Regular paperPretreatment with Endothelin-1 Mimics Ischemic Preconditioning Against Infarction in Isolated Rabbit Heart☆
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Cardioprotective signalling: Past, present and future
2018, European Journal of PharmacologyCitation Excerpt :Extracellular Ca2+, halogenated gases, nitric oxide (NO), reactive oxygen and nitrogen species as well as hydrogen sulphide (H2S) have been shown to induce cardioprotection (Johnson et al., 1991; Miyawaki et al., 1996; Konorev et al., 1999; Sodha et al., 2009; Guerrero-Orriach et al., 2017). In addition, adenosine, acetylcholine, angiotensin, bradykinin, catecholamines, phenylephrine, endothelin, opioids, adrenomedullin, natriuretic peptides, nicotinamide, urocortin, leptin, epoxyeicosanotrienoic acids, insulin-growth factor 1, fibroblast growth factors 1 and 2, and tumor necrosis factor α (TNFα), among others, have all been shown to confer cardioprotection when exogenously administrated (Eddy et al., 1992; Toombs et al., 1992; Yao and Gross, 1993; Liu et al., 1995; Padua et al., 1995; Meng et al., 1996; Wang et al., 1996; Okosi et al., 1998; Cohen et al., 2001; D'Souza et al., 2003; Nithipatikom et al., 2006; Santini et al., 2007; Nishida et al., 2008; Sukhodub et al., 2010). The number of procedures/compounds that could induce cardioprotection is fascinating and every day there are published reports about yet another cardioprotective agent and/or procedure.
Conditioning the whole heart-not just the cardiomyocyte
2012, Journal of Molecular and Cellular CardiologyCitation Excerpt :Endothelin-1 (ET1) receptor agonists were recognised early on as a pharmacological trigger of preconditioning [29], with evidence of ET1 receptors on the myocardial cell surface [29]. However, while ET1 administered as an exogenous bolus to trigger conditioning is effective [29], the endothelial release of ET1 during transient ischaemia/reperfusion is probably insufficient to trigger ischaemic preconditioning on its own, and ET1 receptor antagonists insufficient to attenuate ischaemic preconditioning [30]. Endothelial-derived kinins however have the potential play a far more important role in the preconditioning trigger stimulus [31].
Pathophysiological roles of endothelin receptors in cardiovascular diseases
2012, Journal of Pharmacological SciencesCardioprotective signaling to mitochondria
2009, Journal of Molecular and Cellular CardiologyCitation Excerpt :Ischemic preconditioning (IPC) and ischemic postconditioning are receptor-mediated processes that are triggered by GPCR agonists released by the ischemic heart, primarily bradykinin, opioid peptides, and adenosine [19]. Other GPCR ligands, including acetylcholine, catecholemines, endothelin, and angiotensin II, are also cardioprotective [20–24], but they were found not to be physiological triggers of IPC [14]. A composite diagram of the GPCR signaling pathways is given in Fig. 1.
Cardiovascular endothelins: Essential regulators of cardiovascular homeostasis
2006, Pharmacology and TherapeuticsMechanisms of acetylcholine- and bradykinin-induced preconditioning
2005, Vascular Pharmacology
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Please address all correspondence to: Michael V. Cohen, Department of Physiology, MSB 3050, University of South Alabama, College of Medicine, Mobile, AL 36688, U.S.A.