Cooling-Evoked Hemodynamic Perturbations Facilitate Sympathetic Activity with Subsequent Myogenic Vascular Oscillations via Alpha2-Adrenergic Receptors

Abstract

This study extends our previous work by examining the effects of alpha2-adrenoceptors under cold stimulation involving the increase of myogenic vascular oscillations as increases of very-low-frequency and low-frequency of the blood pressure variability. Forty-eight adult male Sprague-Dawley rats were randomly divided into four groups: vehicle; yohimbine; hexamethonium+yohimbine; guanethidine+yohimbine. Systolic blood pressure, heart rate, power spectral analysis of spontaneous blood pressure and heart rate variability and spectral coherence at very-low-frequency (0.02 to 0.2 Hz), low-frequency (0.2 to 0.6 Hz), and high-frequency (0.6 to 3.0 Hz) regions were monitored using telemetry. Key findings are as follows: 1) Cooling-induced pressor response was attenuated by yohimbine and further attenuated by hexamethonium+yohimbine and guanethidine+yohimbine, 2) Cooling-induced tachycardia response of yohimbine was attenuated by hexame-thonium+yohimbine and guanethidine+yohimbine, 3) Different patterns of power spectrum reaction and coherence value compared hexamethonium+yohimbine and guanethi-dine+yohimbine to yohimbine alone under cold stimulation. The results suggest that sympathetic activation of the postsynaptic alpha2-adrenoceptors causes vasoconstriction and heightening myogenic vascular oscillations, in turn, may increase blood flow to prevent tissue damage under stressful cooling challenge.

Effects of sinoaortic denervation on hemodynamic perturbations of prolonged paradoxical sleep deprivation and rapid cold stress in rats

“…We speculate that pressor and tachycardia responses of SAD/PSD rats under CS are due to the synergic actions of several CS-elicited factors, for instance, adrenergic receptors, nitric oxide, sensory nerves, and non-neural pathways [7,10,11,34,35], which all might produce vasoconstriction, thereby increase SBP. Furthermore, baroreflex failure of SAD unmasks sympathetic inhibition on the heart, thereby increasing HR.…”

“…Sleep disturbances and aversive cold stress (CS) are cardiovascular risk factors [10][11][12], highly prevalent, and often happen together. In the past, we have demonstrated that paradoxical sleep deprivation (PSD) rats in nat-ural baseline (PreCS) result in sympathoexcitation and intensifying myogenic oscillations.…”

“…Spectral analysis of blood pressure variability (BPV) and heart rate variability (HRV) using a frequency domain approach has been widely applied to evaluate the autonomic regulation of cardiovascular function in health and disease-a dynamic interplay among ongoing oscillatory BP and HR and compensatory responses, which depends on a series of interactions among complex neuro-humoral reflexes [10,11,[13][14][15].…”