Enhanced response of pig coronary arteries to endothelin-1 after ischemia–reperfusion. Role of endothelin receptors, nitric oxide and prostanoids

2005 ◽  
Vol 524 (1-3) ◽  
pp. 102-110 ◽  
Author(s):  
Belén Climent ◽  
Nuria Fernández ◽  
Elena Sanz ◽  
Ana Sánchez ◽  
Luis Monge ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Coronary Arteries ◽  
Ischemia Reperfusion ◽  
Endothelin Receptors ◽  
Endothelin 1 ◽  
Pig Coronary Arteries

Nitric oxide attenuates endothelin-1-induced vasoconstriction in canine stomach

1996 ◽  
Vol 271 (1) ◽  
pp. G27-G35
Author(s):  
J. G. Wood ◽  
Q. Zhang ◽  
Z. Y. Yan ◽  
L. Y. Cheung
Keyword(s):  
Nitric Oxide ◽  
Methyl Ester ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Question Mark ◽  
Endothelin 1 ◽  
Vasoconstrictor Response ◽  
Anesthetized Dogs ◽  
Spermine Nonoate

We previously observed that endothelin-1 (ET-1)-induced gastric vasoconstriction is enhanced after ischemia-reperfusion. The purpose of our present study was to examine the role of nitric oxide in regulating ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion. Using a mechanically perfused stomach segment from chloralose-anesthetized dogs, we examined 1) responses to NG-nitro-L-arginine methyl ester (L-NAME) alone and in combination with L-arginine, 2) whether L-NAME affects ET-1-induced vasoconstriction under normal conditions and after ischemia-reperfusion, and 3) if spermine NONOate inverted question mark1,3-propanediamine-N-[4-1-(3-aminopropyl)-2-hydroxy-2-nitrosohydrazi no] butyl; a nitric oxide donor inverted question mark attenuates the augmented response to ET-1 after ischemia-reperfusion. Our results show that 1) L-NAME significantly increased baseline vascular resistance and this response was reduced by L-arginine, 2) ET-1-induced vasoconstriction was enhanced by L-NAME, and 3) administration of spermine NONOate during reperfusion largely attenuated the vasoconstrictor response to ET-1 after ischemia-reperfusion. Our findings are consistent with the hypothesis that nitric oxide modulates responses to ET-1 under normal conditions, and loss of this vasodilator after ischemia-reperfusion results in an augmented response to ET-1.

scholarly journals Role of endothelin receptors, calcium and nitric oxide in the potentiation by endothelin-1 of the sympathetic contraction of rabbit ear artery during cooling

1997 ◽  
Vol 121 (8) ◽  
pp. 1659-1664 ◽  
Author(s):  
A. L. García-Villalón ◽  
J Padilla ◽  
N Fernández ◽  
L Monge ◽  
B Gómez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelin Receptors ◽  
Rabbit Ear Artery ◽  
Endothelin 1 ◽  
Ear Artery ◽  
Rabbit Ear

Coronary vasoconstriction by endothelin-1 in anesthetized goats: role of endothelin receptors, nitric oxide and prostanoids

1996 ◽  
Vol 315 (2) ◽  
pp. 179-186 ◽  
Author(s):  
JoséLuis García ◽  
Nuria Fernández ◽  
Angel Luis García-Villalón ◽  
Luis Monge ◽  
Bernardino Gómez ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelin Receptors ◽  
Coronary Vasoconstriction ◽  
Endothelin 1

The Role of Reactive Oxygen Species, Kinases, Hydrogen Sulfide, and Nitric Oxide in the Regulation of Autophagy and Their Impact on Ischemia and Reperfusion Injury in the Heart

2020 ◽  
Vol 16 ◽  
Author(s):  
Andrey Krylatov ◽  
Leonid Maslov ◽  
Sergey Y. Tsibulnikov ◽  
Nikita Voronkov ◽  
Alla Boshchenko ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Hydrogen Sulfide ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Ischemia And Reperfusion ◽  
Oxygen Species ◽  
Ischemia And Reperfusion Injury ◽  
Adaptive Process

: There is considerable evidence in the heart that autophagy in cardiomyocytes is activated by hypoxia/reoxygenation (H/R) or in hearts by ischemia/reperfusion (I/R). Depending upon the experimental model and duration of ischemia, increases in autophagy in this setting maybe beneficial (cardioprotective) or deleterious (exacerbate I/R injury). Aside from the conundrum as to whether or not autophagy is an adaptive process, it is clearly regulated by a number of diverse molecules including reactive oxygen species (ROS), various kinases, hydrogen sulfide (H2S) and nitric oxide (NO). The purpose this review is to address briefly the controversy regarding the role of autophagy in this setting and to examine a variety of disparate molecules that are involved in its regulation.

Role of nitric oxide in hepatic and pulmonary injury following ischemia-reperfusion of rat liver

2003 ◽  
Vol 124 (4) ◽  
pp. A719-A720
Author(s):  
Yuji Takamatsu ◽  
Kazuo Shimada ◽  
Koji Yamaguchi ◽  
Kazuo Chijiiwa ◽  
Masao Tanaka
Keyword(s):  
Nitric Oxide ◽  
Rat Liver ◽  
Ischemia Reperfusion ◽  
Pulmonary Injury

scholarly journals Role of β-Adrenergic Receptors and Nitric Oxide Signaling in Exercise-Mediated Cardioprotection

Physiology ◽  
2013 ◽  
Vol 28 (4) ◽  
pp. 216-224 ◽  
Author(s):  
John W. Calvert ◽  
David J. Lefer
Keyword(s):  
Nitric Oxide ◽  
Risk Factors ◽  
Adrenergic Receptors ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Signaling ◽  
Factors Associated ◽  
Cardioprotective Effects ◽  
Β Adrenergic Receptors

Exercise promotes cardioprotection in both humans and animals not only by reducing risk factors associated with cardiovascular disease but by reducing myocardial infarction and improving survival following ischemia. This article will define the role that nitric oxide and β-adrenergic receptors play in mediating the cardioprotective effects of exercise in the setting of ischemia-reperfusion injury.

scholarly journals Role of nitric oxide in septal coronary arteries of obese Zucker rats

2014 ◽  
Vol 2 (1) ◽  
Author(s):  
Priyanka Prathipati ◽  
Syed Quadri ◽  
Debra Jackson ◽  
Keith Jackson
Keyword(s):  
Nitric Oxide ◽  
Coronary Arteries ◽  
Zucker Rats ◽  
Obese Zucker Rats
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