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Heusch G, Deussen A, Schipke J, et al. Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo. J Cardiovasc Pharmacol. 1984;6(5):961-8doi: 10.1097/00005344-198409000-00034.
Heusch, G., Deussen, A., Schipke, J., & Thämer, V. (1984). Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo. Journal of cardiovascular pharmacology, 6(5), 961-8. https://doi.org/10.1097/00005344-198409000-00034
Heusch, G, et al. "Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo." Journal of cardiovascular pharmacology vol. 6,5 (1984): 961-8. doi: https://doi.org/10.1097/00005344-198409000-00034
Heusch G, Deussen A, Schipke J, Thämer V. Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo. J Cardiovasc Pharmacol. 1984 Sep-Oct;6(5):961-8. doi: 10.1097/00005344-198409000-00034. PMID: 6209507.
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J Cardiovasc Pharmacol. 1984 Sep-Oct;6(5):961-8. doi: 10.1097/00005344-198409000-00034.

Alpha 1- and alpha 2-adrenoceptor-mediated vasoconstriction of large and small canine coronary arteries in vivo.

Journal of cardiovascular pharmacology

G Heusch, A Deussen, J Schipke, V Thämer

PMID: 6209507 DOI: 10.1097/00005344-198409000-00034

Abstract

The role of alpha-adrenoceptor subtypes mediating vasoconstriction of large epicardial and small resistive coronary arteries was investigated in 26 open-chest dogs. The left circumflex coronary artery was perfused at a constant pressure. Large vessel vasomotion was determined by measurement of circumflex coronary arterial diameter (ultrasonic transit-time technique); the vasomotion of the small resistive coronary arteries was determined from calculated end-diastolic circumflex artery resistance. beta-Receptors were blocked by propranolol (2 mg/kg i.v.) and both vagal nerves were cut. In eight dogs, the intracoronary administration of the alpha 1-adrenoceptor agonist methoxamine (500 micrograms) increased calculated large vessel resistance by 18.8 +/- 5.7% and end-diastolic resistance by 9.5 +/- 0.3%. Intracoronary administration of the alpha 2-adrenoceptor agonist BHT 920 (500 micrograms) did not affect large vessel resistance, but increased end-diastolic resistance by 37.5 +/- 5.6%. In an additional 18 dogs, left cardiac sympathetic nerve stimulation induced an increase in large vessel resistance by 11.1 +/- 0.9% and in end-diastolic resistance by 31.8 +/- 3.0%. The increase in large vessel resistance was prevented by the alpha 1-adrenoceptor antagonist prazosin (1.2 mg/kg i.v.), which still permitted an increase in end-diastolic resistance by 23.0 +/- 3.2%. The increase in end-diastolic resistance was prevented by the alpha 2-adrenoceptor antagonist rauwolscine (0.2 mg/kg i.v.), which still permitted an increase in large vessel resistance by 11.9 +/- 2.4%. The calcium antagonist nifedipine (20 micrograms/kg i.v.) prevented both the increase in large vessel resistance and end-diastolic resistance during sympathetic stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

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