scholarly journals Relaxation of porcine coronary artery to bradykinin. Role of arachidonic acid.

Hypertension ◽  
1994 ◽  
Vol 23 (6_pt_2) ◽  
pp. 976-981 ◽  
Author(s):  
N L Weintraub ◽  
S N Joshi ◽  
C A Branch ◽  
A H Stephenson ◽  
R S Sprague ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Coronary Artery ◽  
Porcine Coronary Artery

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.

2-Chloroadenosine prevents phorbol ester-induced depletion of protein kinase C in porcine coronary artery

1993 ◽  
Vol 264 (5) ◽  
pp. H1465-H1471 ◽  
Author(s):  
R. B. Marala ◽  
K. Ways ◽  
S. J. Mustafa
Keyword(s):  
Protein Kinase C ◽  
Coronary Artery ◽  
Protein Kinase ◽  
Phorbol Ester ◽  
Chronic Exposure ◽  
Porcine Coronary Artery ◽  
Kinase C ◽  
Adenosine Analogue ◽  
Presence And Absence

In this study we investigated the role of the adenosine analogue 2-chloroadenosine (CAD) in the regulation of protein kinase C (PKC) in porcine coronary artery. Arterial rings were contracted with endothelin-1 (ET-1; 10(-10) to 10(-7) M) and phorbol 12,13-dibutyrate (PDBu; 10(-7) M) after incubating them for 1 and 2 days with PDBu (200 nM) in the presence and absence of CAD (10(-4) M). Chronic exposure to PDBu alone attenuated ET-1-induced contractions, while inclusion of CAD during incubation protected against the PDBu-induced blunting of ET-1-induced contraction. Similarly, PDBu (10(-7) M)-induced contraction of the arterial rings was attenuated upon chronic incubation with PDBu, and once again, inclusion of CAD showed an improved response to PDBu-induced contraction when compared with PDBu alone. Incubation with PDBu (200 nM) for 20 min caused the PKC translocation from cytosol to membrane, whereas CAD totally blocked this translocation. Chronic (1 and 2 days) incubation with PDBu caused a substantial depletion of PKC activities in cytosol and membrane. The presence of CAD protected the PDBu-induced depletion of PKC in both cytosol and membrane. To replete PKC, after incubation with the drugs, the arteries were incubated in the absence of drugs for another 2 days. Arteries incubated with PDBu in the presence and absence of CAD recovered significantly in their response to ET-1 as well as PDBu. These results indicate that CAD protects against the PDBu-induced activation and depletion of PKC in porcine coronary artery.

Relationship of Arachidonic Acid Release to Porcine Coronary Artery Relaxation

Hypertension ◽  
1995 ◽  
Vol 26 (4) ◽  
pp. 684-690 ◽  
Author(s):  
Neal L. Weintraub ◽  
Alan H. Stephenson ◽  
Randy S. Sprague ◽  
Lorraine McMurdo ◽  
Andrew J. Lonigro
Keyword(s):  
Arachidonic Acid ◽  
Coronary Artery ◽  
Arachidonic Acid Release ◽  
Porcine Coronary Artery ◽  
Acid Release ◽  
Relationship Of

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

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.

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