activity (SNA) was estimated by the magnitude of depressor response after ganglionic blockade with hexamethonium bromide (C6; 25 mg/kg weight). The depressor effects of C6 were significantly less in bordedline-hypertensive Hiroshima rats (BHR) than in deoxycorticosterone acetate (DOCA)-salt hypertensive rats (DOCA rats) or in spontaneously hypertensive rats (SHR), but they were not different in BHR and normotensive control Wistar rats (NCR). After sympatho-inhibition, the depressor effects of a selective vasopressin V1 receptor antagonist (V1A; 10 μg/kg: [d(CH2)51, O-Me-Tyr2, Arg8]-vasopressin) were significantly greater in BHR than in DOCA rats, SHR or NCR. In a previous study, we reported that the depressor effects of C6 were significantly less in BHR than in SHR, but after sympatho-inhibition, the depressor effects of V1A were significantly greater in BHR than in SHR (Hypertens Res 2002; 25: 241-248). After high-salt diet loading in the present study (8% salt-containing diet for 10 weeks), the magnitudes of increase in mean arterial pressure in BHR and NCR were almost the same. There was almost no difference in the depressor effects of V1A after sympatho-inhibition between BHR with high-salt intake and BHR without high-salt intake. The depressor effects of an anglotensin-converting enzyme inhibitor, captopril (1 mg/kg), were almost the same between BHR and NCR both before and after sympatho-inhibition. However, these effects were completely inhibited after the high-salt diet. The results show that SNA was within the normal range in BHR and that no further accelerated responsiveness of endogenous vasopressin was observed in BHR after high-salt intake.