Differential H1- and H2-receptor-mediated histamine responses of canine epicardial conductance and distal resistance coronary vessels.

Miller, Wayne L.; Bové, Alfred A.

doi:10.1161/01.res.62.2.226

Cited by 16 publications

(7 citation statements)

References 32 publications

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“…Histamine, formed from histidine by histidine-decarboxylase and stored in mast cells and basophils, plays an important role in hypersensitivity and allergic reactions and can modulate vasomotor tone via stimulation of H 1 and H 2 receptors in the vascular wall. In the coronary circulation, H 1 receptors located on vascular smooth muscle cells of large and small arteries mediate vasoconstriction, while H 2 receptors located on vascular smooth muscle cells of arterioles mediate vasodilation (312,403). In addition, H 1 receptors located on the endothelium can stimulate NO release to produce coronary vasodilation (312,586).…”

Section: Autacoidsmentioning

confidence: 99%

Regulation of Coronary Blood Flow During Exercise

Duncker

Bache

2008

Physiological Reviews

784

684

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Exercise is the most important physiological stimulus for increased myocardial oxygen demand. The requirement of exercising muscle for increased blood flow necessitates an increase in cardiac output that results in increases in the three main determinants of myocardial oxygen demand: heart rate, myocardial contractility, and ventricular work. The approximately sixfold increase in oxygen demands of the left ventricle during heavy exercise is met principally by augmenting coronary blood flow (~5-fold), as hemoglobin concentration and oxygen extraction (which is already 70-80% at rest) increase only modestly in most species. In contrast, in the right ventricle, oxygen extraction is lower at rest and increases substantially during exercise, similar to skeletal muscle, suggesting fundamental differences in blood flow regulation between these two cardiac chambers. The increase in heart rate also increases the relative time spent in systole, thereby increasing the net extravascular compressive forces acting on the microvasculature within the wall of the left ventricle, in particular in its subendocardial layers. Hence, appropriate adjustment of coronary vascular resistance is critical for the cardiac response to exercise. Coronary resistance vessel tone results from the culmination of myriad vasodilator and vasoconstrictors influences, including neurohormones and endothelial and myocardial factors. Unraveling of the integrative mechanisms controlling coronary vasodilation in response to exercise has been difficult, in part due to the redundancies in coronary vasomotor control and differences between animal species. Exercise training is associated with adaptations in the coronary microvasculature including increased arteriolar densities and/or diameters, which provide a morphometric basis for the observed increase in peak coronary blood flow rates in exercise-trained animals. In larger animals trained by treadmill exercise, the formation of new capillaries maintains capillary density at a level commensurate with the degree of exercise-induced physiological myocardial hypertrophy. Nevertheless, training alters the distribution of coronary vascular resistance so that more capillaries are recruited, resulting in an increase in the permeability-surface area product without a change in capillary numerical density. Maintenance of alpha- and ss-adrenergic tone in the presence of lower circulating catecholamine levels appears to be due to increased receptor responsiveness to adrenergic stimulation. Exercise training also alters local control of coronary resistance vessels. Thus arterioles exhibit increased myogenic tone, likely due to a calcium-dependent protein kinase C signaling-mediated alteration in voltage-gated calcium channel activity in response to stretch. Conversely, training augments endothelium-dependent vasodilation throughout the coronary microcirculation. This enhanced responsiveness appears to result principally from an increased expression of nitric oxide (NO) synthase. Finally, physical conditioning decreases e...

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Section: Autacoidsmentioning

confidence: 99%

Regulation of Coronary Blood Flow During Exercise

Duncker

Bache

2008

Physiological Reviews

784

684

View full text Add to dashboard Cite

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“…Histamine, an autocoid which is stored in both mast cells and basophils, is formed by the enzymatic decarboxylation of histidine and plays an essential role in allergic responses, inflammation, and injury. Upon release from immune cells, histamine modulates vascular tone through two cognate receptors (i.e., H1 and H2) resulting in arteriolar vasodilation via H2 receptors, venoconstriction via H1 receptors and enhanced capillary permeability (676,953). The coordinated response of these actions is the notable tissue edema seen in acute allergic responses or localized tissue damage.…”

