Histamine and Human Heart

Triggiani, Massimo; Genovese, Arturo; Vigorito, Carlo; Marone, Gianni

doi:10.1159/000233777

Cited by 13 publications

(2 citation statements)

References 10 publications

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“…The heart contains histamine under normal physiological conditions, with the quantity varying between chambers and also between species [59,60]. Consistently though, the right atrium contains the most histamine, with descending amounts found in the left atrium, right ventricle, and left ventricle [60].…”

Section: Histaminementioning

confidence: 88%

Histamine receptors in heart failure

Levick

2021

Heart Fail Rev

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The biogenic amine, histamine, is found predominantly in mast cells, as well as specific histaminergic neurons. Histamine exerts its many and varied actions via four G-protein-coupled receptors numbered one through four. Histamine has multiple effects on cardiac physiology, mainly via the histamine 1 and 2 receptors, which on a simplified level have opposing effects on heart rate, force of contraction, and coronary vasculature function. In heart failure, the actions of the histamine receptors are complex, the histamine 1 receptor appears to have detrimental actions predominantly in the coronary vasculature, while the histamine 2 receptor mediates adverse effects on cardiac remodeling via actions on cardiomyocytes, fibroblasts, and even endothelial cells. Conversely, there is growing evidence that the histamine 3 receptor exerts protective actions when activated. Little is known about the histamine 4 receptor in heart failure. Targeting histamine receptors as a therapeutic approach for heart failure is an important area of investigation given the over-the-counter access to many compounds targeting these receptors, and thus the relatively straight forward possibility of drug repurposing. In this review, we briefly describe histamine receptor signaling and the actions of each histamine receptor in normal cardiac physiology, before describing in more detail the known role of each histamine receptor in adverse cardiac remodeling and heart failure. This includes information from both clinical studies and experimental animal models. It is the goal of this review article to bring more focus to the possibility of targeting histamine receptors as therapy for heart failure.

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Section: Histaminementioning

confidence: 88%

Histamine receptors in heart failure

Levick

2021

Heart Fail Rev

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“…In isolated perfused kidney of sen sitized guinea pigs, antigen challenge causes the re lease of leukotriene C4 and thromboxane B2 (the stable metabolite of thromboxane A2 which is a potent vasoconstrictor like leukotriene C4) and marked re duction in renal perfusion rate . Although antiIgE serum has been shown to induce the release of histamine, leukotriene C4, D4, E4 and thromboxane B2 from human kidney and heart in vitro [6,9,10,13], this is indirect evidence of the presence of mast cells (MC) and IgE, and the ability of IgE to play its usual role of MC sensitization. This paper deals with the di rect demonstration of MC in the two organs, their histochemical properties (which is important, in view'of the known heterogeneity of MC), and, most impor tantly, their sensitization with IgE.…”

mentioning

confidence: 99%

Demonstration of IgE-Sensitized Mast Cells in Human Heart and Kidney

Assem

Ghanem²

1988

Int Arch Allergy Immunol

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Transmural changes in mast cell density in rat heart after infarct induction in vivo

Engels

Reiters

Daemen

et al. 1995

The Journal of Pathology

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The cardiac distribution of mast cells was investigated after the induction of acute myocardial infarction in the rat. The left anterior descending coronary artery (LAD) was occluded by ligation in the infarct group, whereas in sham rats only a superficial ligature was placed beside the LAD. Rats of both groups were killed at 4, 7, 14, 21, 35, and 85 days following surgery. Hearts were excised and formalin-fixed. Mast cell densities were monitored in subepicardial and subendocardial layers of the left ventricle (LV) in 6 microns thick toluidine blue-stained cross-sections. In control (non-operated) animals, mast cell densities were comparable in the LV subepicardial and subendocardial layers (1.5-2.0 cells per mm2). Following infarction, the mast cell density at the subepicardial site of the infarction gradually increased, reaching a maximum of 25 cells per mm2 on day 21, while a non-significant increase was observed at the subendocardial site. In the non-infarcted regions, the mast cell density increased transiently to reach a maximum of 7 cells per mm2 on day 35 in the subepicardial layer. Again, changes in mast cell density in the subendocardial layer were non-significant. In the sham group, a gradual increase to 9 cells per mm2 on day 21 and a subsequent decrease to 5 cells per mm2 on day 85 were observed in the subepicardial layers. These findings indicate a massive accumulation of mast cells in the subepicardial layers of the infarcted region and a small but significant effect of the surgical procedure on cardiac mast cell deposition, especially in the outer layers of the left ventricle.

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Histamine and Human Heart

Cited by 13 publications

References 10 publications

Histamine receptors in heart failure

Histamine receptors in heart failure

Demonstration of IgE-Sensitized Mast Cells in Human Heart and Kidney

Transmural changes in mast cell density in rat heart after infarct induction in vivo

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