Intrathecal Administration of a V1a Antagonist has No Effect on Arterial Pressure in Conscious Rats under Acute or Chronic Osmotic Stress

Abstract

Previous studies suggest a role for spinal vasopressin in the regulation of arterial pressure (AP) in conscious rats. However, the evidence that spinal V1a receptors regulate AP under physiological or pathophysiological conditions in conscious animals is limited. We tested the hypothesis that acute and chronic osmotic stimuli increase AP, in part, via activation of spinal V1a receptors. In all studies, rats were chronically instrumented with an indwelling catheter, for intrathecal (i.t.) administration of a V1a antagonist, and a radiotelemeter to measure AP. Acute intravenous hypertonic saline (n = 7; 1.4ml/kg at 3M) increased AP (ΔAP=20±3mmHg), and the response was unaffected by pretreatment with i.t. V1a antagonist (ΔAP=22±4; 100ng). 48‐hour water deprivation elevated AP 9±4 mmHg (n = 4) and i.t. V1a antagonist caused no change in AP (ΔAP=5±2; 100ng). Finally, the AP response to i.t. V1a antagonist was investigated in rats with chronic osmotic stress induced by 4 weeks of DOCA‐salt treatment (n =4). Although basal AP was elevated in DOCA‐salt rats (140±6), acute i.t. V1a antagonist had no effect on AP (ΔAP=3±5; 100ng). Taken together, these data do not support the hypothesis that spinal V1a receptors are responsible for the regulation of AP under conditions of acute or chronic osmotic stress. Supported by NIH Grant HL064178.