Role of nitric oxide in the regulation of vascular responses mediated by prostaglandin and endothelium-derived hyperpolarizing factor in the porcine coronary artery

2011 ◽  
Author(s):  
Kin-hong Chow
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Vascular Responses ◽  
Porcine Coronary Artery

Effects of L-arginine analogues on vasomotion of isolated porcine coronary arteries

1995 ◽  
Vol 268 (5) ◽  
pp. H1966-H1972 ◽  
Author(s):  
R. Nakaike ◽  
H. Shimokawa ◽  
H. Yasutake ◽  
H. Sumimoto ◽  
A. Ito ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Coronary Arteries ◽  
Isometric Tension ◽  
Vascular Responses ◽  
Porcine Coronary Artery ◽  
Coronary Vasomotion ◽  
Vasoconstrictor Effect ◽  
Dose Dependent

L-Arginine analogues have been widely used to examine the role of endothelium-derived nitric oxide (NO) in vascular responses; however, the effects of the agents on coronary vasomotion are not fully understood. In this study, we examined the effects of the analogues on vasomotion of isolated porcine coronary arteries. Strips of the porcine coronary artery were suspended for isometric tension recording in Krebs-Henseleit solution. L-Arginine analogues, N omega-nitro-L-arginine methyl ester (L-NAME, 10(-9)-10(-3) M), NG-monomethyl-L-arginine (L-NMMA, 10(-9)-10(-3) M), and NG-nitro-L-arginine (L-NNA, 10(-9)-10(-3) M), caused dose-dependent contractions, which were greater in strips with than in those without endothelium. Those endothelium-dependent contractions were almost abolished by indomethacin (10(-5) M) and FeCl2 (10(-3) M). The latter reduces prostaglandin H2 to 12-heptadecatrienoic acid, which has no vasoconstrictor effect. These results indicate that the L-arginine analogues cause endothelium-dependent contractions that are mediated by prostaglandin endoperoxides and suggest that they have properties other than simple inhibition of NO synthesis in porcine coronary arteries.

Two mechanisms mediate relaxation by bradykinin of pig coronary artery: NO-dependent and -independent responses

1991 ◽  
Vol 261 (3) ◽  
pp. H830-H835 ◽  
Author(s):  
C. L. Cowan ◽  
R. A. Cohen
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Coronary Artery ◽  
Thromboxane A2 ◽  
Porcine Coronary Artery ◽  
Cyclic Monophosphate ◽  
Pig Coronary Artery ◽  
Endothelium Dependent Relaxation

The role of nitric oxide and guanosine 3',5'-cyclic monophosphate (cGMP) accumulation in the endothelium-dependent relaxation of the porcine coronary artery to bradykinin was investigated by comparing relaxation and cGMP accumulation in the presence or absence of NG-monomethyl-L-arginine (L-NMMA) and methylene blue. Rings were treated with indomethacin to eliminate the effects of prostaglandins. Relaxation to bradykinin of rings contracted with the thromboxane A2 mimetic U-46619 was not affected by L-NMMA and was only minimally inhibited by methylene blue. Rings contracted with elevated potassium (25 mM) also relaxed completely to bradykinin. However, L-NMMA or methylene blue effectively inhibited relaxation to bradykinin in rings contracted with potassium. cGMP accumulation was stimulated by bradykinin and inhibited by L-NMMA or methylene blue in rings contracted with either U-46619 or potassium. These results suggest that in the absence of nitric oxide-induced cGMP accumulation, a nonprostanoid mechanism exists that is capable of completely relaxing U-46619-contracted coronary artery. This mechanism is either inhibited in or unable to relax potassium-contracted rings. These results also demonstrate that nitric oxide mediates the bradykinin-induced cGMP accumulation that is largely responsible for the relaxation during contraction with potassium.

scholarly journals Cilnidipine, a slow-acting Ca2+ channel blocker, induces relaxation in porcine coronary artery: role of endothelial nitric oxide and [Ca2+ ]i

2006 ◽  
Vol 147 (1) ◽  
pp. 55-63 ◽  
Author(s):  
Hok Sum Leung ◽  
Xiaoqiang Yao ◽  
Fung Ping Leung ◽  
Wing Hung Ko ◽  
Zhen-Yu Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Channel Blocker ◽  
Porcine Coronary Artery ◽  
Endothelial Nitric Oxide

Role of nitric oxide in adenosine receptor-mediated relaxation of porcine coronary artery

1995 ◽  
Vol 269 (5) ◽  
pp. H1672-H1678 ◽  
Author(s):  
W. Abebe ◽  
T. Hussain ◽  
H. Olanrewaju ◽  
S. J. Mustafa
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery ◽  
Porcine Coronary Artery ◽  
Cyclic Monophosphate ◽  
Enhanced Production ◽  
Cgs 21680 ◽  
Synthase Inhibitor ◽  
Ly 83583

In the present study, using porcine coronary artery rings in vitro, we examined the role of the nitric oxide (NO) pathway in endothelium-dependent vasorelaxant effects of the 5'-uronamide adenosine agonists, 5'-(N-ethylcarboxamido)adenosine (NECA) and 2-[p-(2-carboxyethyl)]phenylethyl-amino-5'-N-ethylcarboxamidoadenosine (CGS-21680) as opposed to the endothelium-independent actions of the C2- and N6-substituted analogues, 2-chloroadenosine (CAD) and N6-cyclopentyladenosine (CPA). The NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA, 30 microM), and the NO-destroying agent, 6-anilino-5,8-quinolinedione (LY-83583, 10 microM), attenuated the relaxations of endothelium-intact but not -denuded rings to NECA and CGS-21680. The effect of L-NMMA on NECA-induced relaxation was reversed by L-arginine (100 microM), a substrate for NO synthesis. In the endothelium-intact tissues, both NECA and CGS-21680 elicited enhanced production of nitrite, a stable metabolite of NO. This was also attenuated by L-NMMA or endothelium removal. Furthermore, NECA (10 microM) induced augmentation of guanosine 3',5'-cyclic monophosphate (cGMP) production in the intact arteries, which was also inhibited by L-NMMA, LY-83583, or endothelium removal. In contrast, vasorelaxant responses generated by CAD and CPA were not altered by either L-NMMA or LY-83583. Both agents (10 microM) were also unable to alter nitrite and/or guanosine 3',5'-cyclic monophosphate (cGMP) levels of the coronary artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of endothelium-formed nitric oxide on vascular responses

1990 ◽  
Vol 21 (5) ◽  
pp. 575-587 ◽  
Author(s):  
Jesús Marín ◽  
Carlos F. Sánchez-Ferrer
Keyword(s):  
Nitric Oxide ◽  
Vascular Responses
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