Journal article
Platelet Activation in Carotid Sinuses Triggers Reflex Sympathoinhibition and Hypotension
Hypertension (Dallas, Tex. 1979), Vol.27(3), pp.584-590
03/1996
DOI: 10.1161/01.HYP.27.3.584
PMID: 8613208
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 (3 x 10(8) 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.
Details
- Title: Subtitle
- Platelet Activation in Carotid Sinuses Triggers Reflex Sympathoinhibition and Hypotension
- Creators
- Hui Z Mao - From the Department of Internal Medicine, University of Iowa College of Medicine, and the Department of Veterans Affairs Medical Center, Iowa City, IowaZhi Li - University of IowaMark 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
- Resource Type
- Journal article
- Publication Details
- Hypertension (Dallas, Tex. 1979), Vol.27(3), pp.584-590
- DOI
- 10.1161/01.HYP.27.3.584
- PMID
- 8613208
- ISSN
- 0194-911X
- eISSN
- 1524-4563
- Language
- English
- Date published
- 03/1996
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
- Record Identifier
- 9984025680302771
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