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Descending vasomotor pathways from the dorsomedial hypothalamic nucleus: role of medullary raphe and RVLM. Am J Physiol Regul Integr Comp Physiol 287: R824R832. 2004. First published June 17, 2004, 10.1152/ajpregu. 00221.2004.--The dorsomedial hypothalamic nucleus (DMH) is believed to play a key role in mediating vasomotor and cardiac responses evoked by an acute stress. Inhibition of neurons in the rostral ventrolateral medulla (RVLM) greatly reduces the increase in renal sympathetic nerve activity (RSNA) evoked by activation of the DMH, indicating that RVLM neurons mediate, at least in part, the vasomotor component of the DMH-evoked response. In this study, the first aim was to determine whether neurons in the medullary raphe pallidus (RP) region also contribute to the DMH-evoked vasomotor response, because it has been shown that the DMH-evoked tachycardia is mediated by the RP region. The second aim was to directly assess the effect of DMH activation on the firing rate of RVLM sympathetic premotor neurons. In urethane-anesthetized rats, injection of the GAB[A.sub.A] receptor agonist muscimol (but not vehicle solution) in the RP region caused a modest (~25%) but significant reduction in the increase in RSNA evoked by DMH disinhibition (by microinjection of bicuculline). In other experiments, disinhibition of the DMH resulted in a powerful excitation (increase in firing rate of ~400%) of 5 out of 6 spinally projecting barosensitive neurons in the RVLM. The results indicate that neurons in the RP region make a modest contribution to the renal sympathoexcitatory response evoked from the DMH and also that sympathetic premotor neurons in the RVLM receive strong excitatory inputs from DMH neurons, consistent with the view that the RVLM plays a key role in mediating sympathetic vasomotor responses arising from the DMH. renal sympathetic nerve activity: tachycardia; raphe pallidus; stress

Potts, P. D., A. M. Allen, J. Horiuchi, and R. A. L. Dampney. Does angiotensin II have a significant tonic action on cardiovascular neurons in the rostral and caudal VLM? Am J Physiol Regulatory Integrative Comp Physiol 279: R1392-R1402, 2000.--The peptidic ANG II receptor antagonists [[Sar.sup.1], [Ile.sup.8]]ANG II (sarile) or [[Sar.sup.1], [Thr.sup.8]]ANG II (sarthran) are known to decrease arterial pressure and sympathetic activity when injected into the rostral part of the ventrolateral medulla (VLM). In anesthetized rabbits and rats, the profound depressor and sympathoinhibitory response after bilateral microinjections of sarile or sarthran into the rostral VLM was unchanged after prior selective blockade of angiotensin type 1 ([AT.sub.1]) and ANG-(1-7) receptors, although this abolished the effects of exogenous ANG II. Unlike the neuroinhibitory compounds muscimol or lignocaine, microinjections of sarile in the rostral VLM did not affect respiratory activity. Sarile or sarthran in the caudal VLM resulted in a large pressor and sympathoexcitatory response, which was also unaffected by prior blockade of [AT.sub.1] and ANG-(1-7) receptors. The results indicate that the peptidic ANG receptor antagonists profoundly inhibit the tonic activity of cardiovascular but not respiratory neurons in the VLM and that these effects are independent of ANG II or ANG-(1-7) receptors. sympathetic vasomotor tone; arterial pressure; medulla oblongata