Adrenoceptor and cholinoceptor modulation of rat pulmonary vein cardiac muscle contractility

Abstract Cardiac muscle extends into mammalian pulmonary veins for variable distances according to species. This study has addressed the autonomic control of electrically paced cardiac muscle of the pulmonary vein of the rat. Contractile responses of Wistar rat pulmonary veins were investigated unde...

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Bibliographic Details
Published in:Vascular pharmacology 2007-03, Vol.46 (3), p.166-170
Main Authors: Sweeney, Catherine M, Jones, James F.X, Bund, Stuart J
Format: Article
Language:English
Subjects:
Acetylcholine
Acetylcholine - metabolism
Acetylcholine - pharmacology
Animals
Atenolol - pharmacology
Atropine - pharmacology
Autonomic
Cardiac muscle
Cardiovascular
In Vitro Techniques
Male
Myocardial Contraction - drug effects
Myocardial Contraction - physiology
Noradrenaline
Norepinephrine - metabolism
Norepinephrine - pharmacology
Pulmonary vein
Pulmonary Veins - drug effects
Pulmonary Veins - physiology
Rats
Rats, Wistar
Receptors, Adrenergic - drug effects
Receptors, Adrenergic - metabolism
Receptors, Cholinergic - drug effects
Receptors, Cholinergic - metabolism
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Summary:Abstract Cardiac muscle extends into mammalian pulmonary veins for variable distances according to species. This study has addressed the autonomic control of electrically paced cardiac muscle of the pulmonary vein of the rat. Contractile responses of Wistar rat pulmonary veins were investigated under isometric conditions in vitro. Vessels were electrically paced at 1 Hz (10 V, 1 ms pulse width). Acetylcholine (ACh, 1 nM–10 μM) attenuated the contractile response (maximum inhibition at 1 μM, 41 ± 15%, mean ± SD). The attenuation was inhibited by atropine ( p < 0.05) and partially inhibited (7 ± 4%, mean ± SD, p < 0.01) by removal of the endothelium. Noradrenaline (NA, 1 nM–10 μM) augmented the cardiac muscle contractility in a fashion partially inhibited by atenolol; augmentation at 10 μM was reduced from 169 ± 9% ( n = 6) to 135 ± 9% ( n = 5), ( p < 0.05). The ability of ACh to attenuate the contractile responses was unaffected by the presence of NA. In conclusion, ACh has a muscarinic receptor-mediated negative inotropic effect upon the cardiac muscle of the pulmonary vein of the rat mediated in part by the endothelium. The cardiac muscle expresses a positive inotropic response to NA partly mediated by β1-adrenoceptors that can be antagonised by ACh. Therefore, pulmonary vein cardiac muscle function is modulated by competing autonomic influences which may be of significance to the generation of atrial fibrillation events.
ISSN:1537-1891
1879-3649
DOI:10.1016/j.vph.2006.09.005