Differential regulation of sympathetic outflows to vasoconstrictor and thermoregulatory effectors.

The medullary premotor neurons determining the sympathetic outflow regulating cardiac function and vasoconstriction are located in the rostral ventrolateral medulla (RVLM). The present study sought evidence for differential characteristics and baroreceptor reflex sensitivities between the sympathetic nerve activity (SNA) controlling brown adipose tissue (BAT) metabolism and thermogenesis and cardiovascular SNA such as that controlling mesenteric vasoconstriction via the splanchnic (SPL) nerve. The tonic discharge of sympathetic nerves is determined by the inputs to functionally specific sympathetic preganglionic neurons from supraspinal populations of premotor neurons. Under normothermic conditions, BAT SNA was nearly silent, while SPL SNA exhibited sustained, large-amplitude bursts. Disinhibition of neurons in the rostral raphe pallidus (RPa), a potential site of sympathetic premotor neurons controlling BAT SNA, or icv injection of prostaglandin E2, a pyrogenic stimulus, elicited a dramatic increase in BAT SNA. SPL SNA was strongly influenced by the baroreceptor reflex as indicated by a high coherence to the arterial pressure, while activated BAT SNA exhibited no correlation with the arterial pressure. Since these characteristics and reflex responses in sympathetic outflow have been shown to arise from the ongoing or altered discharge of sympathetic premotor neurons, the marked differences between SPL SNA and BAT SNA provide strong evidence supporting the hypothesis that vasoconstriction and thermogenesis (metabolism) are controlled by distinct populations of sympathetic premotor neurons, the former in the RVLM and strongly baroreceptor-modulated and the latter potentially in the RPa exhibiting little influence of baroreceptor reflex activation.