[The roles of protein kinase C and Na(+)-H+ exchange in the angiotensin II-induced hypertrophic response].
In order to study the roles of protein kinase C (PKC) and Na(+)-H+ exchange in [Sar1] ANG II-induced hypertrophic response, 3H-Leucine incorporation into serum-free cultured neonatal rat cardiomyocytes were interfered with staurosporine, phorbol 12-myristate 13-acetate (PMA) or amiloride. With [Sar1] ANG II, a dose dependent augmentation of protein synthesis was observed. Activator of PKC (PMA) could also accelerate the rate of protein synthesis to a significant extent, while pretreatment of cardiac myocytes with PKC inhibitor (staurosporine) or Na(+)-H+ exchanger inhibitor (amiloride) would block [Sar1] ANG II-induced increase 3H-Leucine incorporation. These results demonstrated that activation of PKC and Na(+)-H+ exchange might mediate the hypertrophic response initiated by [Sar1] ANG II. However, inhibition of cellular Na(+)-H+ exchange did not affect the increase in protein synthesis due to activation of PKC, a finding indicating that the two resorts to regulate cell growth are mediated by independent pathways.
Laboratory of Cardiovascular Physiology, Human Medical University, Changsha.
X L
XL
Ding
C Y
CY
Zhou
Y X
YX
Li
D000470:Alkaloids / Q000494:pharmacology; D000584:Amiloride / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D016895:Culture Media, Serum-Free; D005260:Female; D008297:Male; D009206:Myocardium / Q000166:cytology*; D011493:Protein Kinase C / Q000037:antagonists & inhibitors / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors / Q000502:physiology*; D019311:Staurosporine
D000470:Alkaloids; D016895:Culture Media, Serum-Free; D017923:Sodium-Hydrogen Exchangers; D000804:Angiotensin II; D000584:Amiloride; D011493:Protein Kinase C; D019311:Staurosporine