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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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