The effects of acidosis on the phosphorylation of phospholamban and
troponin-i in rat cardiac muscle.
Mundi[tilde]na-Weilenmann, C., L. Vittone, H. E. Cingolani, and C. H.
Orchard.
Centro de Investigaciones Cardiovasculares Department of
Physiology, Facultad de Ciencias M[acute]edicas University of Leeds,
Universidad Nacional de la Plata Leeds, 60 y 120, 1900 La Plata LS2
9JT, Argentina U.K.
APStracts 2:0269C, 1995.
Acidosis inhibits Ca2+ transport by the sarcoplasmic reticulum of
cardiac muscle, and decreases the Ca2+ sensitivity of the contractile
proteins, although the mechanisms underlying these changes are
unclear. We have investigated the hypothesis that changes in the
phosphorylation of the regulatory proteins phospholamban and
troponin-I might play a role in the acidosis-induced changes in the
function of the sarcoplasmic reticulum and the myofilaments
respectively. Langendorff-perfused rat hearts were labelled with 32P,
and then perfused with either control (pH 7.4) or acid (pH 6.8)
physiological salt solution, in both the absence and presence of
isoproterenol. The incorporation of 32P into phospholamban and
troponin-I was determined by SDS-page electrophoresis of sarcoplasmic
reticulum and myofibrillar proteins, followed by autoradiography and
liquid scintillation counting. The data show that acidosis has no
effect on the phosphorylation of phospholamban in the absence of
isoproterenol, but that in the presence of isoproterenol, acidosis
increased the phosphorylation of phospholamban. However acidosis
increased the phosphorylation of troponin-I, in both the absence and
the presence of isoproterenol. Acidosis did not alter the cAMP
content of the hearts, but did inhibit type 1 phosphatase. These data
show that acidosis can alter the phosphorylation of these two
proteins, and suggest that these changes underlie, in part, the
changes observed in cardiac muscle during acidosis.
Received 14 April 1995; accepted in final form 12 July 1995.
APS Manuscript Number C211-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 30 July 1995.