Adrenoceptor and cholinoceptor modulation of rat pulmonary vein cardiac muscle contractility

• 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
• ISSN: 1537-1891; 1879-3649
• DOI: 10.1016/j.vph.2006.09.005

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.