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Deussen A, Busch P, Schipke J, et al. Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels. Basic Res Cardiol. 1990;85:193-206doi: 10.1007/978-3-662-11038-6_16.
Deussen, A., Busch, P., Schipke, J., Thämer, V., & Heusch, G. (1990). Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels. Basic research in cardiology, 85193-206. https://doi.org/10.1007/978-3-662-11038-6_16
Deussen, A, et al. "Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels." Basic research in cardiology vol. 85 (1990): 193-206. doi: https://doi.org/10.1007/978-3-662-11038-6_16
Deussen A, Busch P, Schipke J, Thämer V, Heusch G. Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels. Basic Res Cardiol. 1990;85:193-206. doi: 10.1007/978-3-662-11038-6_16. PMID: 1965398.
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Basic Res Cardiol. 1990;85:193-206. doi: 10.1007/978-3-662-11038-6_16.

Contribution of postsynaptic alpha 2-adrenoceptors to reflex sympathetic constriction of stenotic coronary vessels.

Basic research in cardiology

A Deussen, P Busch, J Schipke, V Thämer, G Heusch

Affiliations

  1. Zentrum für Physiologie, Heinrich-Heine-Universität Düsseldorf, FRG.

PMID: 1965398 DOI: 10.1007/978-3-662-11038-6_16

Abstract

Increases in the activity of efferent cardiac sympathetic nerves by 35 +/- 9% were induced by 60 s bilateral occlusion of the common carotid arteries (BCO) in anesthetized dogs. Under control conditions the reflex rise in sympathetic nerve activity enhanced left ventricular pressure (115 +/- 4 mm Hg) by 47% and regional myocardial oxygen consumption (9.7 +/- 1.1 ml/min.100 g) by 56%. Simultaneously, end-diastolic circumflex coronary resistance (0.99 +/- 0.11 mm Hg.min.100 g/ml) decreased by 16%. After exhaustion of coronary dilator reserve by production of a severe coronary stenosis, BCO enhanced left ventricular pressure (107 +/- 4 mm Hg) by 49%, oxygen consumption of the poststenotic area (7.6 +/- 0.8 ml/min.100 g) increased by 21%, and circumflex coronary resistance (0.54 +/- 0.05 mm Hg.min.100 g/ml) also increased by 19%. The reflex increase in coronary resistance during BCO was abolished after infusion of the alpha 2-adrenoceptor antagonist rauwolscine (0.2 mg/kg i.v.). Administration of rauwolscine, however, did not prevent the reflex increase of left ventricular pressure and regional myocardial oxygen consumption. Comparable increases in poststenotic coronary resistance during BCO were found in dogs which either received propranolol (2 mg/kg i.v.) or in which the reflex rise in mean aortic pressure was limited to 13 +/- 3 mm Hg. In both experimental groups, rauwolscine also effectively prevented the BCO-induced rise in coronary resistance. In contrast, the reflex increase of total peripheral resistance was not significantly reduced by rauwolscine, but was blunted after additional administration of the selective alpha 1-adrenoceptor antagonist prazosin (1.2 mg/kg i.v.). We conclude that: 1) Poststenotic coronary vasoconstriction occurs during shortlasting increases in efferent cardiac sympathetic discharge within the physiological range. 2) This increase in poststenotic coronary resistance is significantly reduced after administration of the alpha 2-adrenoceptor antagonist rauwolscine. 3) In contrast to poststenotic coronary resistance, functionally innervated alpha 2-adrenoceptors are of minimal importance for the reflex increase in total peripheral resistance.

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