Role of vasopressin V1 antagonist in the action of vasopressin on the cooling-evoked hemodynamic perturbations of rats.

Abstract

We aimed to investigate the role of arginine vasopressin (AVP) acting via the AVPV1 receptor in the autonomic cardiovascular responses to cold stress (CS). The study was conducted on adult male Sprague-Dawley rats with telemetry transmitters implanted to monitor heart rate (HR) and systolic blood pressure (SBP) throughout the experiment course. Rats were divided into four groups and were given, respectively, saline (control group), AVPV1 antagonist (V1880) alone, and V1880 following the removal of sympathetic outflows using hexamethonium (HEX+V1880) or guanethidine (GUA + V1880). Rats were subjected to the CS stimuli (rapid immersion of the rat's limbs into 4 °C water). Hemodynamic responses were recorded at baseline (PreCS), during CS, and after CS. Data analysis was performed using descriptive methods and spectral and cross-spectral analysis of blood pressure variability (BPV) and heart rate variability (HRV). Key results showed that at PreCS, inhibition of AVPV1 increases SBP and HR as well as very-low-frequency BPV and low-frequency BPV, which is attenuated by hexamethonium (effect on SBP only) and guanethidine (effect on both SBP and HR). HEX+V1880 results in increased high-frequency BPV and attenuated very-low-frequency HRV, while GUA + V1880 results in increased high-frequency HRV and attenuated very-low-frequency HRV. During CS, we observed that SBP and HR, as well as very-low-frequency BPV and low-frequency BPV, were similar in the control group and the group with AVPV1 inhibition, while AVPV1 inhibition results in attenuated high-frequency BPV. Furthermore, we observed that changes produced by AVPV1 inhibition alone were affected differently by HEX+V1880 and GUA + V1880, particularly in low-frequency HRV and very-low-frequency HRV. The results support that AVPV1 mediates autonomic cardiovascular responses at both baseline and CS stimuli conditions are associated with central mechanism engagement.