Effects of Histamine on Porcine Isolated Myocardium

Du, Xiao Y.; Schoemaker, Regien G.; Bax, Willem A.; Bos, Egbert; Saxena, Pramod R.

doi:10.1097/00005344-199309000-00019

Cited by 13 publications

(5 citation statements)

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“…The PIE of histamine is mediated by H 1 -receptors in the porcine ventricle, whereas the PIE of histamine in human ventricles is mainly mediated by H 2 -receptors (Du et al 1993). Hence, an animal model that expresses both functional human 5-HT 4 -receptors and human H 2 -receptors in the ventricle and the atrium is currently lacking and would be a relevant and a convenient model for preparations from the human myocardium.…”

Section: Introductionmentioning

confidence: 99%

Functional interaction of H2-receptors and 5HT4-receptors in atrial tissues isolated from double transgenic mice and from human patients

Neumann

Schwarzer

Fehse

et al. 2021

Naunyn-Schmiedeberg's Arch Pharmacol

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In the past, we generated transgenic mice that overexpress the human histamine 2 (H2)-receptor (H2-TG) or that overexpress the human serotonin 4 (5-HT4)-receptor (5-HT4-TG) in the heart. Here, we crossbred these lines of mice to generate double transgenic mice that overexpress both receptors (DT). This was done to study a conceivable interaction between these receptors in the mouse heart as a model for the human heart. When in left atria, initially, force of contraction was elevated maximally with 1 µM serotonin, and subsequently, histamine was cumulatively applied; a biphasic effect of histamine was noted: the force of contraction initially decreased, maximally at 10 nM histamine, and thereafter, the force of contraction increased again at 1 µM histamine. Notably, functional interaction between 5-HT and histamine was also identified in isolated electrically stimulated trabeculae carneae from human right atrium (obtained during cardiac surgery). These functional and biochemical data together are consistent with a joint overexpression of inotropically active H2-receptors and 5-HT4-receptors in the same mouse heart. We also describe an antagonistic interaction on the force of contraction of both receptors in the mouse atrium (DT) and in the human atrial muscle strips. We speculate that via this interaction, histamine might act as a “brake” on the cardiac actions of 5-HT via inhibitory GTP-binding proteins acting on the activity of adenylyl cyclase.

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Section: Introductionmentioning

confidence: 99%

Functional interaction of H2-receptors and 5HT4-receptors in atrial tissues isolated from double transgenic mice and from human patients

Neumann

Schwarzer

Fehse

et al. 2021

Naunyn-Schmiedeberg's Arch Pharmacol

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“…Histamine is a neurohormonal mediator that binds to histamine H1, H2, and H3 receptors, thereby inducing various cellular functions [ 108 , 109 ] as well as cardiac hypertrophy ( Figure 1 ) [ 110 ]. Notably, cardiomyocytes express the histamine H2 receptor, which is coupled to the beta receptor and Gs proteins [ 111 , 112 , 113 , 114 , 115 ]. Consistently, histamine triggers positive inotropic effects [ 116 , 117 ].…”

Section: The Role Of Immune Cells In Cardiac Hypertrophymentioning

confidence: 99%

The Microenvironment of the Pathogenesis of Cardiac Hypertrophy

Bazgir

Nau

Nakhaei‐Rad

et al. 2023

Cells

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Pathological cardiac hypertrophy is a key risk factor for the development of heart failure and predisposes individuals to cardiac arrhythmia and sudden death. While physiological cardiac hypertrophy is adaptive, hypertrophy resulting from conditions comprising hypertension, aortic stenosis, or genetic mutations, such as hypertrophic cardiomyopathy, is maladaptive. Here, we highlight the essential role and reciprocal interactions involving both cardiomyocytes and non-myocardial cells in response to pathological conditions. Prolonged cardiovascular stress causes cardiomyocytes and non-myocardial cells to enter an activated state releasing numerous pro-hypertrophic, pro-fibrotic, and pro-inflammatory mediators such as vasoactive hormones, growth factors, and cytokines, i.e., commencing signaling events that collectively cause cardiac hypertrophy. Fibrotic remodeling is mediated by cardiac fibroblasts as the central players, but also endothelial cells and resident and infiltrating immune cells enhance these processes. Many of these hypertrophic mediators are now being integrated into computational models that provide system-level insights and will help to translate our knowledge into new pharmacological targets. This perspective article summarizes the last decades’ advances in cardiac hypertrophy research and discusses the herein-involved complex myocardial microenvironment and signaling components.

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“…However, it was antagonised in muscle strips from the right and left human ventricles using cimetidine, and ThEA was ineffective [ 161 ]. Much later, Du et al, 1993 [ 102 ] found a transient negative inotropic effect to histamine in some human left ventricular muscle strips, but only in half of the patients studied. Some data were also presented [ 89 ] that may be interpreted as a negative inotropic effect of histamine H 1 receptor stimulation in human ventricular preparations.…”

Section: Histamine H 1 Receptor In Human Heartsmentioning

confidence: 99%

“…For the human ventricle, at least one publication reported a direct negative inotropic effect of histamine, probably via histamine H 1 receptor stimulation. However, this negative inotropic effect under conditions specific for histamine H 1 receptors stimulation was only seen in approximately half of the patients, but clinical details were not given [ 102 ]. Moreover, NIE were noted when they generated a cumulative concentration–response curve.…”

Section: Histamine H 1 Receptor In Human Heartsmentioning

confidence: 99%

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Function and Role of Histamine H1 Receptor in the Mammalian Heart

et al. 2023

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Histamine can change the force of cardiac contraction and alter the beating rate in mammals, including humans. However, striking species and regional differences have been observed. Depending on the species and the cardiac region (atrium versus ventricle) studied, the contractile, chronotropic, dromotropic, and bathmotropic effects of histamine vary. Histamine is present and is produced in the mammalian heart. Thus, histamine may exert autocrine or paracrine effects in the mammalian heart. Histamine uses at least four heptahelical receptors: H1, H2, H3 and H4. Depending on the species and region studied, cardiomyocytes express only histamine H1 or only histamine H2 receptors or both. These receptors are not necessarily functional concerning contractility. We have considerable knowledge of the cardiac expression and function of histamine H2 receptors. In contrast, we have a poor understanding of the cardiac role of the histamine H1 receptor. Therefore, we address the structure, signal transduction, and expressional regulation of the histamine H1 receptor with an eye on its cardiac role. We point out signal transduction and the role of the histamine H1 receptor in various animal species. This review aims to identify gaps in our knowledge of cardiac histamine H1 receptors. We highlight where the published research shows disagreements and requires a new approach. Moreover, we show that diseases alter the expression and functional effects of histamine H1 receptors in the heart. We found that antidepressive drugs and neuroleptic drugs might act as antagonists of cardiac histamine H1 receptors, and believe that histamine H1 receptors in the heart might be attractive targets for drug therapy. The authors believe that a better understanding of the role of histamine H1 receptors in the human heart might be clinically relevant for improving drug therapy.

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Effects of Histamine on Porcine Isolated Myocardium

Cited by 13 publications

References 0 publications

Functional interaction of H2-receptors and 5HT4-receptors in atrial tissues isolated from double transgenic mice and from human patients

Functional interaction of H2-receptors and 5HT4-receptors in atrial tissues isolated from double transgenic mice and from human patients

The Microenvironment of the Pathogenesis of Cardiac Hypertrophy

Function and Role of Histamine H1 Receptor in the Mammalian Heart

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