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Subarachnoid Hemorrhage‐Induced Activation of Protein Kinase C and Suppression of Voltage‐Gated Potassium Channels
Author(s) -
Rudy Robert F,
Koide Masayo,
Wellman George C.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.925.3
Subject(s) - protein kinase c , depolarization , subarachnoid hemorrhage , vasoconstriction , constriction , medicine , myocyte , potassium channel , activator (genetics) , endocrinology , chemistry , anesthesia , cardiology , kinase , biology , microbiology and biotechnology , receptor
Subarachnoid hemorrhage (SAH) caused by aneurysm rupture is often associated with decreased cerebral blood flow and the development of severe neuronal deficits in patients. One cause of this disability is intracerebral (parenchymal) artery constriction. This constriction may be due in part to suppression of voltage‐gated potassium (K V ) channels causing membrane potential depolarization, enhanced Ca 2+ influx and vasoconstriction. Previous studies have shown that protein kinase C (PKC) is activated following SAH and that K V currents are suppressed in myocytes of larger diameter cerebral arteries from SAH model animals. Here, we examined PKC involvement in SAH‐induced K V current suppression in parenchymal arterioles using the conventional whole cell patch clamp technique. We found that K V currents were suppressed in myocytes obtained from SAH model rats compared to cells obtained from control animals. We also observed that the PKC activator 1,2‐dioctanoyl‐glycerol suppressed K V currents in control but not SAH myocytes, indicating PKC may be maximally active following SAH. In summary, our data indicate that PKC activity is increased following SAH and contributes to suppression of K V channels. Supported by the National Institutes of Health (NIH; P01‐HL095488), the Totman Medical Research Trust, the University of Vermont Summer Internship Grant and the Peter Martin Fund.