Open AccessRole of Na+/Phosphate-Cotransporter in Myocardial Contractile Responses to α1-Agonist
Author(s) -
Michael O. Onwochei
Publication year - 1995
Publication title -
journal of cardiovascular pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.762
H-Index - 100
eISSN - 1533-4023
pISSN - 0160-2446
DOI - 10.1097/00005344-199505000-00021
Subject(s) - phenylephrine , prazosin , chemistry , cotransporter , contraction (grammar) , agonist , pi , endocrinology , medicine , extracellular , calcium , pharmacology , sodium , biochemistry , receptor , antagonist , biology , organic chemistry , blood pressure
The interaction of cardiac sodium/phosphate (Na+/Pi)-cotransporter and the phosphoinositide pathway (PIP) in influencing myocardial contraction was investigated. Specifically, the study was performed to determine if myocardial positive inotropic response (+dP/dt) to phenylephrine (PE, an activator of PIP) can be potentiated by inorganic phosphate (Pi, the substrate of Na+/Pi-cotransporter). Contractile responses of the isolated perfused rat heart were studied in conditions of controlled extracellular calcium activity and constant preload. The data showed that phenylephrine-induced increase in +dP/dt was potentiated by Pi. Prazosin inhibited this increase in +dP/dt, indicating alpha 1-adrenergic involvement. This Pi-potentiated increase in +dP/dt was also inhibited by phosphonoformate (PFA); however, only partial inhibition was obtained with concentrations of PFA that selectively inhibited Na+/Pi-cotransporter. Isoproterenol-induced increase in +dP/dt was not potentiated by Pi, showing that potentiation of +dP/dt is not a common effect of Pi. The data support an important interaction between PIP and Na+/Pi-cotransporter in regulating myocardial contraction.