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Inotropic effects of Ca 2+ channel agonist and antagonists in neuraminidase‐treated left atria of rats
Author(s) -
Hattori Yuichi,
Hazama Setsuro,
Kanno Mono,
Nakao Yasuo
Publication year - 1986
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1986.tb10818.x
Subject(s) - diltiazem , sarcolemma , verapamil , inotrope , medicine , endocrinology , chemistry , contractility , nifedipine , sialic acid , agonist , neuraminidase , propranolol , calcium , biology , receptor , myocyte , biochemistry , enzyme
1 The effects of removal of sialic acid from cardiac sarcolemma on contractile functions and on inotropic responses to Ca 2+ channel agonist and antagonists were investigated in rat left atria. 2 About 64% of the total sialic acid content of the left atria was removed during a 90 min exposure to neuraminidase (2 u ml −1 ). 3 The removal of sialic acid neither affected the development of twitch tension induced by stimulation at a frequency of 0.5 Hz, nor altered the interval‐dependent changes in contractility such as the force‐frequency relationship and post rest contractions. 4 The positive inotropic effects produced by isoprenaline, and by an increase in extracellular Ca 2+ concentration were the same in the neuraminidase‐treated preparations as those in the untreated preparations. Bay K 8644, a Ca 2+ channel agonist, induced an increase in conractility in the neuraminidase‐treated preparations comparable to that in the untreated ones. 5 Neuraminidase treatment significantly attenuated the negative inotropic effects of verapamil and diltiazem, whereas it had no effect on that of nifedipine. 6 The results indicate that sialic acid removal modifies neither the basal contractile functions nor the positive inotropism which is associated with an enhancement of the slow inward Ca 2+ current. However, sialic acid, which constitutes the glycocalyx of the cardiac sarcolemma, may be involved in the mechanism of the Ca 2+ channel antagonistic actions of verapamil and diltiazem, but not that of nifedipine. Thus, our results provide pharmacological evidence that verapamil and diltiazem behave differently from the dihydropyridine compounds.