Angiotensin II stimulates PGF2 αrelease in cultured neonatal rat ventricular myocytes via L-type calcium channels

Abstract

Angiotensin II (Ang II) has been shown to cause Prostaglandin F2 α(PGF2α) release in neonatal rat ventricular myocytes and smooth muscle cells. In these cells, Ang II has also been shown to regulate growth. We used neonatal rat ventricular myocytes to investigate the role of calcium in maintenance of Ang II-induced PGF2 αrelease. The amount of PGF2 αproduced was determined by radioimmunoassay. Ang II-induced PGF2 αrelease. Pretreatment of neonatal rat ventricular myocytes with different doses (10−8M, 10−7M, 10−6M and 10−5M) of diltiazm (voltage-sensitive L-type calcium channel blocker) produced significant inhibition in Ang II-induced PGF2αrelease. Inhibition was first noted at 10−8M and was complete at 10−6M. Conversely, pretreatment of neonatal rat ventricular myocytes with different doses (10−8M, 10−7M, 10−6M and 10−5M) of calcium channel blockers (conotoxin; voltage-sensitive N-type calcium channel blocker or thapsigargin; intracellular calcium channel blocker) produced no changes in Ang II-induced PGF2αrelease. These results strongly suggest that Ang II-induced PGF2 αrelease in neonatal rat ventricular myocytes is maintained, at least in part, via increase in extracellular calcium influx.