Altered vascular permeability responses to substance P in diabetic rats: Interactions with a nitric oxide synthesis inhibitor

1993 ◽  
Vol 240 (2-3) ◽  
pp. 163-168 ◽  
Author(s):  
Ronald Mathison ◽  
Joseph S. Davison
Keyword(s):  
Nitric Oxide ◽  
Substance P ◽  
Vascular Permeability ◽  
Diabetic Rats ◽  
Nitric Oxide Synthesis ◽  
Synthesis Inhibitor

Mechanism underlying the response to vasodilator nerve stimulation in isolated dog and monkey cerebral arteries

1990 ◽  
Vol 259 (5) ◽  
pp. H1511-H1517 ◽  
Author(s):  
N. Toda ◽  
T. Okamura
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Coronary Artery ◽  
Substance P ◽  
Nerve Stimulation ◽  
Cerebral Arteries ◽  
Inhibitory Effect ◽  
Synthesis Inhibitor ◽  
Transmural Stimulation ◽  
Stimulation Of

Relaxant responses to transmural electrical stimulation and nicotine of cerebral artery strips obtained from dogs and Japanese monkeys were abolished by tetrodotoxin and hexamethonium, respectively, and suppressed by treatment with NG-monomethyl-L-arginine (L-NMMA), a nitric oxide (NO) synthesis inhibitor. The inhibitory effect was prevented and reversed by L-arginine but not by D-arginine. The relaxations suppressed by L-NMMA were not increased by exogenously applied NO. Endothelium denudation did not alter the response to transmural stimulation and nicotine or the inhibitory effect of L-NMMA. D-NMMA did not inhibit the response to vasodilator nerve stimulation. Dog coronary artery relaxations caused by transmural stimulation were not inhibited by L-NMMA but reversed to contractions by propranolol. Relaxations caused by substance P of dog cerebral arteries treated with indomethacin were dependent on endothelium and inhibited by L-NMMA, whereas those by NO and nitroglycerin, endothelium-independent relaxations, were unaffected. It is concluded that chemical and electrical stimulation of vasodilator nerves relaxes dog and monkey cerebral arteries, possibly by a mediation of NO rather than a stimulating action of NO on the release of vasodilator transmitter. Endothelium-dependent relaxations by substance P of dog cerebral arteries appear to be mediated by NO.

scholarly journals Endogenous Nitric Oxide Synthesis Inhibitor Asymmetric Dimethyl l -Arginine Accelerates Endothelial Cell Senescence

2004 ◽  
Vol 24 (10) ◽  
pp. 1816-1822 ◽  
Author(s):  
Fortunato Scalera ◽  
Jürgen Borlak ◽  
Bibiana Beckmann ◽  
Jens Martens-Lobenhoffer ◽  
Thomas Thum ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cell ◽  
Cell Senescence ◽  
Nitric Oxide Synthesis ◽  
Synthesis Inhibitor ◽  
Endogenous Nitric Oxide

scholarly journals Effects of centrally administered nitric oxide synthesis inhibitor on the cardiovascular regulation

1998 ◽  
Vol 76 ◽  
pp. 51
Author(s):  
Shigeki Moriguchi ◽  
Nobuhiro Koga ◽  
Kenji Honda ◽  
Ryo Saito ◽  
Yukio Takano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Regulation ◽  
Nitric Oxide Synthesis ◽  
Synthesis Inhibitor

scholarly journals Nebivolol Ameliorates Nitric Oxide–Deficient Hypertension

2002 ◽  
Vol 2 ◽  
pp. 1676-1684 ◽  
Author(s):  
L.A. Fortepiani ◽  
M.C. Ortiz ◽  
N.M. Atucha ◽  
Joaquin Garcia-Estan
Keyword(s):  
Nitric Oxide ◽  
Arterial Hypertension ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
No Synthase ◽  
Nitric Oxide Synthesis ◽  
Synthesis Inhibitor ◽  
Angiotensin System ◽  
Calcium Dependent ◽  
Adrenoceptor Antagonist

Nebivolol is a new selective beta 1-adrenoceptor antagonist with nitric oxide (NO)–releasing properties. In the present study we have analyzed whether nebivolol affects the development of the arterial hypertension that follows the chronic inhibition of nitric oxide synthesis. Nebivolol (1 mg/kg/day, 14 days) was given concurrently with the NO synthesis inhibitor Nw-nitro-L-arginine methyl ester (L-NAME, 0.1, 1, and 10 mg/kg/day, 14 days) to several groups of rats. Blood pressure, renal function, plasma renin activity (PRA), and NO activity and metabolites were measured at the end of the treatment period. L-NAME treatment alone increased mean arterial pressure dose dependently (103.5 ± 2.4, 110.9 ± 2.0, and 125.8 ± 2.2 mmHg, respectively). Nebivolol completely prevented the development of arterial hypertension in the groups treated with L-NAME at the doses of 0.1 and 1 mg/kg/day and reduced the increase achieved with the L-NAME dose of 10 mg/kg/day (110.3 ± 2.7). There were no differences in glomerular filtration rate or natriuresis between nebivolol-treated and -untreated rats. Plasma nitrates+nitrites and calcium-dependent NO synthase activity in the kidney also decreased dose dependently with L-NAME treatment and nebivolol did not significantly modify it. However, PRA was lower in all groups treated with nebivolol and L-NAME as compared to the rats receiving only L-NAME. These data indicate that nebivolol prevents the development of the arterial hypertension associated with chronic NO deficit and this effect seems to be dependent on the inhibition of renin-angiotensin system.

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