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1 Department of Physiology and Pharmacology, The Oregon Health Sciences University, Portland, Oregon 97201; and 2 Departments of Psychology and Pharmacology and the Cardiovascular Center, University of Iowa, Iowa City, Iowa 52242
Central administration of the serotonin receptor ligand methysergide delays the decompensatory response to hypotensive hemorrhage. This study was performed to determine the receptor subtype that mediates this effect. Lateral ventricular (LV) injection of methysergide (40 µg) delayed the hypotensive, bradycardic, and sympathoinhibitory responses to blood withdrawal (1.26 ml/min) in conscious rats. The response was quantified, in part, as the blood volume withdrawal that produced a 40-mmHg fall in blood pressure. The delayed hypotensive response produced by methysergide (8.2 ± 0.2 vs. 5.6 ± 0.2 ml, P < 0.01) was reversed by the 5-hydroxytryptamine (HT)1A antagonist WAY-100635 (30 µg iv: 6.7 ± 0.4 ml, P < 0.01; 100 µg iv: 5.6 ± 0.1 ml, P < 0.01). LV injection of the 5-HT1A agonist (+)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) also delayed the hypotensive (10 µg: 8.6 ± 0.3, P < 0.01; 20 µg: 9.2 ± 0.3 ml, P < 0.01), bradycardic, and sympathoinhibitory responses to hemorrhage. WAY-100635 (10 µg iv) completely reversed the effects of 8-OH-DPAT (20 µg: 5.4 ± 0.3 ml). Neither selective blockade of 5-HT2 receptors nor stimulation of 5-HT1B/1D receptors had any effect on hemorrhage responses. These data indicate that methysergide stimulates 5-HT1A receptors to delay the decompensatory responses to hemorrhage.
blood pressure; renal sympathetic activity; serotonin
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