Comparison of the positive inotropic effects of serotonin,histamine, angiotensin II,endothelin and isoprenaline in the isolated human right atrium |
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Authors: | Hans-Reinhard Zerkowski Andrea Broede Klaus Kunde Steffen Hillemann Ellen Schäfer Magdalene Vogelsang Martin C Michel Otto-Erich Brodde |
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Institution: | (1) Abteilung Thorax- und Kardiovaskuläre Chirurgie, Universitätsklinikum Essen, Hufelandstrasse 55, W-4300 Essen 1, Federal Republic of Germany;(2) Biochemisches Forschungslabor, Medizinische Klinik und Poliklinik, Abteilung Nieren- und Hochdruckkrankheiten, Universitätsklinikum Essen, Hufelandstrasse 55, W-4300 Essen 1, Federal Republic of Germany |
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Abstract: | Summary The receptor systems through which serotonin (5-HT), histamine, angiotensin II and endothelin increase the force of contraction were studied in isolated right atria from patients without apparent heart failure.All agonists increased the atrial force of contraction in a concentration-dependent manner; maximal effects, however, were significantly less than those evoked by isoprenaline or Ca2+. 5-HT and histamine, but not angiotensin II and endothelin, activated adenylate cyclase, whereas endothelin and angiotensin II stimulated inositol phosphate generation. Experiments with subtype-selective antagonists revealed that histamine effects were mediated by H2-receptors (sensitive to ranitidine), 5-HT-effects by 5-HT4-receptors (sensitive to SDZ 205-557) and angiotensin II effects by AT1-receptors (sensitive to losartan).We conclude that in human right atria the force of contraction can be increased by cyclic AMP-dependent (histamine, 5-HT) and -independent (angiotensin II, endothelin) pathways. Compared to -adrenoceptors, however, all other receptor systems increase the force of contraction only submaximally indicating that the -adrenoceptor pathway is the most important physiological mechanism to regulate force of contraction and/or heart rate in the human heart.Correspondence to O. E. Brodde at the above address |
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Keywords: | Serotonin Histamine Angiotensin II Endothelin Cardiac adenylate cyclase Cardiac inositol phosphates Human heart |
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