Sodium nitroprusside protects adult rat cardiac myocytes from cellular injury induced by simulated ischemia: Role for a non-cGMP-dependent mechanism of nitric oxide protection

Gerreffa, A, Woodman, O, Cao, A and Ritchie, R 2006, 'Sodium nitroprusside protects adult rat cardiac myocytes from cellular injury induced by simulated ischemia: Role for a non-cGMP-dependent mechanism of nitric oxide protection', Journal of Cardiovascular Pharmacology, vol. 47, no. 1, pp. 1-8.


Document type: Journal Article
Collection: Journal Articles

Title Sodium nitroprusside protects adult rat cardiac myocytes from cellular injury induced by simulated ischemia: Role for a non-cGMP-dependent mechanism of nitric oxide protection
Author(s) Gerreffa, A
Woodman, O
Cao, A
Ritchie, R
Year 2006
Journal name Journal of Cardiovascular Pharmacology
Volume number 47
Issue number 1
Start page 1
End page 8
Total pages 8
Publisher Lippincott Williams & Wilkins
Abstract The cardioprotective actions of nitric oxide (NO) have largely been attributed to cGMP. NO may, however, elicit some biological actions independently of cGMP. We tested the hypothesis that the NO donor sodium nitroprusside specifically protects isolated cardiomyocytes from injury at least in part independently of its ability to elevate cGMP by using metabolic inhibition to simulate ischemia. Metabolic inhibition-induced injury of adult rat cardiomyocytes (increased activity of lactate dehydrogenase and creatine kinase) was significantly reduced by sodium nitroprusside by at least 30% at all concentrations studied (0.3-100 ?M). Sodium nitroprusside (1 ?M) increased cardiomyocyte cGMP content, but neither a stable analogue of cGMP (8-bromo-cGMP) nor a potent cGMP stimulus (atrial natriuretic peptide) mimicked the protective effects of sodium nitroprusside. Moreover, inhibition of soluble guanylyl cyclase failed to inhibit sodium nitroprusside cardiomyocyte protection. Conversely, inhibition of either ATP-sensitive potassium (KATP) channels with glibenclamide (10 ?M) or calcium-sensitive potassium (KCa) channels with tetraethylammonium bromide (1 mM) or iberiotoxin (20 nM) markedly attenuated the cardioprotective actions of sodium nitroprusside. In conclusion, sodium nitroprusside protects isolated cardiomyocytes from metabolic inhibition independently of cGMP; rather, inhibition of KCa and KATP channels reverses the sodium nitroprusside actions, thus unmasking another mechanism for NO-mediated protection in cardiomyocytes.
Subject Basic Pharmacology
DOI - identifier 10.1097/01.fjc.0000189601.12276.8b
Copyright notice © 2006 by Lippincott Williams & Wilkins.
ISSN 0160-2446
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