Role of Alpha 2-Adrenoceptors in Hemodynamic Instability in Rats under Cooling Challenge: Investigation by Spectral Analysis

Cooling causes hemodynamic instability manifested as changes in blood pressure variability and heart rate variability (BPV, HRV). We previously observed that increased sympathomyogenic responses to cooling indexed as very-low-frequency BPV (VLF BPV ) and low-frequency BPV (LF BPV ) were dependent on the evoked pressor effect in rats. As a follow-up, the present study was designed to explore whether the alpha 2-adrenoceptor (α2-ADR) is involved in such responses. Hemodynamic changes were telemectrically 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±2 o C). Plasma nitric oxide (NO) was measured in the presence and absence of the added hexamethonium. 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) BPV versus HRV were assessed. Our results generally showed 1) control cooling-induced pressor was significantly attenuated after YOH pretreatments, 2) Compared to control vehicle prior to CI initiation, YOH produced tachycardia and increased most frequency powers but reduced normalized HF HRV power (nHF HRV ), 3) In contrast, compared with control vehicle throughout the CI trial, YOH produced less pressor, more tachycardia, and increased nHF HRV but attenuated most other frequency powers. Furthermore, the dicrotic notch was undetectable and NO was increased in CI after YOH pretreatment; however, the increase in NO was diminished after hexamethonium addition. These findings substantialized the sympathomyogenic role for α2-ADR during the cooling-induced hemodynamic instability.