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Am J Physiol Heart Circ Physiol 274: H43-H51, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 1, H43-H51, January 1998

Central methysergide prevents renal sympathoinhibition and bradycardia during hypotensive hemorrhage

Karie E. Scrogin1, Roland Veelken2, and Alan Kim Johnson1

1 Departments of Psychology and Pharmacology and Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242; and 2 Department of Nephrology, University of Erlangen/Nürnberg, Erlangen 91052, Germany

Mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) were measured in conscious rats during either hemorrhage or cardiopulmonary chemoreceptor stimulation with phenylbiguanide (PBG) after intracerebroventricular injection of the 5-HT1/5-HT2-receptor antagonist, methysergide (40 µg). Progressive hemorrhage caused an initial rise (109 ± 33%) followed by a fall in RSNA (-60 ± 7%) and a fall in HR (-126 ± 7 beats/min). Methysergide delayed the hypotension and prevented both the sympathoinhibitory and bradycardic responses to hemorrhage. Systemic 5-HT3-receptor blockade did not influence responses to hemorrhage. The PBG infusion caused transient depressor (-25 ± 6 mmHg), bradycardic (-176 ± 40 beats/min), and renal sympathostimulatory (182 ± 47% baseline) responses that were not affected by central methysergide (-20 ± 6 mmHg, -162 ± 18 beats/min, 227 ± 46% baseline). These data indicate that a central serotonergic receptor-mediated component contributes to the sympathoinhibitory and bradycardic responses to hypotensive hemorrhage in conscious rats. Furthermore, the same central 5-HT-receptor populations involved in reflex responses to hypotensive hemorrhage probably do not mediate the sympathoinhibitory response to cardiopulmonary chemosensitive 5-HT3 receptors.

phenylbiguanide; renal sympathetic nerve activity


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