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Kinins in the Heart

  • Chapter
Hormones and the Heart in Health and Disease

Part of the book series: Contemporary Endocrinology ((COE,volume 21))

Abstract

Kinins are polypeptides that contain the sequence of the nonapeptide, bradykinin, in their structure. In mammals, the main kinins are bradykinin and lysine-bradykinin. They are generated by a group of enzymes known as kininogenases, which include plasma and tissue kallikrein Kininogenases release kinins from low- (LMWK) and high-molecularweight kininogen (HMWK), which are present in high concentrations in plasma. Kinins are rapidly hydrolyzed in various tissues and plasma by a group of enzymes known as kininases; the best known are angiotensin-converting enzyme (ACE) and neutral endopeptidase 24.11 (NEP). Kinins release various endothelial autacoids, particularly nitric oxide (NO), endothelium-derived hyperpolarizing factor (EDHF), eicosanoids, and tissue plasminogen activator (tPA). These substances exert a cardioprotective effect by causing hemodynamic changes and/or by a direct effect on the heart. The heart and vascular tissue contain the components of the kallikrein-kinin system, and kinins are also present in the venous effluent of isolated hearts perfused with saline buffers. Myocardial ischemia increases local release of kinins, which is enhanced further by ACE inhibitors. Kinins are also found in vascular and cardiac tissue in higher concentrations than in plasma. In isolated cardiac arteries and microvessels, angiotensin stimulates the formation of cyclic guanosine 3’,5’-monophosphate (cGMP), and this effect is mediated by the release of kinins and NO. The beneficial cardiovascular effects of ACE inhibitors, which are well documented, have generally been attributed to blockade of the renin-angiotensin system (RAS); however, there is a significant amount of evidence suggesting that kinins also participate in the cardioprotective effects of ACE inhibitors, especially in myocardial infarction (MI) induced by ischemia and reperfusion, left ventricular remodeling after MI, and heart failure (HF). Recent evidence suggests that some of the effects of angiotensin (ANG) type 1 receptor (AT1) antagonists are caused by activation of type 2 receptors, which may act via release of kinins and NO. This chapter will address the role of kinins within the heart, with emphasis on their role in the reduction of MI by ischemic preconditioning and the cardioprotective effect of ACE inhibitors in hypertension, as well as during MI induced by ischemia-reperfusion, left ventricular remodeling after MI, and HF post-MI.

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Authors
  1. Oscar A. Carretero
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Editors and Affiliations

  1. Department of Physiology, The University of Tennessee, Memphis, TN, USA

    Leonard Share PhD

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© 1999 Springer Science+Business Media New York

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Carretero, O.A. (1999). Kinins in the Heart. In: Share, L. (eds) Hormones and the Heart in Health and Disease. Contemporary Endocrinology, vol 21. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-708-6_9

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  • DOI: https://doi.org/10.1007/978-1-59259-708-6_9

  • Publisher Name: Humana Press, Totowa, NJ

  • Print ISBN: 978-1-4757-5420-9

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