Effeects of PMA on Protein Kinase C in Perfused Rat Heart
Protein kinase C (PKC), the phospholipid, Ca2+-dependent protein kinase has been implicated in cardiac hypertrophy (Simpson et al. J. Molec. Cell. Cardiol. 18, suppl. 5, 45–58, 1985) and more recently in cardiac glucose transport (Van de Werve et al. Diabetes 36, 310–314, 1987). In addition α1 adrenergic agonists as well as muscarinic agonists increase phosphatidylinositol (PI) turnover in heart thus implying a role for PKC as part of the signal transduction processes. α-Adrenergic agonists also activate cardiac trans-sarcolemma electron efflux (Löw et al. Biochim. Biophys. Acta 844, 142–148, 1985). Since neither PI-turnover nor electron efflux is affected by β-agonists it appeared possible that PKC activation and electron efflux were uniquely involved in α-adrenergic receptor activation and were causally related. In the present study three questions were addressed: — (i) αl-adrenergic receptor activation associated with PKC activation?; (ii) what is the effect of treatment of the perfused rat heart with tumour-promoting phorbol ester (PMA), a putative activator of PKC?; and (iii) what is the relationship between PKC and trans-sarcolemma electron efflux?