Nitric oxide synthesis in endothelial cytosol: Evidence for a calcium-dependent and a calcium-independent mechanism

Author(s):  
Alexander M�lsch ◽  
Eberhard Bassenge ◽  
Rudi Busse
1998 ◽  
Vol 177 (2) ◽  
pp. 489-492 ◽  
Author(s):  
Pietro D'Agostino ◽  
Marzia La Rosa ◽  
Caterina Barbera ◽  
Francesco Arcoleo ◽  
Gloria Di Bella ◽  
...  

1995 ◽  
Vol 269 (5) ◽  
pp. H1679-H1684 ◽  
Author(s):  
Y. Hatano ◽  
K. Mizumoto ◽  
T. Yoshiyama ◽  
M. Yamamoto ◽  
H. Iranami

Caffeine (10(-4)-10(-3) M) induced concentration-dependent relaxations of phenylephrine-precontracted rat aortic rings with endothelium. Endothelial denudation significantly, but only partially, attenuated caffeine-induced relaxation. Pretreatment with NG-nitro-L-arginine, oxyhemoglobin, and methylene blue attenuated the relaxations to an extent similar to endothelial denudation. Guanosine 3',5'-cyclic monophosphate (cGMP) and adenosine 3',5'-cyclic monophosphate (cAMP) contents of aortic strips with endothelium increased significantly after exposure to caffeine (10(-3) M). Endothelial denudation attenuated caffeine-induced cGMP increase. Pretreatment with ryanodine (2 x 10(-5) M), which has been shown to combine with receptors on endoplasmic reticulum (ER) of endothelium, attenuated caffeine-induced relaxation and cGMP content increase of rings with endothelium. Pretreatment with caffeine potentiated sodium nitroprusside-induced relaxations and cGMP increase of rings without endothelium. These results demonstrated that caffeine-induced relaxation comprises two components. In the endothelium-dependent mechanism, caffeine promotes nitric oxide synthesis in endothelium by release of Ca2+ from ER through a ryanodine-sensitive Ca2+ channel, and the suppression of cGMP degradation also contributes to the relaxation. In the endothelium-independent mechanism, caffeine acts as a 3',5'-cyclic-nucleotide phosphodiesterase inhibitor.


2002 ◽  
Vol 2 ◽  
pp. 1676-1684 ◽  
Author(s):  
L.A. Fortepiani ◽  
M.C. Ortiz ◽  
N.M. Atucha ◽  
Joaquin Garcia-Estan

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.


1998 ◽  
Vol 68 (3) ◽  
pp. 180-186 ◽  
Author(s):  
Leonor Pinilla ◽  
Dolores González ◽  
Manuel Tena-Sempere ◽  
Enrique Aguilar

Author(s):  
O. V. Bazilyuk ◽  
Anatolii V. Kotsuruba ◽  
Lyubov. G. Stepanenko ◽  
Sergey A. Talanov ◽  
Yu. P. Korchak ◽  
...  

Circulation ◽  
1995 ◽  
Vol 92 (9) ◽  
pp. 2636-2644 ◽  
Author(s):  
Akira Ito ◽  
Kensuke Egashira ◽  
Toshiaki Kadokami ◽  
Yoshihiro Fukumoto ◽  
Tsuneo Takayanagi ◽  
...  

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