A role for spinal vasopressin (V1a) receptors in regulation of arterial pressure (AP) in conscious rats

Abstract

Studies suggest that vasopressinergic PVN neurons increase sympathetic nerve activity (SNA), and therefore AP, via direct projections to the spinal cord and that this pathway is activated during acute osmotic stress. Our laboratory is interested in the role of this pathway in models of chronic osmotic stress such as the DOCA‐salt rat. In this study, we hypothesized that vasopressin can act on spinal V1a receptors to increase AP in conscious rats. Rats were chronically instrumented with telemetry transmitters for measurement of AP and intrathecal catheters for injection of a V1a specific agonist without (N=7) or with (N=6) a V1a specific antagonist pretreatment. Drugs were administered in 10 microliters of saline followed by a 23 microliter saline flush. Injection of the V1a agonist increased AP (33 ± 2 mmHg) and this response was attenuated by pretreatment with the V1a antagonist (22±4). These results are consistent with the hypothesis that spinal V1a receptors may play a role in regulating AP in conscious rats. Initial studies of intrathecal infusion of the V1a antagonist in DOCA‐salt rats suggest these receptors may be active in this chronic model of hypertension. Supported by NIH Grant HL064178.