Studies on the mechanism of carbon monoxide-induced vasodilation in the isolated perfused rat heart

McFaul, Steve J.; McGrath, James J.

doi:10.1016/0041-008x(87)90252-3

Cited by 75 publications

(34 citation statements)

References 13 publications

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“…Indeed, Rich et al (23) showed a hyperpolarization of about 10 mV in rabbit corneal epithelial cells, and a hyperpolarization of about 20 mV was observed in single VSMCs by Wang (27). Thus these data confirm that the CO effect is endothelium-independent, as suggested in several reports using different techniques and protocols (14,15,27).…”

Section: Does This Increase In 4-ap-sensitive Currents Have Functionasupporting

confidence: 76%

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

Barbé

Dubuis²,

Rochetaing

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes. Am J Physiol Heart Circ Physiol 282: H2031-H2038, 2002. First published January 24, 2002 10.1152/ajpheart.00807.2001.-A physiological role of carbon monoxide has been suggested for coronary myocytes; however, direct evidence is lacking. The objective of this study was to test the effect of chronic carbon monoxide exposure on the K ϩ currents of the coronary myocytes. The effect of 3-wk chronic exposure to carbon monoxide was assessed on K ϩ currents in isolated rat left coronary myocytes by the use of the patch-clamp technique in the whole cell configuration. Moreover, membrane potential studies were performed on coronary artery rings using intracellular microelectrodes, and coronary blood flow in isolated heart preparation was recorded. Carbon monoxide did not change the amplitude of global whole cell K ϩ current, but it did increase the component sensitive to 1 mM 4-aminopyridine. Carbon monoxide exposure hyperpolarized coronary artery segments by ϳ10 mV and, therefore, increased their sensitivity to 4-aminopyridine. This effect was associated with an enhancement of coronary blood flow. We conclude that chronic carbon monoxide increases a 4-aminopyridinesensitive current in isolated coronary myocytes. This mechanism could, in part, contribute to hyperpolarization and to increased coronary blood flow observed with carbon monoxide.voltage-gated K ϩ channels; membrane currents; vasodilation; 4-aminopyridine CARBON MONOXIDE (CO) is an endogenously generated gas that regulates vascular tone. Several lines of investigation provide evidence that CO is a vasodilator acting directly on vascular smooth muscle cells (VSMCs) (27) and that it inhibits smooth muscle cell proliferation (17). In coronary circulation, acute and chronic exogenous CO exposure induced an increase in coronary blood flow (1, 16). Several mechanisms have been suggested to explain this effect, including a direct effect of CO on coronary artery cells (8). Indeed, acute CO induced in vitro an endothelium-independent relaxation of the preconstricted coronary artery (8,14). Nevertheless, the cellular mechanism by which acute or chronic CO increases in coronary blood flow is unknown.Plasma membranes of coronary VSMCs show a dense expression of voltage-gated K ϩ (K V ) channels and high-conductance Ca 2ϩ -activated K ϩ (BK Ca ) channels. Moreover, the expression levels of these two-gene families are altered in some chronic cardiovascular pathologies, such as arterial hypertension (3). CO can influence the open-state probability of BK Ca channels in VSMC membranes (27), and it can activate K V channels in jujenal circular smooth muscle cells (6), thereby regulating the level of resting membrane potential (E m ) and contractile force in VSMCs. In the VSMCs of arterial circulation, the hyperpolarizing effect of K V and BK Ca channels contributes to the regulation of vascular tone and blood pressure by limiting voltage-dependent Ca 2ϩ influx through dihydropy...

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Section: Does This Increase In 4-ap-sensitive Currents Have Functionasupporting

confidence: 76%

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

Barbé

Dubuis²,

Rochetaing

et al. 2002

American Journal of Physiology-Heart and Circulatory Physiology

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“…inhibition of platelet aggregation [65] and vascular smooth muscle relaxation [67], and is accompanied by increases in intraceliular CAMP. The characteristics and mechanism of GC-S activation by CO also seem to be identical with NO [65].…”

Section: Carbon Monoxidementioning

confidence: 99%

NO^•, CO and ^•OH Endogenous soluble guanylyl cyclase‐activating factors

Schmidt

1992

FEBS Letters

190

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Several low molecular weight compounds are capable of activating soluble guanylyl cyclase. Recent evidence suggests that some of these are formed under physiological conditions: the nitric oxide radical, carbon monoxide and the hydroxyl radical. Thus, multiple signal transduction pathways appear to exist that form a family of guanylyl cyclase activating faclors and thereby regulate the intracellular cyclic guanosine 3',5'-monophosphatc Ievcl.

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“…Interestingly, CO also induces relaxations of vascular tissues (Coburn, 1979;Lin & McGrath, 1988;Graser et al, 1990) and cultured vascular smooth muscle cells (Ramos et al, 1989). The vascular eects of CO are not due to hypoxia or functional hypoxia (McFaul & McGrath, 1987), not mediated by prostaglandins and not related to the stimulation of adrenoceptors or adenosine (Martin et al, 1985;. Despite many eorts and years of investigation, the eects of exogenous or endogenous CO on dierent vascular tissues or vascular smooth muscle cells have not been systemically characterized and the mechanisms underlying CO-mediated vasorelaxation remain largely elusive.…”

Section: Introductionmentioning

confidence: 99%

Carbon Monoxide-Induced Vasorelaxation and the Underlying Mechanisms

Wang¹,

Zhao²

2001

Carbon Monoxide and Cardiovascular Functions

111

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1 Carbon monoxide (CO) induced a concentration-dependent relaxation of isolated rat tail artery tissues which were precontracted with phenylephrine or U-46619. This vasorelaxing eect of CO was independent of the presence of the intact endothelium. 2 The CO-induced vasorelaxation was partially inhibited by the blockade of either the cyclicGMP pathway or big-conductance calcium-activated K (K Ca ) channels. When both the cyclicGMP pathway and K Ca channels were blocked, the CO-induced vasorelaxation was completely abolished. 3 Incubation of vascular tissues with hemin, in order to enhance the endogenous production of CO, suppressed the phenylephrine-induced vasocontraction in a time-and concentration-dependent manner. The hemin-induced suppression of the vascular contractile response to phenylephrine was abolished after the vascular tissues were co-incubated with either oxyhaemoglobin or zinc protoporphyrin-IX, suggesting an induced endogenous generation of CO from vascular tissues. 4 The eect of hemin incubation on vascular contractility did not involve the endogenous generation of nitric oxide. 5 Our results suggest that CO may activate both a cyclicGMP signalling pathway and K Ca channels in the same vascular tissues, and that the endogenously generated CO may signi®cantly aect the vascular contractile responses.

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Studies on the mechanism of carbon monoxide-induced vasodilation in the isolated perfused rat heart

Cited by 75 publications

References 13 publications

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

NO^•, CO and ^•OH Endogenous soluble guanylyl cyclase‐activating factors

Carbon Monoxide-Induced Vasorelaxation and the Underlying Mechanisms

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Studies on the mechanism of carbon monoxide-induced vasodilation in the isolated perfused rat heart

Cited by 75 publications

References 13 publications

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

A 4-AP-sensitive current is enhanced by chronic carbon monoxide exposure in coronary artery myocytes

NO•, CO and •OH Endogenous soluble guanylyl cyclase‐activating factors

Carbon Monoxide-Induced Vasorelaxation and the Underlying Mechanisms

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NO^•, CO and ^•OH Endogenous soluble guanylyl cyclase‐activating factors