Interaction between endothelin-1 and endothelium-derived relaxing factor in human arteries and veins.

Lüscher, Thomas F.; Yang, Zhihong; Tschudi, Marcel R.; Segesser, Ludwig von; Stulz, P; Boulanger, Chantal; Siebenmann, R; Turina, Marko; Bühler, Fritz R.

doi:10.1161/01.res.66.4.1088

Cited by 279 publications

(127 citation statements)

References 41 publications

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“…The maximal contraction to endothelin-l was 6.56 ± 0.77 g (64.35 ± 7.55 mN, n = 14, combining our results for the lower phasic and nifedipine-treated curves), approximately double that of Chester et al (1989;38.7 ± 6.4 mN, n = 34 Luscher et al, 1990;8.01, Costello et al, 1990), human saphaneous vein (8.40, LUscher et al, 19908.12, Costello et al, 1990) and porcine coronary artery (approximately 9.3, Yanagisawa et al, 1988). As with U46619, the difference in pECm values for endothelin-1 between the phasic curves probably reflects the relative sensitivity of phasic activity to vasoconstrictors.…”

Section: Discussionsupporting

confidence: 81%

Pharmacological reactivity of human epicardial coronary arteries: phasic and tonic responses to vasoconstrictor agents differentiated by nifedipine

Stork

Cocks

1994

British J Pharmacology

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1 Human epicardial coronary artery rings, freshly obtained from cardiac transplantation patients, commonly exhibited phasic contractile activity in vitro. This activity occurred either spontaneously or in response to vasoconstrictor stimulation.2 Nifedipine pretreatment (1 nM-0.1 ;LM) reduced both types of phasic contractions in a concentrationdependent manner. At 0.1 StM nifedipine, spontaneous contractions were completely abolished, as were phasic contractions induced by U46619, endothelin-1 or 5-hydroxytryptamine (5-HT). 3 For U46619 (0.1-100nM), the largest phasic contractions (amplitude peak to trough) occurred over the mid-range of concentrations used (1-10 nM). At higher concentrations (30-100 nM), phasic activity was reduced as the response reached a maximum. Estimated pEC50 values for the upper phasic and lower phasic curves were significantly different (8.71 ± 0.13 versus 7.90 ± 0.11; P<0.05; n = 10). In the presence of nifedipine (0.1 gM), the purely tonic contraction curve to U46619 was similar to the lower phasic curve in the absence of nifedipine (pECm = 8.14 ± 0.06, n = 10). Similar results were obtained for endothelin-1 (0.1-100 nM). 4 Responses to 5-HT (1 nM-3 gLM) were more variable. The largest phasic contractions were spread unevenly throughout the concentration-response curve. In the presence of nifedipine (0.1 gM), the curve to 5-HT was significantly depressed in range but not sensitivity (pECm) when compared with the phasic curves.5 In conclusion, activation of dihydropyridine-sensitive voltage-operated Ca2l channels mediated the phasic contractions commonly observed in human epicardial coronary arteries. These contractions amplified the contractile responses to low concentrations of vasoconstrictors. Inhibition of phasic activity by the Ca2" channel antagonist, nifedipine, allowed the tonic vasoconstrictor profile of human isolated coronary artery to be determined which is important information for the accurate quantitative assessment of vasodilator responses in this tissue in vitro.

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Section: Discussionsupporting

confidence: 81%

Pharmacological reactivity of human epicardial coronary arteries: phasic and tonic responses to vasoconstrictor agents differentiated by nifedipine

Stork

Cocks

1994

British J Pharmacology

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“…4) Other relaxing factors released by the endothelium include endothelium-derived hyperpolarizing factor, prostacyclin, C-type natriuretic factor, 5-hydroxytryptamine serotonin, adenosine triphosphate, substance P, and acetylcholine. 5,6) Additionally, ECs can also produce and release vascular constricting factors. Endothelin is a potent vasoconstrictor peptide originally isolated from ECs.…”

Section: Autonomic Nervous System (Ans) and Vascular Diseasementioning

confidence: 99%

The Relationship between Vascular Function and the Autonomic Nervous System

Amiya

Watanabe

Komuro

2014

Annals of Vascular Diseases

106

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Endothelial dysfunction and autonomic nervous system dysfunction are both risk factors for atherosclerosis. There is evidence demonstrating that there is a close interrelationship between these two systems. In hypertension, endothelial dysfunction affects the pathologic process through autonomic nervous pathways, and the pathophysiological process of autonomic neuropathy in diabetes mellitus is closely related with vascular function. However, detailed mechanisms of this interrelationship have not been clearly explained. In this review, we summarize fi ndings concerning the interrelationship between vascular function and the autonomic nervous system from both experimental and clinical studies. The clarifi cation of this interrelationship may provide more comprehensive risk stratifi cation and a new effective therapeutic strategy against atherosclerosis.

