Mechanisms of Modulation of Thermoregulatory Reactions during Cooling in Hypertensive Rats by the Sympathetic Nervous System

Abstract

Susceptibility of thermoregulatory responses to cold to blockage of α(1)- and β-adrenoreceptors differs in health and hypertension. α(1)-Adrenoceptor blockade reduces vessel reactivity during cooling and vessel reaction to cold becomes similar to that in intact normotensive rats. Changes in the structure of metabolic response to cold in favor of non-shivering thermogenesis typical of hypertensive animals becomes even more pronounced under conditions of α(1)-adrenoceptor blockade due to inhibition of cold shivering. Blockage of β-adrenoceptors does not affect parameters of vascular response to cooling. In hypertensive rats, in contrast to normotensive animals, β-adrenoceptor blockade during cooling increased temperature thresholds for total metabolic reaction and shivering. The maximum shivering intensity also increased, which partially compensated inhibition of non-shivering thermogenesis. In the whole organism, blockade of one type of adrenoceptors during cooling leads to intensification of compensatory mechanisms realized through adrenoceptors of the other type. In hypertensive rats, compensatory capacities of thermogenic processes controlled by α(1)- and β-adrenoceptors are impaired in comparison with normotensive animals under conditions of inhibition of both shivering and non-shivering thermogenesis.

Neurovascular mechanisms underlying augmented cold‐induced reflex cutaneous vasoconstriction in human hypertension

“…Our findings are also in agreement with exaggerated sympathetic responses to cold stress in rat models of hypertension (Morley et al . ; Tkachenko & Kozyreva, ) and with reports of sympathetic hyper‐reactivity to cold exposure (albeit indirectly assessed) in human hypertension (Hintsala et al . b ; Hintsala et al .…”