Control of coronary vascular tone by nitric oxide.

Kelm, Malte; Schrader, Jürgen

doi:10.1161/01.res.66.6.1561

Cited by 659 publications

(298 citation statements)

References 51 publications

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“…No effect of the NOS inhibitors was observed on basal coronary flow, excluding the role of NO in the regulation of basal coronary vascular tone. This observation conflicts with in vitro findings in guinea pig Langendorff heart preparations, in which NOS inhibition reduced basal coronary vascular flow (21)(22)(23).…”

Section: Respiratory Acidosiscontrasting

confidence: 83%

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Effects of acid-base imbalance on vascular reactivity

Celotto

Capellini

Baldo

et al. 2008

Braz J Med Biol Res

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Acid-base homeostasis maintains systemic arterial pH within a narrow range. Whereas the normal range of pH for clinical laboratories is 7.35-7.45, in vivo pH is maintained within a much narrower range. In clinical and experimental settings, blood pH can vary in response to respiratory or renal impairment. This altered pH promotes changes in vascular smooth muscle tone with impact on circulation and blood pressure control. Changes in pH can be divided into those occurring in the extracellular space (pH o ) and those occurring within the intracellular space (pH i ), although, extracellular and intracellular compartments influence each other. Consistent with the multiple events involved in the changes in tone produced by altered pH o , including type of vascular bed, several factors and mechanisms, in addition to hydrogen ion concentration, have been suggested to be involved. The scientific literature has many reports concerning acid-base balance and endothelium function, but these concepts are not clear about acid-base disorders and their relations with the three known mechanisms of endothelium-dependent vascular reactivity: nitric oxide (NO/cGMP-dependent), prostacyclin (PGI 2 /cAMP-dependent) and hyperpolarization. During the last decades, many studies have been published and have given rise to confronting data on acid-base disorder and endothelial function. Therefore, the main proposal of this review is to provide a critical analysis of the state of art and incentivate researchers to develop more studies about these issues.

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Section: Respiratory Acidosiscontrasting

confidence: 83%

“…A number of publications have implicated NO in the vasodilatory response of the cerebral vasculature to hypercapnia (22), although more recent evidence suggests that the role of NO may be "permissive" rather than "causative" in this vascular bed (23).…”

Section: Respiratory Acidosismentioning

confidence: 99%

Effects of acid-base imbalance on vascular reactivity

Celotto

Capellini

Baldo

et al. 2008

Braz J Med Biol Res

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“…NS). In keeping with a role for NO in determining basal coronary tone (Kelm & Schrader, 1990), L-NAME by itself caused a small but signi®cant decrease in coronary conductance of 0.025+0.009 ml min 71 mmHg 71 .…”

Section: E Ect Of Ador Antagonists On Atp-and Adenosine-mediated Incrsupporting

confidence: 53%

“…L-NAME also attenuated vasodilations caused by 2-MeSATP (Figure 9b). This ®nding suggests that nitric oxide plays a role in the receptor-e ector signal transduction of both A 2A -adenosine and P 2Y1 receptors (Vials & Burnstock, 1993;Kelm & Schrader, 1990). In contrast, glibenclamide did not attenuate the vasodilations caused by 2-MeSATP (Figure 9a), indicating that activation of K ATP channels is not required for P 2Y1 receptor-mediated vasodilation.…”

Section: Mechanism Of a 2a -Ador Activation By Atpmentioning

confidence: 87%

Role of A_2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart

Erga

Seubert

Liang

et al. 2000

British J Pharmacology

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1 Adenosine-5'-triphosphate (ATP) and adenosine are potent coronary vasodilators. ATP is rapidly converted to adenosine by ectonucleotidases. We examined whether coronary vasodilation caused by exogenous ATP is mediated by P 2 receptor activation or by A 2A -adenosine receptor activation. 2 E ects of interventions on coronary conductance were determined by measuring coronary perfusion pressure in guinea-pig isolated hearts perfused at a constant¯ow of 10 ml min 71 . 3 ATP and adenosine both caused sustained, concentration-dependent increases of coronary conductance. Maximal responses to both agonists were equivalent. The values of pD 2 (+s.e.mean) for ATP and adenosine were 6.68+0.04 and 7.06+0.05, respectively. Adenosine was signi®cantly more potent than ATP (P50.0001, n=10).4 The values of pIC 50 for the selective A 2A -adenosine receptor antagonist SCH58261 to antagonize equivalent responses to ATP and adenosine were 8.28+0.08 and 8.28+0.06 (P=0.99, n=6), respectively. 5 The non-selective adenosine receptor antagonists xanthine amine congener (XAC) and CGS15943 antagonized similarly the equivalent vasodilations caused by ATP (pIC 50 values 7.48+0.04 and 7.45+0.06, respectively) and adenosine (pIC 50 values 7.37+0.13 and 7.56+0.11). 6 In contrast to ATP and adenosine, the two P 2 agonists 2-methylthio-ATP and uridine-5'-triphosphate failed to cause stable increases of coronary conductance, caused desensitization of vasodilator responses, and were not antagonized by SCH 58261, 8-parasulphophenyltheophylline, or XAC. 7 Glibenclamide attenuated coronary vasodilations caused by ATP and adenosine by 88 and 89%, respectively, but failed to attenuate those caused by 2-methylthio-ATP.

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“…This uncertainty derives mainly from the fact that the techniques used to quantify NO in oxygen-containing aqueous solutions are unable to discriminate between NO and labile NO donors. NOX is frequently detected by its biological activity on target cells (smoothmuscle cells [1,3] or platelets [12]) and target enzymes (soluble guanylyl cyclase [13][14][15]), by formation of methaemoglobin from HbO2 [16,17] and by the stable NO. metabolite nitrite via a diazotization reaction [18,19]).…”

Section: Introductionmentioning

confidence: 99%

NO accounts completely for the oxygenated nitrogen species generated by enzymic l-arginine oxygenation

Mülsch

Vanin

Mordvintcev

et al. 1992

Biochemical Journal

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Control of coronary vascular tone by nitric oxide.

Abstract: A specific difference-spectrophotometric method was used to measure nitric oxide (NO) release into the coronary effluent perfusate of isolated, constant-flow-perfused guinea pig hearts. Authentic NO

Cited by 659 publications

References 51 publications

Effects of acid-base imbalance on vascular reactivity

Effects of acid-base imbalance on vascular reactivity

Role of A_2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart

NO accounts completely for the oxygenated nitrogen species generated by enzymic l-arginine oxygenation

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Control of coronary vascular tone by nitric oxide.

Abstract: A specific difference-spectrophotometric method was used to measure nitric oxide (NO) release into the coronary effluent perfusate of isolated, constant-flow-perfused guinea pig hearts. Authentic NO

Cited by 659 publications

References 51 publications

Effects of acid-base imbalance on vascular reactivity

Effects of acid-base imbalance on vascular reactivity

Role of A2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart

NO accounts completely for the oxygenated nitrogen species generated by enzymic l-arginine oxygenation

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Role of A_2A‐adenosine receptor activation for ATP‐mediated coronary vasodilation in guinea‐pig isolated heart