Pronounced cholinergic but only moderate purinergic effects in isolated atrial and ventricular heart muscle from cats.
1. The effects of cholinergic and purinergic stimulation on action potential, force of contraction and 86Rb efflux were investigated in cat atrial and/or ventricular heart muscle. 2. Acetylcholine and carbachol exerted a concentration-dependent negative inotropic effect in cat atrial heart muscle. Carbachol 10 mumol l-1 completely abolished the force of contraction and increased the rate constant of 86Rb efflux 2-3 fold, whereas the action potential duration was shortened to about 1/10 of its length under control conditions. 3. The effects of acetylcholine and carbachol in cat atrial heart muscle were mimicked, qualitatively, by adenosine and its analogues 5'-(N-ethyl)-carboxamido-adenosine (NECA) and (-)-N6-(R-phenyl-isopropyl)-adenosine (R-PIA). Maximal purinergic effects, however, amounted to about 15-50% in comparison to those of cholinergic stimulation. 4. In cat ventricular heart muscle, cholinergic or purinergic stimulation had no significant effects on the force of contraction in the absence of a cyclic AMP-dependent positive inotropic effect. Carbachol antagonized the positive inotropic effect elicited by either 3-isobutyl-1-methylxanthine, isoprenaline or cyclic 8-(4-chlorphenylthio)adenosine-3':5'-monophosphate; NECA and R-PIA were less effective. The inhibition by carbachol of the effects of isoprenaline was not related to a change in the rate constant of 86Rb efflux. 5. It is concluded that the effects of cholinoceptor and purinoceptor agonists in the cat heart involve a change in the potassium conductance in the atrium, whereas the effects in the ventricle may be related to changes of intracellular cyclic AMP levels. It seems reasonable to assume that, in comparison to cholinergic stimulation, a low density of purinoceptors in the cat heart is responsible for the relatively weak effects of adenosine agonists in this species.
Kemmer
M
M
Pharmakologisches Institut, Universität Mainz, Federal Republic of Germany.
Jakob
H
H
Nawrath
H
H
D000109:Acetylcholine / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects; D000241:Adenosine / Q000494:pharmacology; D019830:Adenosine-5'-(N-ethylcarboxamide); D000818:Animals; D016275:Atrial Function; D002217:Carbachol / Q000494:pharmacology; D002415:Cats; D004176:Dipyridamole / Q000494:pharmacology; D005260:Female; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects; D010660:Phenylisopropyladenosine / Q000494:pharmacology; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000502:physiology*; D011983:Receptors, Purinergic / Q000187:drug effects / Q000502:physiology*; D012414:Rubidium Radioisotopes; D016276:Ventricular Function
D011950:Receptors, Cholinergic; D011983:Receptors, Purinergic; D012414:Rubidium Radioisotopes; D010660:Phenylisopropyladenosine; D019830:Adenosine-5'-(N-ethylcarboxamide); D004176:Dipyridamole; D002217:Carbachol; D000241:Adenosine; D000109:Acetylcholine