What question did this study set out to answer?

To determine whether protein kinase C acts as the intracellular messenger transducing lipopolysaccharide signaling into elevated nitric oxide synthase activity and impaired contractility in cardiac myocytes.

December 1, 1995AJP Heart and Circulatory Physiology

PKC mediates LPS- and phorbol-induced cardiac cell nitric oxide synthase activity and hypocontractility

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Authors

TMThomas M. McKennaUnited States Air Force Research Laboratory SLS. LiAlberta Children's Hospital STShiying TaoVA Palo Alto Health Care System

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Implication

In vitro study reveals that protein kinase C mediates nitric oxide synthase activation and contractile depression in rat myocytes, highlighting an intracellular target in sepsis.

Key Points

To determine whether protein kinase C acts as the intracellular messenger transducing lipopolysaccharide signaling into elevated nitric oxide synthase activity and impaired contractility in cardiac myocytes.
Cultured rat cardiac myocytes were exposed to lipopolysaccharide (100 ng/ml) or the protein kinase C activator beta-phorbol 12,13-dibutyrate.
Myocytes were evaluated for protein kinase C activity, inducible nitric oxide synthase expression, and electrical-stimulated contractility in the presence or absence of protein kinase C inhibitors, protein kinase C depletion, or the nitric oxide synthase inhibitor L-NAME.
Lipopolysaccharide and beta-phorbol 12,13-dibutyrate significantly enhanced protein kinase C activity, inducible nitric oxide synthase expression, and overall nitric oxide synthase activity while depressing myocyte contractility.
Pharmacological inhibition of protein kinase C with sphingosine, chelerythrine, or calphostin-C, as well as prolonged phorbol-induced kinase depletion, abolished the increase in nitric oxide synthase activity and prevented contractile dysfunction.
Direct nitric oxide synthase inhibition using L-NAME fully reversed the contractile depression induced by protein kinase C activation.

Cite This Study

McKenna et al. (1995) studied this question.

synapsesocial.com/papers/6a9afab2491e2ec77d8b36ee https://doi.org/10.1152/ajpheart.1995.269.6.h1891

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Implication

In vitro study reveals that protein kinase C mediates nitric oxide synthase activation and contractile depression in rat myocytes, highlighting an intracellular target in sepsis.

PKC mediates LPS- and phorbol-induced cardiac cell nitric oxide synthase activity and hypocontractility

Discussion

Member takes

Implication

Key Points

Cite This Study

PKC mediates LPS- and phorbol-induced cardiac cell nitric oxide synthase activity and hypocontractility

Discussion

Member takes

Implication

Key Points

Cite This Study

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