Prolonged exposure of canine coronary arteries to a nitric oxide donor desensitizes soluble guanylate cyclase

2005 ◽  
Vol 123 (1) ◽  
pp. 82-88 ◽  
Author(s):  
Paul Sorajja ◽  
David G. Cable ◽  
Chad E. Hamner ◽  
Hartzell V. Schaff
Keyword(s):  
Nitric Oxide ◽  
Coronary Arteries ◽  
Guanylate Cyclase ◽  
Prolonged Exposure ◽  
Soluble Guanylate Cyclase ◽  
Nitric Oxide Donor

The nitric oxide donor cis-[Ru(bpy)2(SO3)NO](PF6) increases gastric mucosa protection in mice – Involvement of the soluble guanylate cyclase/KATP pathway

Nitric Oxide ◽  
2015 ◽  
Vol 45 ◽  
pp. 35-42 ◽  
Author(s):  
Ana Paula M. Santana ◽  
Bruno M. Tavares ◽  
Larisse T. Lucetti ◽  
Florêncio S. Gouveia ◽  
Ronaldo A. Ribeiro ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gastric Mucosa ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Nitric Oxide Donor

Agonist-specific impairment of coronary vascular function in genetically altered, hyperlipidemic mice

1999 ◽  
Vol 276 (4) ◽  
pp. R1023-R1029 ◽  
Author(s):  
Kathryn G. Lamping ◽  
Daniel W. Nuno ◽  
David A. Chappell ◽  
Frank M. Faraci
Keyword(s):  
Nitric Oxide ◽  
Coronary Arteries ◽  
Guanylate Cyclase ◽  
Vascular Function ◽  
Soluble Guanylate Cyclase ◽  
Plasma Cholesterol ◽  
High Cholesterol Diet ◽  
Cholesterol Diet ◽  
High Cholesterol ◽  
Deficient Mice

The objectives of the present study were to 1) examine mechanisms involved in endothelium-dependent responses of coronary arteries from normal mice and 2) determine whether vascular responses of coronary arteries are altered in two genetic models of hypercholesterolemia [apolipoprotein E (apoE)-deficient mice (apoE −/−) and combined apoE and low-density lipoprotein receptor (LDLR)-deficient mice (apoE + LDLR −/−)]. Plasma cholesterol levels were higher in both apoE −/− and apoE + LDLR −/− compared with normal mice on normal and high-cholesterol diets (normal chow: normal 110 ± 5 mg/dl, apoE −/− 680 ± 40 mg/dl, apoE + LDLR −/− 810 ± 40 mg/dl; high-cholesterol chow: normal 280 ± 60 mg/dl, apoE −/− 2,490 ± 310 mg/dl, apoE + LDLR −/− 3,660 ± 290 mg/dl). Coronary arteries from normal (C57BL/6J), apoE −/−, and apoE + LDLR −/− mice were isolated and cannulated, and diameters were measured using videomicroscopy. In normal mice, vasodilation in response to ACh and serotonin was markedly reduced by 10 μM N ω-nitro-l-arginine (an inhibitor of nitric oxide synthase) or 20 μM 1 H-[1,2,4]oxadiazolo[4,3- a]quinoxalin-1-one (ODQ; an inhibitor of soluble guanylate cyclase). Vasodilation to nitroprusside, but not papaverine, was also inhibited by ODQ. Dilation of arteries from apoE −/− and apoE + LDLR −/− mice on normal diet in response to ACh was similar to that observed in normal mice. In contrast, dilation of arteries in response to serotonin from apoE −/− and apoE + LDLR −/− mice was impaired compared with normal. In arteries from both apoE −/− and apoE + LDLR −/− mice on high-cholesterol diet, dilation to ACh was decreased. In apoE + LDLR −/− mice on high-cholesterol diet, dilation of coronary arteries to nitroprusside was increased. These findings suggest that dilation of coronary arteries from normal mice in response to ACh and serotonin is dependent on production of nitric oxide and activation of soluble guanylate cyclase. Hypercholesterolemia selectively impairs dilator responses of mouse coronary arteries to serotonin. In the absence of both apoE and the LDL receptor, high levels of cholesterol result in a greater impairment in coronary endothelial function.

Glutathione causes coronary vasodilation via a nitric oxide- and soluble guanylate cyclase-dependent mechanism

1997 ◽  
Vol 273 (3) ◽  
pp. H1231-H1238 ◽  
Author(s):  
P. Y. Cheung ◽  
R. Schulz
Keyword(s):  
Nitric Oxide ◽  
Ethyl Ester ◽  
Guanylate Cyclase ◽  
Coronary Flow ◽  
Soluble Guanylate Cyclase ◽  
Specific Inhibitor ◽  
Nitric Oxide Donor ◽  
Coronary Vasodilation ◽  
Vasodilator Action ◽  
Dependent Mechanism

The actions of thiols on coronary vascular tone in the intact heart are unknown. Glutathione (GSH), glutathione disulfide (GSSG), and L-cysteine (10-1,000 microM each) and GSH ethyl ester (3-300 microM) were infused into isolated rat hearts perfused with Krebs buffer at a constant pressure by the Langendorff method. GSH, GSSG, and GSH ethyl ester, but not L-cysteine, caused a concentration-dependent increase in coronary flow with the following order of potency: GSH ethyl ester > GSH = GSSG. The nitric oxide synthase inhibitor NG-monomethyl-L-arginine (300 microM), prevented the increase in coronary flow with GSH and attenuated that with GSSG (300 microM each). The vasodilation with GSH or GSSG and the associated increase in myocardial guanosine 3',5'-cyclic monophosphate were abolished by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (a specific inhibitor of soluble guanylate cyclase) at 1 and 3 microM, respectively. The vasodilator action of GSH was abolished by superoxide dismutase (50 U/ml). Inhibition of GSH reductase abolished GSSG-induced vasodilation. Neither glibenclamide (1 microM) nor indomethacin (4 microM) affected the vasodilator action of GSH and GSSG. We conclude that GSH and GSSG cause coronary vasodilation that is mediated by a nitric oxide- and guanylate cyclase-dependent mechanism, possibly mediated by the reaction between GSH and peroxynitrite to form S-nitrosoglutathione, a nitric oxide donor.

Nitric oxide-independent stimulation of soluble guanylate cyclase reduces organ damage in experimental low-renin and high-renin models

2010 ◽  
Vol 28 (8) ◽  
pp. 1666-1675 ◽  
Author(s):  
Yuliya Sharkovska ◽  
Philipp Kalk ◽  
Bettina Lawrenz ◽  
Michael Godes ◽  
Linda Sarah Hoffmann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Organ Damage ◽  
Stimulation Of

YC-1, a nitric oxide-independent activator of soluble guanylate cyclase, inhibits platelet-rich thrombosis in mice

1997 ◽  
Vol 320 (2-3) ◽  
pp. 161-166 ◽  
Author(s):  
Che-Ming Teng ◽  
Chin-Chung Wu ◽  
Feng-Nien Ko ◽  
Fang-Yu Lee ◽  
Sheng-Chu Kuo
Keyword(s):  
Nitric Oxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase

O14. Functional knockout of the soluble guanylate cyclase alpha 1 subunit leads to gender-specific hypertension while retaining sensitivity to nitric oxide

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 4-5
Author(s):  
Patrick Yves Sips ◽  
Emmanuel Buys ◽  
Elke Rogge ◽  
Sofie Nimmegeers ◽  
Mieke Dewerchin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Gender Specific
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