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“…Indeed, the contractions to the peptide are enhanced after endothelial removal, in dicating that basal production of EDNO reduces the response to the peptide. 38 Stimulation of the formation of EDNO by acetylcholine reverses endothelin-in duced contractions in most blood vessels although this mechanism appears to be less potent in veins. 38 …”

Section: Endothelinmentioning

confidence: 99%

“…3 6 , 3 7 In human arterial and venous coronary bypass vessels, it causes marked contractions. 38 The circulating levels of endothelin-1 are very low, however, suggesting that little of the peptide is formed under physiological conditions.39 This may be related 35 ; 2) cAMP-dependent inhibition 42 ; and 3) an inhibitory fac tor produced by vascular smooth muscle cells. 43 The cGMP-dependent mechanism can be activated by EDNO, nitroglycerine, 3-morpholino sydnominine (SIN-1), 44 and atrial natriuretic peptide (which acti vates particulate guanylyl cyclase).…”

Section: Cyclooxygenase-dependent Endothelium-derived Contract Ing Famentioning

confidence: 99%

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Endothelial Regulation of Vascular Tone and Growth

Lüscher

Tanner

1993

American Journal of Hypertension

101

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The endothelium regulates vascular tone by releasing factors involved in relaxation and contraction, in coagulation and thrombus formation, and in growth inhibition and stimulation. Endothelium-dependent relaxations are elicited by transmitters, hormones, platelet substances, and the coagulation system, and by physical stimuli such as the shear stress from circulating blood. They are mediated by the endothelium-derived relaxing factor, recently identified as nitric oxide, which causes vasodilation and platelet deactivation. Other proposed endothelium-derived relaxing factors include a hyperpolarizing factor, lipooxygenase products, and the cytochrome P450 pathway. Endothelium-derived contracting factors are produced by the cyclooxygenase pathway and by endothelial cells, which produce the peptide endothelin-1, a potent vasoconstrictor that under normal conditions circulates at low levels. The endothelium produces both growth inhibitors-normally dominant-and growth stimuli. Denuded or dysfunctional endothelium leads to a proliferative response and intimal hyperplasia in the vessel wall; moreover, platelets adhere to the site and release potent growth factors. Endothelial dysfunction has numerous causes: Aging is associated with increased formation of contracting factor and decreased relaxing factor; denudation, such as by coronary angioplasty, impairs the capacities of regenerated endothelial cells; oxidized low-density lipoproteins and hypercholesterolemia interfere with nitric oxide production; hypertension morphologically and functionally alters the endothelium; and atherosclerosis markedly attenuates some endothelium-dependent relaxations. For patients with coronary bypass grafts, differences in endotheliumderived vasoactive factors between the internal mammary artery and the saphenous vein may be important determinants of graft function, with the mammary artery having more pronounced relaxations than the saphenous vein and thus a higher patency rate. Am J Hypertens 1993;6:283S-293S KEY WORDS: Endothelial regulation, endothelial dysfunction, vascular tone, endothelium-derived relaxing factors, endothelium-derived contracting factors, nitric oxide.T he endothelium takes part in the regulation of vascular tone 1 by releasing relaxing and contracting factors both under basal conditions and when activated by neurotransmitters, hormones, autacoids, or physical stimuli. In addition, endothelial cells release factors involved in coagulation and thrombus formation and in growth inhibition and stimulation.Owing to its strategic anatomic position, the endothelium is a target organ for hypertension, diabetes, and hyperlipidemia. 1 Alterations in endothelial function may contribute to the pathogenesis as well as to the progression and complications of hypertension and its sequelae such as atherosclerotic vascular disease. ENDOTHELIUM-DEPENDENT REGULATION OF VASCULAR TONERelaxing Factors Endothelium-dependent relaxa tions occur both in vitro and in vivo 2^; transmitters, hormones, substances derived from platelets, and t...

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Interaction between endothelin-1 and endothelium-derived relaxing factor in human arteries and veins.

Cited by 279 publications

References 41 publications

Pharmacological reactivity of human epicardial coronary arteries: phasic and tonic responses to vasoconstrictor agents differentiated by nifedipine

Pharmacological reactivity of human epicardial coronary arteries: phasic and tonic responses to vasoconstrictor agents differentiated by nifedipine

The Relationship between Vascular Function and the Autonomic Nervous System

Endothelial Regulation of Vascular Tone and Growth

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