Cooling-evoked hemodynamic perturbations facilitate sympathetic activity with subsequent myogenic vascular oscillations via alpha2-adrenergic receptors.

摘要

This study extends our previous work by examining the effects ofalpha2-adrenoceptors under cold stimulation involving theincrease of myogenic vascular oscillations as increases ofvery-low-frequency and low-frequency of the blood pressurevariability. Forty-eight adult male Sprague-Dawley rats wererandomly divided into four groups: vehicle; yohimbine;hexamethonium+yohimbine; guanethidine+yohimbine. Systolicblood pressure, heart rate, power spectral analysis ofspontaneous blood pressure and heart rate variability andspectral 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 asfollows: 1) Cooling-induced pressor response was attenuated byyohimbine and further attenuated by hexamethonium+yohimbineand guanethidine+yohimbine, 2) Cooling-induced tachycardiaresponse of yohimbine was attenuated by hexamethonium+yohimbine and guanethidine+yohimbine, 3) Differentpatterns of power spectrum reaction and coherence valuecompared hexamethonium+yohimbine and guanethidine+yohimbine to yohimbine alone under cold stimulation. Theresults suggest that sympathetic activation of the postsynapticalpha2-adrenoceptors causes vasoconstriction and heighteningmyogenic vascular oscillations, in turn, may increase blood flowto prevent tissue damage under stressful cooling challenge.