Haemodynamic effects of H<sub>2</sub>‐receptor antagonists

Hinrichsen, Holger; Halabi, Atef; Kirch, Wilhelm

doi:10.1111/j.1365-2362.1992.tb01929.x

Cited by 13 publications

(4 citation statements)

References 67 publications

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“…The ranitidine-induced reduction of circulating aldosterone concentration on the day of ex vivo experiments is a potential confounder in the present experiments, as it may have masked adverse vascular effects of the aldosterone-histamine interaction. The present study confirms a negative chronotropic effect of H 2 antagonists on heart rate observed previously [ 25 ]. Likewise, H 2 antagonists can acutely but transiently reduce arterial blood pressure [ 25 ].…”

Section: Discussionsupporting

confidence: 93%

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Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

Assersen,

Jensen,

Enggaard

et al. 2024

Pflugers Arch - Eur J Physiol

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Aldosterone through the mineralocorticoid receptor MR has detrimental effects on cardiovascular disease. It reduces the bioavailability of nitric oxide and impairs endothelium-dependent vasodilatation. In resistance arteries, aldosterone impairs the sensitivity of vascular smooth muscle cells to nitric oxide by promoting the local secretion of histamine which activates H2 receptors. The present experiments tested in vivo and ex vivo the hypothesis that systemic H2-receptor antagonism reduces arterial blood pressure and improves vasodilatation in angiotensin II–induced chronic hypertension. Hypertension was induced by intravenous infusion of angiotensin II (60 ng kg−1 min−1) in conscious, unrestrained mice infused concomitantly with the H2-receptor antagonist ranitidine (27.8 µg kg−1 min−1) or vehicle for 24 days. Heart rate and arterial blood pressure were recorded by indwelling arterial catheter. Resistance (mesenteric) and conductance (aortae) arteries were harvested for perfusion myography and isometric tension recordings by wire myography, respectively. Plasma was analyzed for aldosterone concentration. ANGII infusion resulted in elevated arterial blood pressure and while in vivo treatment with ranitidine reduced plasma aldosterone concentration, it did not reduce blood pressure. Ranitidine improved ex vivo endothelial function (acetylcholine 10−9 to 10−6 mol L−1) in mesenteric resistance arteries. This was abolished by ex vivo treatment with aldosterone (10−9 mol L−1, 1 h). In aortic segments, in vivo ranitidine treatment impaired relaxation. Activation of histamine H2 receptors promotes aldosterone secretion, does not affect arterial blood pressure, and protects endothelial function in conduit arteries but promotes endothelial dysfunction in resistance arteries during angiotensin II–mediated hypertension. Aldosterone contributes little to angiotensin II–induced hypertension in mice.

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Section: Discussionsupporting

confidence: 93%

“…The present study confirms a negative chronotropic effect of H 2 antagonists on heart rate observed previously [ 25 ]. Likewise, H 2 antagonists can acutely but transiently reduce arterial blood pressure [ 25 ]. This effect is presumably due to concomitant blockade of α 1 -adrenoceptors [ 32 ].…”

Section: Discussionsupporting

confidence: 93%

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

Assersen,

Jensen,

Enggaard

et al. 2024

Pflugers Arch - Eur J Physiol

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“…Second, H2-blockers have a procholinergic effect [19,20], although it is uncertain whether this effect is due to stimulation of muscarinergic receptors, increased release of acetylocholine, or inhibition of acetylcholinesterase [21]. Although none of the subjects showed cholinergic adverse effects such as lacrimation, salivation, emesis, or diarrhea during ranitidine treatment, it is possible that a cholinergic-like effect of ranitidine contributes to the increase in vagal tone.…”

Section: Discussionmentioning

confidence: 98%

H2-Blocker modulates heart rate variability

et al. 1999

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The use of H2-blockers in the treatment of patients with peptic ulcer has become popular. However, this treatment has adverse cardiovascular effects. The aim of this study was to investigate proarrhythmic rhythm and autonomic nervous activity by analyzing heart rate variability in patients treated with omeprazole, ranitidine, and plaunotol. Nineteen patients (mean age 67.5 +/- 2.7 years) with active gastric ulcer were treated with omeprazole (20 mg/day) for 8 weeks, then ranitidine (300 mg/day) for the next 4 months, and finally plaunotol (240 mg/day). At each stage of the treatment, Holter electrocardiography was performed, and heart rate variability and arrhythmias analyzed. Heart rate variability yielded power in the low- (0.04-0.15 Hz) and high-frequency components (0.15-0.4 Hz). Although both ranitidine and omeprazole induced little change in cardiac rhythm, the high-frequency power was higher (10.3 +/- 0.8 vs 8.6 +/- 0.6 ms, P < 0.05) and the ratio of low-to-high frequency power was lower (1.41 +/-0.10 vs 1.59 +/- 0.09. P < 0.05) during ranitidine than during plaunotol treatment. Cosinor analysis of heart rate variability revealed a decreased amplitude of low-frequency power during omeprazole compared with during ranitidine and plaunotol treatment. Ranitidine modulated high-frequency power which may be related to the adverse cardiovascular effects of H2-blocker.

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“…Histamine has various effects on the coronary arteries and the myocardium (7).The main source of histamine in the heart is the mast cell, but a non-mast cell pool of histamine has been proposed (10). Histamine acts on myocardial H2 receptors to increase the heart rate and contractility, to lower the ventricular fibrillation threshold and to slow the AV conduction (5). The H2 antagonists widely used in the treatment of peptic ulcer produce cardiac side effects in some patients, suggesting that histamine might play a role in the physiological regulation of the heart (1).…”

Section: Discussionmentioning

confidence: 99%

Mast cells in human coronary arteries; is there any correlation with luminal narrowing?

Falck

Halgunset

1996

APMIS

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Histamine in the human coronary arteries is harboured in mast cells and possibly in a non-mast cell store. Upon histamine exposure atherosclerotic coronary arteries react differently than normal coronary arteries, and histamine has been proposed to provoke vasospasms, ischaemia and sudden cardiac death. Previous reports have indicated a correlation between the mast cell density and the histamine content on the one hand and the degree of atherosclerosis on the other hand. Since previous reports applied visual assessment of the luminal narrowing only, we reexamined these results utilising planimetric methods. The study was accomplished by examining coronary arteries from autopsy cases (50-70 years, N=29) with a diagnosis of sudden death, myocardial infarction or a non-cardiac cause. The mast cell density was calculated as the ratio between the mast cell count and the adventitial area as seen by light microscopy, and was compared to the degree of luminal narrowing. We were not able to find any correlation between the mast cell density and the luminal narrowing. The myocardial infarction group had the most severe degree of luminal narrowing, but there was no significant difference in mast cell density between the groups. We therefore question the previous notion that there is a correlation between the adventitial mast cell density in the coronary arteries and the luminal narrowing. Earlier reports may have been biased by visual assessment and by erroneously treating several measurements from the same person as independent samples.

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Haemodynamic effects of H₂‐receptor antagonists

Cited by 13 publications

References 67 publications

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

H2-Blocker modulates heart rate variability

Mast cells in human coronary arteries; is there any correlation with luminal narrowing?

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Haemodynamic effects of H2‐receptor antagonists

Cited by 13 publications

References 67 publications

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

Histamine H2-receptor antagonism improves conduit artery endothelial function and reduces plasma aldosterone level without lowering arterial blood pressure in angiotensin II–hypertensive mice

H2-Blocker modulates heart rate variability

Mast cells in human coronary arteries; is there any correlation with luminal narrowing?

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Haemodynamic effects of H₂‐receptor antagonists