Role of Alpha 2‐adrenoceptors in Hemodynamic Instability in Rats Under Cooling Stress

Abstract

Cooling causes hemodynamic instability as changes in blood pressure variability and heart rate variability (BPV, HRV). We observed that increased sympathomyogenic responses (SMR) as changes in very‐low frequency of BPV (VLFBPV) and low frequency of BPV (LFBPV) which were dependent on the evoked pressor to cooling; the present study was designed to examine whether the α2‐adrenoceptor (AR) is involved in such cooling effects of rats. Hemodynamic changes were telemetry monitored throughout the experiments. Vehicle or yohimbine (YOH, 2.5 or 5.0 mg/kg) was administered with a latency (5 min, 30 min) before a cooling impact (CI, 4±2oC). Plasma nitric oxide (NO) was measured in presence or absence of the added hexamethonium (HEX). Spectral powers of high frequency (HF, 0.6‐3.0 Hz), low frequency (LF, 0.2‐0.6 Hz), and very‐low frequency (VLF, 0.02‐0.2 Hz) in BPV bands were compared with those in HRV bands. Results generally showed 1) cooling‐evoked pressor was significantly attenuated after YOH treatment, 2) Compared with vehicle prior to the CI start, YOH produced tachycardia and increased most frequency powers but reduced the normalized HFHRV (nHFHRV), 3) In contrast, compared with control vehicle throughout the CI trial, YOH produced less pressor, more tachycardia, and increased nHFHRV but reduced most the other frequency powers. Besides, the dicrotic notch was undetectable and NO was increased in CI trial after YOH treatment, in which the increase in NO was diminished after HEX addition. This study confirmed a functional role of α2‐AR which is imperative for the immediate SMR to the cooling‐induced hemodynamic instability.