Inhibition of the nitric oxide/cyclic guanosine monophosphate pathway limited the cardioprotective effect of post-conditioning in hearts with apical myocardial infarction

Correa, Francisco; Buelna‐Chontal, Mabel; Chagoya, Victoria; García‐Rivas, Gerardo; Vigueras, Rosa María; Pedraza‐Chaverrí, José; García-Niño, Wylly Ramsés; Hernández-Pando, Rogelio; León-Contreras, Juan Carlos; Zazueta, Cecilia

doi:10.1016/j.ejphar.2015.09.018

Cited by 20 publications

(13 citation statements)

References 38 publications

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“… 55 The cardioprotective effects of ischemic or pharmacological post-conditioning were abolished by L-NAME or 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, inhibitor of sGC), where NO donors restored the cardioprotection even in the presence of L-NAME or ODQ. 56 …”

Section: Pathophysiological Implications Of Nitric Oxide System In Camentioning

confidence: 99%

Altered Nitric Oxide System in Cardiovascular and Renal Diseases

et al. 2016

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Nitric oxide (NO) is synthesized by a family of NO synthases (NOS), including neuronal, inducible, and endothelial NOS (n/i/eNOS). NO-mediated effects can be beneficial or harmful depending on the specific risk factors affecting the disease. In hypertension, the vascular relaxation response to acetylcholine is blunted, and that to direct NO donors is maintained. A reduction in the activity of eNOS is mainly responsible for the elevation of blood pressure, and an abnormal expression of iNOS is likely to be related to the progression of vascular dysfunction. While eNOS/nNOS-derived NO is protective against the development of atherosclerosis, iNOS-derived NO may be proatherogenic. eNOS-derived NO may prevent the progression of myocardial infarction. Myocardial ischemia/reperfusion injury is significantly enhanced in eNOS-deficient animals. An important component of heart failure is the loss of coronary vascular eNOS activity. A pressure-overload may cause severer left ventricular hypertrophy and dysfunction in eNOS null mice than in wild-type mice. iNOS-derived NO has detrimental effects on the myocardium. NO plays an important role in regulating the angiogenesis and slowing the interstitial fibrosis of the obstructed kidney. In unilateral ureteral obstruction, the expression of eNOS was decreased in the affected kidney. In triply n/i/eNOS null mice, nephrogenic diabetes insipidus developed along with reduced aquaporin-2 abundance. In chronic kidney disease model of subtotal-nephrectomized rats, treatment with NOS inhibitors decreased systemic NO production and induced left ventricular systolic dysfunction (renocardiac syndrome).

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Section: Pathophysiological Implications Of Nitric Oxide System In Camentioning

confidence: 99%

Altered Nitric Oxide System in Cardiovascular and Renal Diseases

et al. 2016

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“…14,15 Recently, it has been shown that remote intrathecal fentanyl preconditioning induces cardioprotective effects in rats via the activation of NOS, and that the NOS inhibitor -N omega--nitro-L-arginine methyl ester (L-NAME) abolished this effect. 16,17 Further studies highlight the role of the increased expression and activity of NOS in delayed protective effects of IPC. 18 POC also increases NOS activity; likewise, the NOS blockade with L-NAME abrogates the beneficial effect of POC.…”

Section: Discussionmentioning

confidence: 99%

Opioidergic conditioning of the human heart muscle in nitric oxide-dependent mechanism

et al. 2018

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“…Mitochondrial ATP-sensitive potassium channels (mKATP) control the activity of the mPTPs [13]. NO in low concentration was documented to be a potent mKATP opener through activation of anti-apoptotic cascade of enzymes called RISK pathway [14][15][16][17].…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide signaling in the ischemic postconditioning of human heart muscle (RCD code: III)

Kunecki

Płazak

Podolec

et al. 2016

Journal of Rare Cardiovascular Diseases

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Background: Ischemic heart conditioning is well documented to trigger the intrinsic protective mechanisms of resistance against ischemia/reperfusion (I/R) injury. Previous studies on animal model have suggested that the nitric oxide (NO) mediates the beneficial effect of ischemic postconditioning (POC). We tested the hypothesis that POC provide cardioprotection in the NO-dependent mechanism in the human myocardium. Methods: Human atrial trabeculae were subjected to simulated I/R injury. To achieve POC triple brief hypoxia periods were followed by the lethal hypoxia. Non-selective inhibitor of NO synthase: NG-monomethyl-L-arginine (L-NMMA) was used at the time of re-oxygenation in the POC protocol. Contractility of the myocardium was assessed as the maximal force of a contraction (Amax), the rate of rise of the force of a contraction (Slope L) and cardiac muscle relaxation -as the rate of decay of the force of a contraction (Slope T). Results: Co-application of L-NMMA with POC resulted in the decrease of Amax, Slope L and Slope T during re-oxygenation period as compared to POC only. Conclusions: At re-oxygenation period, the blockade of NO synthesis has deleterious effect on systolic and diastolic function of human myocardium, as well as attenuates the beneficial effect of ischemic POC. JRCD 2016; 2 (6): 181-184

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Inhibition of the nitric oxide/cyclic guanosine monophosphate pathway limited the cardioprotective effect of post-conditioning in hearts with apical myocardial infarction

Cited by 20 publications

References 38 publications

Altered Nitric Oxide System in Cardiovascular and Renal Diseases

Altered Nitric Oxide System in Cardiovascular and Renal Diseases

Opioidergic conditioning of the human heart muscle in nitric oxide-dependent mechanism

Nitric oxide signaling in the ischemic postconditioning of human heart muscle (RCD code: III)

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