Gk. Oriji, Angiotensin II stimulates PGF(2 alpha) release in cultured neonatal rat ventricular myocytes via L-type calcium channels, PROS LEUK E, 65(2), 2001, pp. 73-77
Citations number
26
Categorie Soggetti
Cell & Developmental Biology
Journal title
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS
Angiotensin II (Ang II) has been shown to cause Prostaglandin F-2 alpha (PG
F(2 alpha)) release in neonatal rat ventricular myocytes and smooth muscle
cells. In these cells, Ang II has also been shown to regulate growth. We us
ed neonatal rat ventricular myocytes to investigate the role of calcium in
maintenance of Ang II-induced PGF(2 alpha) release. The amount of PGF(2 alp
ha) produced was determined by radioimmunoassay. Ang II-induced PGF(2 alpha
) release. Pretreatment of neonatal rat ventricular myocytes with different
doses (10(-8) M, 10(-7) M, 10(-6) M and 10(-5) M) of diltiazm (voltage-sen
sitive L-type calcium channel blocker) produced significant inhibition in A
ng II-induced PGF(2 alpha) release. Inhibition was first noted at 10(-8) M
and was complete at 10(-6) M. Conversely, pretreatment of neonatal rat vent
ricular myocytes with different doses (10(-8) M, 10(-7) M, 10(-6) M and 10(
-5) M) of calcium channel blockers (conotoxin; voltage-sensitive N-type cal
cium channel blocker or thapsigargin; intracellular calcium channel blocker
) produced no changes in Ang II-induced PGF(2 alpha) release. These results
strongly suggest that Ang II-induced PGF(2 alpha) release in neonatal rat
ventricular myocytes is maintained, at least in part, via increase in extra
cellular calcium influx. (C) 2001 Harcourt Publishers Ltd.