Platelet inhibition by endothelium‐derived relaxing factor from the rabbit perfused aorta

Bult, Hidde; Fret, Hermine R.L.; Bossche, Rita M. Van den; Herman, Arnold G.

doi:10.1111/j.1476-5381.1988.tb11769.x

Cited by 37 publications

(20 citation statements)

References 23 publications

(24 reference statements)

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“…The dose-response curve of BRL 37344 was then performed in the presence of methylene blue (10 M), an agent that inhibits activation of soluble guanylyl cyclase by NO in various biological systems (14,15). A 30-min pretreatment of methylene blue alone had no significant effect on basal peak tension (52.4Ϯ8.8 and 49.7Ϯ9.1 N in control and methylene blue-treated biopsies, respectively; n ϭ 8).…”

Section: Resultsmentioning

confidence: 99%

The negative inotropic effect of beta3-adrenoceptor stimulation is mediated by activation of a nitric oxide synthase pathway in human ventricle.

Gauthier¹,

Leblais²,

Kobzik³

et al. 1998

J. Clin. Invest.

345

294

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Abstract␤ 1 -and ␤ 2 -adrenoceptors in heart muscle cells mediate the catecholamine-induced increase in the force and frequency of cardiac contraction. Recently, in addition, we demonstrated the functional expression of ␤ 3 -adrenoceptors in the human heart. Their stimulation, in marked contrast with that of ␤ 1 -and ␤ 2 -adrenoceptors, induces a decrease in contractility through presently unknown mechanisms. In the present study, we examined the role of a nitric oxide (NO) synthase pathway in mediating the ␤ 3 -adrenoceptor effect on the contractility of human endomyocardial biopsies. The negative inotropic effects of a ␤ 3 -adrenoceptor agonist, BRL 37344, and also of norepinephrine in the presence of ␣ -and

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Section: Resultsmentioning

confidence: 99%

The negative inotropic effect of beta3-adrenoceptor stimulation is mediated by activation of a nitric oxide synthase pathway in human ventricle.

Gauthier¹,

Leblais²,

Kobzik³

et al. 1998

J. Clin. Invest.

345

294

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“…One of these factors could be nitric oxide (NO), 20,21 one of the most vasoactive autacoids. NO is important in regulating vascular tone, 20 inhibits platelet aggregation, 22 and limits platelet-endothelial interactions. 20 Moreover, NO may play a role in maintaining the normal mitogenic state of vascular smooth muscle by inhibiting proliferation.…”

mentioning

confidence: 99%

Continuous Perivascularl-Arginine Delivery Increases Total Vessel Area and Reduces Neointimal Thickening After Experimental Balloon Dilatation

Bosmans

Vrints

Kockx

et al. 1999

ATVB

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The aim of this study was to evaluate whether vascular remodeling and neointimal thickening occur after balloon dilatation of the nonatherosclerotic rabbit carotid artery, and whether both processes are influenced by continuous perivascular delivery of L-arginine or the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). In the first experiment, histological and morphometric evaluation of arteries was performed at different time points after balloon dilatation: 10 minutes (n=7), and 1 (n=7), 2 (n=9), 3 (n=20), or 10 (n=5) weeks. Neointimal thickening progressively contributed to luminal narrowing for at least 10 weeks after angioplasty. During the first 2 weeks after dilatation, a significant decrease of the total vessel area was measured. Ten weeks after dilatation, both the neointimal and total vessel area were increased without further changing of the luminal area. In the second experiment, endothelial injured rabbits were randomly assigned to receive 2 weeks of continuous local perivascular physiological salt solution (n=6), L-arginine (n=8), or L-NAME (n=7), starting immediately after balloon dilatation (ie, local drug delivery during the first phase of the biphasic vascular remodeling process). Perivascular L-arginine delivery significantly reduced the neointimal area, despite an increased number of neointimal Ki-67-positive smooth muscle cells. Both the luminal area and total vessel area were significantly increased. Serum L-arginine levels remained unchanged. L-NAME administration had no effect on the neointimal area, nor on the luminal and total vessel area. Neointimal formation and biphasic vascular remodeling occur after experimental balloon dilatation of the nonatherosclerotic rabbit carotid artery, and can be influenced by continuous local perivascular delivery of L-arginine.

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“…Aortic effluent was collected in the presence of indomethacin (1O ZM) between 90 and 30 s before, and from 30 to 90 s after each injection of ACh. PGI2 was determined by radioimmunoassay of 6-oxo-PGFI, as described by Beetens et al (1986) and Bult et al (1988).…”

Section: Organ Chamber Studiesmentioning

confidence: 99%

Influence of chronic treatment with a nitric oxide donor on fatty streak development and reactivity of the rabbit aorta

Bult

Meyer

Herman

1995

British J Pharmacology

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1 The influence of chronic treatment with molsidomine, pro-drug of the nitric oxide (NO) donor, 3-morpholino-sydnonimine (SIN-1), on fatty streak development and release of NO and prostacyclin (PGI2) was studied in the aorta of normal and cholesterol-fed rabbits. 2 Groups of 10 rabbits received standard diet (150g day-'), or diets with 0.3% cholesterol, with 0.02% molsidomine or with the combination of cholesterol and molsidomine for 16 weeks. Lesion area and thickness, maximum change in isometric force (E.,,.) and sensitivity (-log EC3. or pD2) to constricting and relaxing agonists were assessed in segments of arch, thoracic and abdominal aorta. Bioassay was used to assess NO release. 3 Cholesterol-induced fatty streaks tapered off towards the abdominal aorta. Area, thickness, weight and cholesterylester content of the lesions were augmented by the NO donor, whereas the hypercholesterolaemia remained unchanged. The exacerbation was attributed to co-release of superoxide anion from the sydnonimine. 4 As fatty streaks progressed, amplitude and pD2 of acetylcholine (ACh)-induced relaxations decreased, whereas cyclic GMP and cyclic AMP second messenger systems were not influenced, since Em., and sensitivity to SIN-1 and forskolin remained unchanged. However, extensive lesions apparently trapped some NO, as the pD2 of authentic NO decreased. 5The fatty streaks curtailed the biosynthesis of PGI2 and the overflow of NO from the perfused thoracic aorta. The latter defect was not restored by L-arginine and appears to be consistent with a functional change of the endothelial muscarinic receptors. 6 The NO donor desensitized the aorta to cyclic GMP-mediated -relaxations (ACh, SIN-1 and NO), without affecting cyclic AMP-mediated relaxation to forskolin or constrictor responses to phenylephrine and 5-hydroxytryptamine. 7 The drug also suppressed the ACh-induced overflow of NO, without changing PGI2 release. This selective reduction of endothelial NO release and the desensitization of cyclic GMP-mediated relaxations occurred independently of fatty streak formation. 8 The results indicate that chronic exposure to exogenous NO downregulates endothelial NO release and cyclic GMP-mediated relaxations, and provide evidence for the existence of negative feed-back regulations of the L-arginine NO pathway under in vivo conditions.

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Platelet inhibition by endothelium‐derived relaxing factor from the rabbit perfused aorta

Cited by 37 publications

References 23 publications

The negative inotropic effect of beta3-adrenoceptor stimulation is mediated by activation of a nitric oxide synthase pathway in human ventricle.

The negative inotropic effect of beta3-adrenoceptor stimulation is mediated by activation of a nitric oxide synthase pathway in human ventricle.

Continuous Perivascularl-Arginine Delivery Increases Total Vessel Area and Reduces Neointimal Thickening After Experimental Balloon Dilatation

Influence of chronic treatment with a nitric oxide donor on fatty streak development and reactivity of the rabbit aorta

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