Key result
Idazoxan microinjection into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR in spontaneously hypertensive rats, but not in normotensive rats.
Baroreflex regulation of arterial pressure in spontaneously hypertensive rats is highly dependent on NTS adrenergic mechanisms, unlike in normotensive rats.
Animal data indicate selective NTS adrenergic dependence in hypertensive baroreflex control; leaves open human translation and therapeutic targeting.
We examined the effect of alpha(2)-adrenoreceptor blockade in the nucleus of the solitary tract (NTS) on baroreflex responses elicited by electrical stimulation of the left aortic depressor nerve (ADN) in urethane-anesthetized spontaneously hypertensive rats (SHR, n = 11) and normotensive Wistar-Kyoto rats (WKY, n = 11). ADN stimulation produced a frequency-dependent decrease in mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). In SHR, unilateral microinjection of idazoxan into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR and had a disproportionately greater influence on baroreflex control of MAP than of RSNA. In WKY, idazoxan microinjections did not significantly alter baroreflex function relative to control vehicle injections. These results suggest that baroreflex regulation of arterial pressure in SHR is highly dependent on NTS adrenergic mechanisms. The reflex regulation of sympathetic outflow to the kidney is less influenced by the altered alpha(2)-adrenoreceptor mechanisms in SHR.
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Hayward et al. (2002) studied Hypertension (n=22). Idazoxan microinjection into the NTS vs. Control vehicle injections was evaluated on Baroreflex control of mean arterial pressure (MAP), renal sympathetic nerve activity (RSNA), and heart rate (HR). Idazoxan microinjection into the NTS markedly reduced baroreflex control of MAP, RSNA, and HR in spontaneously hypertensive rats, but not in normotensive rats.
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