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Molecular and Cellular Mechanisms of Cardiovascular Regulation pp 327–351Cite as

The Role of Phosphoinositide Hydrolysis in the Regulation of Cardiac Function via α-Adrenergic, Endothelin, and Angiotensin Receptors

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Summary

Activation of myocardial a,-adrenergic, endothelin, and angiotensin receptors leads to acceleration of the hydrolysis of phosphoinositide, with resultant production of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol. In spite of the wide range of species-dependent variation in the induction of the positive inotropic effect among mammalian species, there is an excellent correlation between the extent of acceleration of the hydrolysis of phosphoinositide and the positive inotropic effect under most experimental conditions after the administration of the respective agonists in the rabbit ventricular muscle. Moreover, the positive inotropic effect of the agonists of these receptors is consistently associated with a negative lusitropic effect and an increase in the sensitivity of myofilaments to Ca2+ ions. Furthermore, the positive inotropic effect can be selectively inhibited by inhibitors of protein kinase C such as staurosporine, NA 0345, and H-7, with little associated effect on the hydrolysis of phosphoinositide and the positive inotropic effect of isoproterenol and Bay K 8644 in the rabbit ventricular muscle. An activator of protein kinase C, phorbol 12,13-dibutyrate (PDBu), likewise selectively inhibited the positive inotropic effect and acceleration of phosphoinositide hydrolysis induced by these receptor agonists in the rabbit. By contrast, the regulation of action potentials and membrane ionic currents induced by these receptor agonists shows quite a wide range of variation in rabbit ventricular cardiomyocytes. α-Adrenoceptor agonists cause monophasic prolongation of the action potential, while endothelin-1 and angiotensin II elicit a biphasic change in the duration of action potential, namely a transient abbreviation that is followed by a long-lasting prolongation. Endothelin-1 also modifies the calcium current (ICa,) in a biphasic manner, while α-agonists scarcely affected ICa, and angiotensin II has a weak and variable effect on ICa. The potassium current, IKl, is suppressed by α-agonists, whereas it is transiently activated by angiotensin II. Angiotensin II activates a slowly developing Cl- current, while endothelin-1 does not induce such a current. These results suggest that the products of hydrolysis of phosphoinositide might play a crucial role as intracellular messengers in the regulation of cardiac function that is induced upon activation of angiotensin, endothelin, and α-adrenergic receptors in the rabbit ventricular myocardium. The signal-transduction process subsequent to cceleration of the hydrolysis of phosphoinositide might, however, show a wide range of variable types of coupling to regulatory proteins in the heart. Alternatively, additional regulatory processes that are specifically triggered by activation of the respective receptors might operate in parallel with the acceleration of phosphoinositide hydrolysis. Thus, the activation of receptors that belong to this class could be involved in diverse types of physiological as well as pathophysiological regulation of myocardial cell function in the mammalian heart.

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Authors and Affiliations

  1. Department of Pharmacology, Yamagata University School of Medicine, 990-23, Yamagata, Japan

    Masao Endoh & Hideyuki Morita

  2. Department of Pharmacology, Fukushima Medical College, 960-12, Fukushima, Japan

    Junko Kimura

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  1. Masao Endoh
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  2. Hideyuki Morita
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Editors and Affiliations

  1. Department of Pharmacology, Yamagata University School of Medicine, 2-2-2 Iida-nishi, 990-23, Yamagata, Japan

    Masao Endoh M.D., Ph.D. (Professor) (Professor)

  2. Georgetown University Medical Center, 3900 Reservoir Rd., NW, 20007, Washington, D.C., USA

    Martin Morad Ph.D. (Professor of Pharmacology and Medicine) (Professor of Pharmacology and Medicine)

  3. Pharmakologisches Institut, Universitäts-Krankenhaus Eppendorf, Martinistrasse 52, D-20246, Hamburg, Germany

    Hasso Scholz M.D. (Professor) (Professor)

  4. Department of Pharmacology, Akita University School of Medicine, 1-1-1 Hondoh, Akita 010, Japan

    Toshihiko Iijima M.D., Ph.D. (Professor) (Professor)

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Endoh, M., Morita, H., Kimura, J. (1996). The Role of Phosphoinositide Hydrolysis in the Regulation of Cardiac Function via α-Adrenergic, Endothelin, and Angiotensin Receptors. In: Endoh, M., Morad, M., Scholz, H., Iijima, T. (eds) Molecular and Cellular Mechanisms of Cardiovascular Regulation. Springer, Tokyo. https://doi.org/10.1007/978-4-431-65952-5_25

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