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(Hypertension. 1996;27:584-590.)
© 1996 American Heart Association, Inc.

Articles

Platelet Activation in Carotid Sinuses Triggers Reflex Sympathoinhibition and Hypotension

Hui Z. Mao; Zhi Li; Mark W. Chapleau

From the Department of Internal Medicine, University of Iowa College of Medicine, and the Department of Veterans Affairs Medical Center, Iowa City, Iowa.

Correspondence to Mark W. Chapleau, PhD, Assistant Professor, Department of Internal Medicine, E327 General Hospital, University of Iowa College of Medicine, 200 Hawkins Dr, Iowa City, IA 52242.

Abstract The carotid sinuses, one of the major sites of baroreceptor innervation, are also a common site of atherosclerotic lesions and platelet aggregation. The goal of the present study was to determine whether platelet activation in carotid sinuses causes reflex-mediated changes in renal sympathetic nerve activity and arterial pressure. Rabbit platelets were isolated, resuspended in Krebs' buffer, and activated by thrombin. Injection of activated platelets (3x10⁸ platelets/mL) into the vascularly isolated carotid sinuses of anesthetized rabbits essentially eliminated sympathetic nerve activity and acutely decreased mean arterial pressure from 126±5 to 53±4 mm Hg (n=16; P<.05). Sympathetic activity and arterial pressure returned to control levels over a period of minutes despite sustained exposure to activated platelets. Injection of U-46619, a thromboxane analogue and vasoconstrictor, into carotid sinuses did not alter sympathetic activity or arterial pressure. However, serotonin (5-hydroxytryptamine [5-HT]), which is known to be released from activated platelets, and the 5-HT₃ receptor agonist phenylbiguanide mimicked the effect of platelets. Furthermore, the platelet-induced reflex inhibition of sympathetic activity and hypotension were not altered by the cyclooxygenase inhibitor indomethacin but were attenuated significantly by 5-HT receptor antagonists. Platelet activation inhibited sympathetic activity to 5±2% of control in the absence of antagonists but to only 35±11 and 76±4% of control after selective blockade of 5-HT₂ and 5-HT₃ receptors with ketanserin and MDL-72222, respectively. The results indicate that (1) platelet activation in carotid sinuses triggers reflex inhibition of sympathetic nerve activity and hypotension; (2) the reflex is not caused by carotid vasoconstriction and is not mediated by prostanoids; and (3) the reflex is mediated by 5-HT acting primarily on 5-HT₃ and to a lesser extent on 5-HT₂ receptors. We speculate that this reflex may contribute to arterial pressure lability and susceptibility to stroke in patients with carotid atherosclerotic disease.

Key Words: blood pressure • sympathetic nervous system • atherosclerosis • pressoreceptors • stroke • serotonin • carotid sinus

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