Section: Neural Controlmentioning

confidence: 99%

Regulation of Coronary Blood Flow

Goodwill

Dick

Kiel

et al. 2017

Comprehensive Physiology

244

248

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The heart is uniquely responsible for providing its own blood supply through the coronary circulation. Regulation of coronary blood flow is quite complex and, after over 100 years of dedicated research, is understood to be dictated through multiple mechanisms that include extravascular compressive forces (tissue pressure), coronary perfusion pressure, myogenic, local metabolic, endothelial as well as neural and hormonal influences. While each of these determinants can have profound influence over myocardial perfusion, largely through effects on end-effector ion channels, these mechanisms collectively modulate coronary vascular resistance and act to ensure that the myocardial requirements for oxygen and substrates are adequately provided by the coronary circulation. The purpose of this series of Comprehensive Physiology is to highlight current knowledge regarding the physiologic regulation of coronary blood flow, with emphasis on functional anatomy and the interplay between the physical and biological determinants of myocardial oxygen delivery.

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“…Indeed, the effect of L-NAME vs. cimetidine on the response to histamine was absolutely identical. Consistent with these observations, the H 2 -receptor mediates vasodilation in rabbit renal arteries as well as in the canine and human coronary circulation (8,26,40). Moreover, cimetidine augments the histamine-induced vasoconstriction at sites of coronary artery spasm in a pig model, and it can induce coronary artery spasm in patients with vasospastic angina (30 -32).…”

Section: Discussionmentioning

confidence: 77%

“…Consistently, H 1 -receptor stimulation induces vasoconstriction in rabbit renal arteries as well as in the canine and human coronary circulation (8,26,40). The small relaxation of RA at high concentrations of histamine in the presence of pyrilamine may be related to release of low amounts of NO, as the presence of a low number of endothelial H 2 -receptors cannot be excluded by the real-time PCR analysis.…”

Section: Discussionmentioning

confidence: 93%

Absence of histamine-induced nitric oxide release in the human radial artery: implications for vasospasm of coronary artery bypass vessels

Stähli

Greutert²,

Mei³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

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Radial artery (RA) bypass grafts can develop severe vasospasm. As histamine is known to induce vasospasm, its effect on RA was assessed compared with the classic bypass vessels internal mammary artery (MA) and saphenous vein (SV). The vessels were examined in organ chambers for isometric tension recording. Histamine induced contractions on baseline; the sensitivity was higher in RA and SV than MA. After precontraction with norepinephrine, histamine did not evoke relaxations of RA but induced relaxations of MA and less of SV at lower concentrations; it induced contractions at higher concentrations, reaching similar levels in all three vessels. Indomethacin did not affect the response of MA and RA but potentiated relaxations and reduced contractions of SV. Endothelium removal, N(omega)-nitro-L-arginine methyl ester (L-NAME), or the H2-receptor blocker cimetidine did not affect the response of RA, but inhibited relaxations and enhanced contractions in MA and inhibited relaxations in SV; in the latter, only L-NAME enhanced contractions. Real-time PCR detected much lower expression of endothelial H2-receptor in RA than MA or SV. Western blots revealed similar endothelial nitric oxide (NO) synthase expression in all three vessels. Relaxations to acetylcholine were identical in RA and MA. Thus histamine releases NO by activating the endothelial H2-receptor, the expression of which is much lower in RA than MA or SV. H2-receptor activation also releases prostaglandins in SV, partially antagonizing NO. The lack of histamine-induced NO production represents a possible mechanism of RA vasospasm.

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Differential H1- and H2-receptor-mediated histamine responses of canine epicardial conductance and distal resistance coronary vessels.

Cited by 16 publications

References 32 publications

Regulation of Coronary Blood Flow During Exercise

Regulation of Coronary Blood Flow During Exercise

Regulation of Coronary Blood Flow

Absence of histamine-induced nitric oxide release in the human radial artery: implications for vasospasm of coronary artery bypass vessels

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