ISSN:
1432-1912
Keywords:
Acetylcholine
;
Ca2+-dependent action potential
;
Isoproterenol
;
Theophylline
;
Gumea-pig papillary muscle
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Effects of acetylcholine (ACh) on the Ca2+-dependent electrical and mechanical response restored by isoproterenol (10−8 M), theophylline (3 mM) or excess Ca2+ (7.2 mM) were investigated in the guinea-pig papillary muscle which was partially depolarized and rendered inexcitable by potassium (27 mM), and were compared with effects of nifedipine, a Ca2+ antagonist. Isoproterenol, theophylline and excess Ca2+ restored the Ca2+-dependent action potential and tension development. ACh at concentrations of 10−6–10−4 M decreased the maximum rate of rise of the action potential restored by isoproterenol or theophylline, but ACh (10−8–10−4 M) had no significant effect on the maximum rate of rise of the action potential restored by excess Ca2+. The actions of ACh on electrial and mechanical responses restored by isoproterenol or theophylline were increased by physostigmine (10−7 M) and were antagonized by atropine (10−7 M) but not by hexamethonium (3×10−4 M). Nifedipine (10−6M) significantly suppressed the maximum rate of rise of the action potential and tension development restored by isoproterenol, theophylline or excess Ca2+. It is concluded that ACh acting via muscarinic receptors suppresses the Ca2+-dependent action potential, that was previously restored by isoproterenol or theophylline, by an increase in calcium conductance (g Ca), which, in turn, may be due to an elevation of the level of cellular cAMP. However, ACh does not affect the action potential restored by excess Ca2+ which probably acts by an increase in the driving force for Ca2+. This mode of action of ACh is different from that of a Ca2+ antagonist, nifedipine. The antagonistic effect of ACh to positive inotropic effects induced by isoproterenol or theophylline may be attributed to this mechanism.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00508630
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