CENTRAL METHYSERGIDE PREVENTS RENAL SYMPATHOINHIBITION AND BRADYCARDIA DURING HYPOTENSIVE HEMORRHAGE

Mean arterial pressure (MAP), heart rate (HR), and renal sympathetic n erve activity (RSNA) were measured in conscious rats during either hem orrhage or cardiopulmonary chemoreceptor stimulation with phenylbiguan ide (PBG) after intracerebroventricular injection of the 5-HT1/5-HT2-r eceptor antagonist, methysergide (40 mu g). Progressive hemorrhage cau sed 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 infl uence responses to hemorrhage. The PBG infusion caused transient depre ssor (-25 +/- 6 mmHg), bradycardic (-176 +/- 40 beats/min), and renal sympathostimulatory (182 +/- 47% baseline) responses that were not aff ected 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. Fu rthermore, the same central 5-HT-receptor populations involved in refl ex responses to hypotensive hemorrhage probably do not mediate the sym pathoinhibitory response to cardiopulmonary chemosensitive 5-HT3 recep tors.