Y. Fukuta et al., ANGIOTENSIN-II AS A STIMULATOR OF NA-DEPENDENT CA2+ EFFLUX FROM FRESHLY ISOLATED ADULT-RAT CARDIOMYOCYTES(), Neuroscience letters, 213(2), 1996, pp. 95-98
In cardiac tissues, angiotensin II causes inotropic and chronotropic e
ffects on the heart. It is indicated that the mechanism of the inotrop
ic effect of angiotensin II is attributed to an increase in cytosolic
free calcium ([Ca2+](i)) in cardiomyocytes. However, increased [Ca2+](
i) should be restored to a physiological level because cumulative elev
ation in [Ca2+](i) leads to irreversible injury in cardiomyocytes. Whe
reas it is known that angiotensin II causes the increase in [Ca2+](i)
in cardiac cells, little is known about the mechanisms of decrease in
[Ca2+](i) in cardiomyocytes upon angiotensin II stimulation. In the pr
esent study, we examined the effect of angiotensin II on Ca2+ efflux f
rom freshly isolated adult rat cardiomyocytes. Angiotensin II stimulat
ed the efflux of Ca-45(2+) from the cells in a concentration dependent
manner (10(-7)-10(-5) M). The Ca-45(2+) efflux from the cells was inh
ibited by type 1 angiotensin II receptor inhibitor. The angiotensin II
-stimulated Ca-45(2+) efflux was not affected by deprivation of the ex
tracellular Ca2+, but was dependent on the presence of extracellular N
a+. These results indicate that angiotensin II stimulates extracellula
r Na+-dependent Ca-45(2+) efflux from freshly isolated adult rat cardi
omyocytes, probably through its stimulatory effect on the plasma membr
ane type 1 angiotensin II receptors which may couple to Na+/Ca2+ excha
nge.