2012
DOI: 10.1177/147323001204000114
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Serum Levels of Calcitonin Gene-Related Peptide and Substance P are Decreased in Patients with Diabetes Mellitus and Coronary Artery Disease

Abstract: OBJECTIVE: This study evaluated serum levels of the neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP) in coronary artery disease (CAD) patients with and without a history of diabetes mellitus (DM). METHODS: Patients undergoing coronary angiography for suspected myocardial ischaemia were divided into four groups depending on their clinical status: control group (no CAD or DM; n = 44), DM group (DM without CAD; n = 46), CAD group (stable CAD without DM; n = 44) and DM + CAD group (stable … Show more

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Cited by 54 publications
(40 citation statements)
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“…Importantly, the adriamycin treatment schedule was earlier applied to produce congestive cardiomyopathy in the rat (Schwarz et al 1998a;Katona et al 2004). In this experimental model and other models of heart failure, the protective role of chemosensitive afferent nerves which express the TRPV1 receptor has been demonstrated and suggested to be mediated through the release of CGRP from cardiac sensory nerves (Ferdinandy et al 1997;Katona et al 2004;Wang and Wang 2005;Ferdinandy and Jancsó 2009;Wang et al 2012). Although the mechanisms of the cardioprotective effect of CGRP-containing sensory nerves are not fully understood, the experimental evidence suggests that impairment of these particular peptidergic sensory nerves aggravates the development and course of cardiac pathologies, such as drug-induced congestive cardiomyopathy and heart failure; conversely, the TRPV1 receptor-activated increased release of CGRP (Zhong and Wang 2008) from cardiac sensory nerves confers protection against heart failure.…”
Section: Discussionmentioning
confidence: 95%
“…Importantly, the adriamycin treatment schedule was earlier applied to produce congestive cardiomyopathy in the rat (Schwarz et al 1998a;Katona et al 2004). In this experimental model and other models of heart failure, the protective role of chemosensitive afferent nerves which express the TRPV1 receptor has been demonstrated and suggested to be mediated through the release of CGRP from cardiac sensory nerves (Ferdinandy et al 1997;Katona et al 2004;Wang and Wang 2005;Ferdinandy and Jancsó 2009;Wang et al 2012). Although the mechanisms of the cardioprotective effect of CGRP-containing sensory nerves are not fully understood, the experimental evidence suggests that impairment of these particular peptidergic sensory nerves aggravates the development and course of cardiac pathologies, such as drug-induced congestive cardiomyopathy and heart failure; conversely, the TRPV1 receptor-activated increased release of CGRP (Zhong and Wang 2008) from cardiac sensory nerves confers protection against heart failure.…”
Section: Discussionmentioning
confidence: 95%
“…The serum CGRP levels are decreased in patients with diabetes mellitus and coronary artery disease [20]. CGRP has been shown to modulate glucose homeostasis by antagonizing insulin action in skeletal muscle and liver [21,22].…”
Section: Discussionmentioning
confidence: 99%
“…In human studies, CGRP lowered blood pressure (see above) and protected against heart failure via positive chronotropic and inotropic effects [72,73]. Additional evidence for a cardioprotective role of CGRP in humans comes from studies showing: (i) decreased CGRP serum levels in coronary artery disease [74]; (ii) improved myocardial contractility after intravenous infusions of CGRP in congestive heart failure [75]; (iii) involvement of CGRP in the response to nitroglycerine in chronic heart failure [76]; and finally (iv) the finding that CGRP might be the effector molecule of nitroxyl (HNO) in the HNO-TRPA1-CGRP axis [77].…”
Section: Cgrp and The [ 1 2 _ T D $ D I F F ] Heartmentioning
confidence: 98%