NG-methylarginine, and inhibitor of endothelium-derived nitric oxide synthesis, is a potent pressor agent in the guinea pig: Does nitric oxide regulate blood pressure in vivo?

Aisaka, Kazuo; Gross, Steven S.; Griffith, Owen W.; Levi, Roberto

doi:10.1016/0006-291x(89)92517-5

Cited by 422 publications

(175 citation statements)

References 19 publications

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“…This finding is consistent with studies in other tissues in vitro (Palmer et al, 1988b;Amezcua et al, 1989;Rees et al, 1989a;1990b;Moore et al, 1990) and in vivo (Aisaka et al, 1989;Rees et al, 1989b;1990b;Gardiner et al, 1990) and further strengthens the belief that basal release on NO modulates vascular tone (Rees et al, 1990b;Amrani et al, 1992;see Moncada et al, 1991). In the vasculature, constitutive NO synthase is localized entirely in the endothelial layer (Knowles et al, 1990).…”

Section: Discussionsupporting

confidence: 87%

Bacterial endotoxin rapidly stimulates prolonged endothelium‐dependent vasodilatation in the rat isolated perfused heart

Baydoun

Foale

Mann

1993

British J Pharmacology

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1 The effects of bacterial lipopolysaccharide (Escherichia coli 011 1-B4; LPS) on coronary vascular tone were examined in the isolated perfused heart of the rat. The role of nitric oxide and/or prostaglandin products of the cyclo-oxygenase pathway in mediating the actions of LPS were also investigated. 2 Coronary vascular tone was raised and maintained by a continuous perfusion of the thromboxanemimetic U46619 (5nM). LPS perfusion (0.1-100itgml-') caused a concentration-dependent fall in coronary tone without any significant change in the force of cardiac contractility.3 At 5 lggml', LPS reduced perfusion pressure by 38±9mmHg. This effect was rapid in onset, maximal within the first 5 min and sustained for 90 + 10 min (n = 6). 4 The vasodilatation induced by LPS was dependent on the presence of an intact endothelium and abolished following endothelial damage caused by air embolism.5 NW-nitro-L-arginine methylester (L-NAME; 50 gM) or N0-nitro-L-arginine (L-NOARG; 50 tM) blocked the vasodilatation induced by LPS (5 jLg ml--). The inhibition caused by these arginine analogues was partially reversed by 1 mM L-but not D-arginine. 6 The vasodilator action of LPS was also completely blocked by the glucocorticoid, dexamethasone (10 jiM) but unaffected by indomethacin (10 jiM).7 These results suggest that LPS evokes rapid release of nitric oxide (NO) in the microvasculature of the rat isolated heart presumably via activation of the constitutive L-arginine-NO pathway in the endothelium. Furthermore, the lack of effect of indomethacin suggests that prostaglandins released via the cyclo-oxygenase pathway are not involved in mediating this action of LPS.

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Section: Discussionsupporting

confidence: 87%

Bacterial endotoxin rapidly stimulates prolonged endothelium‐dependent vasodilatation in the rat isolated perfused heart

Baydoun

Foale

Mann

1993

British J Pharmacology

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“…Thus, while inhibition of NOS led to the well documented elevation in AP (Aisaka et al, 1989; 1 990a ,b), we did not observe any re duction of rCBF as measured by LDF in control animals under the conditions and doses of this study. The maintenance of rCBF was a conse quence of an increase in CVR, indicating that cere brovascular autoregulation was still intact.…”

Section: Discussioncontrasting

confidence: 55%

“…While a continuous low background release of NO from endothelium is believed to provide a tonic level of vasodilation (Aisaka et al, 1989), it is un likely that enlargement of the focal ischemic lesion by NN A is related to reduction of basal rCBF. Thus, while inhibition of NOS led to the well documented elevation in AP (Aisaka et al, 1989; 1 990a ,b), we did not observe any re duction of rCBF as measured by LDF in control animals under the conditions and doses of this study.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Nitric Oxide Synthesis Increases Focal Ischemic Infarction in Rat

Yamamoto

Golanov

Berger

et al. 1992

J Cereb Blood Flow Metab

230

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Summary:We investigated whether inhibition of nitric oxide (NO) biosynthesis with N-w-nitro-L-arginine (NNA), a competitive inhibitor of NO synthase (NOS), would modify the volume of the focal ischemic infarction produced by occlusion of the middle cerebral artery (MCA) in spontaneously hypertensive rats. NNA was in fused for 1 h (2.4 mg/kg/h) immediately following occlu sion of the MCA. NNA increased lesion volume 24 h later by 32% over controls (150.8 ± 16.6 to 199.2 ± 17.4 mm3; p < 0.001, n = 6). This effect was antagonized by co infusion of L-but not D-arginine. The antihypertensive rilmenidine (0.75 mg/kg) reduced the lesion by 27% (p < 0.05, n = 4). Changes in lesion size were confined to the penumbra. NNA increased arterial pressure (AP) (118 ± There is increasing evidence that the endogenous vasodilator nitric oxide (NO) is synthesized in the brain from the amino acid L-arginine (L-Arg) by the enzyme NO synthase (NOS). The principal form of NOS expressed in brain appears to correspond to the constitutive form of the enzyme (Bredt and Sny der, 1990; Hope et ai., 1991)

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“…If viability exceeded 97%, cells were suspended in MEM with 2% fetal bovine serum, 2 mM glutamine, and antibiotics at a density of 5 x 105 cells per ml, and 1 ml was placed into 8 wells of 24-well dishes (Costar). MOT or OVCAR cells were placed in the other 16 wells. A combination of LPS and cytokines (25 A4) was incubated with these cell lines for 22 hr at 37°C in 5% CO2.…”

Section: Methodsmentioning

confidence: 99%