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Effect of histamine on cardiac sarcolemmal calcium binding as indicated by use of ionic lanthanum
S A Barman1, M D Olson, J T Saari
1Department of Physiology, University of North Dakota School of Medicine, Grand Forks 58202.
Insights
Histamine enhances lanthanum binding to cardiac cell membranes, suggesting increased calcium binding. This effect is mediated by H2 receptors, contributing to histamine's positive inotropic effect in heart muscle.
Area of Science:
- Cardiology
- Pharmacology
- Cell Biology
Background:
- Histamine is known to have a positive inotropic effect on cardiac muscle.
- The precise mechanism underlying histamine's inotropic action, particularly its interaction with calcium, remains incompletely understood.
Purpose of the Study:
- To investigate whether histamine's positive inotropic effect is linked to enhanced calcium binding.
- To explore the role of the sarcolemmal-glycocalyx complex in histamine-mediated calcium binding.
Main Methods:
- Rabbit hearts were perfused with histamine, verapamil, and lanthanum under various conditions.
- Transmission electron microscopy was used to visualize lanthanum binding to cardiac myocytes.
- The effects of H1 (diphenhydramine) and H2 (cimetidine) antagonists were assessed.
Main Results:
- Histamine enhanced lanthanum binding to the cardiac cell membrane and cytoplasmic vesicles.
- Verapamil alone prevented lanthanum binding.
- The histamine-induced enhancement of lanthanum binding was not affected by diphenhydramine but was reduced by cimetidine.
Conclusions:
- Histamine appears to increase calcium binding to the sarcolemmal-glycocalyx complex in cardiac muscle.
- This effect, contributing to histamine's positive inotropic action, is at least partially mediated by H2 receptors.
Abstract:
To determine whether the inotropic effect of histamine might be associated with enhanced calcium binding to the sarcolemmal-glycocalyx complex, the effect of histamine on lanthanum binding to the cell membrane in the presence of verapamil was assessed. Rabbit hearts were perfused firstly with histamine, secondly with histamine and verapamil, and subsequently with histamine in the presence of lanthanum and verapamil. Subsequent transmission electron microscopy showed the presence of bound lanthanum on both the cellular surface and cytoplasmic vesicles of most cardiac myocytes, which is in contrast to the absence of lanthanum binding that occurs in the presence of verapamil alone. Furthermore, this histamine mediated enhancement of lanthanum binding is not affected by the H1 antagonist diphenhydramine but is reduced by the H2 antagonist cimetidine. This visual evidence of an apparent enhancement of lanthanum binding under histamine and subsequent attenuation with cimetidine supports the hypothesis that histamine may exert its positive inotropic effect by causing increased calcium binding to the sarcolemmal-glycocalyx complex of cardiac muscle and that the effect is mediated at least in part by H2 receptors.