Nitric Oxide Modulates Thermoregulatory Effector Mechanisms in the Conscious Rabbit

Abstract

Body temperature homeostasis in higher vertebrates is achieved by modulation of thermoregulatory effector mechanisms such as shivering, panting or changes in local vascular tone. Regional cardiovascular control by differentiation of the sympathetic outflow represents a well characterized concept to maintain body temperature homeostasis under conditions of physiological disturbances within the thermoregulatory control circuit (1). Peripheral warming leads to a fall in cutaneous sympathetic nerve activity in conscious rabbits, thus reducing vasomotor tone, whereas visceral and cardiac sympathetic activity increases (1,2). Respiratory frequency and evaporative water loss (REWL) are augmented to allow sufficient heat dissipation at unaltered mean arterial pressure and heart rate, and low rates of metabolic heat production (3). Peripheral cold stimuli produce the reverse pattern of autonomic effector activities. Cutaneous vasodilation occurring during heat exposure requires active neurogenic vasodilation in addition to the release of vasoconstrictor tone. Besides vasoactive intestinal polypeptide (VIP) and ATP, gaseous nitric oxide (NO) might represent one of the mediators involved in nonadrenergic, noncholinergic (NANC) transmission processes (4). NO endogenously derived from the amino acid L-arginine through enzymatic activity of nitric oxide synthase (NOS) isoforms represents a rather novel concept of intercellular signalling (5). Synthesized by vascular endothelial cells, smooth muscle cells and neurons, NO appears to activate soluble intracellular guanylate cyclase activity in a paracrine fashion, finally leading to NANC vaso- or bronchodilation and alteration of neuronal activity, respectively. With regard to its possible role within autonomic regulatory circuits to maintain homeostasis, only scarce information is available (5).