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Am J Physiol Heart Circ Physiol 280: H1528-H1536, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 4, H1528-H1536, April 2001

Angiotensin II stimulates cardiac L-type Ca2+ current by a Ca2+- and protein kinase C-dependent mechanism

E. A. Aiello and H. E. Cingolani

Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata 1900, Argentina

Angiotensin II (ANG II) evokes positive inotropic responses in various species. However, the effects of this peptide on L-type Ca2+ currents (ICa) are still controversial. We report in this study that the effects of ANG II on ICa differ depending on the mode of patch-clamp technique used, standard whole cell (WC) or perforated patch (PP). No significant effects of ANG II (0.5 µM) were observed when WC in cells dialyzed with high EGTA was used. However, when the intracellular milieu was preserved using PP, ANG II induced a significant 77 ± 6% increase in ICa (-2.2 ± 0.3 in control and -3.9 ± 0.6 pA/pF in ANG II, n = 8, P < 0.05). When WC was used in cells dialyzed with low Ca2+ buffer capacity (EGTA 0.1 mM), ANG II was able to induce an increase in ICa (-3.5 ± 0.3 in control vs. -4.8 ± 0.4 pA/pF in ANG II, n = 13, P < 0.05). This increase was prevented when the cells were also dialyzed with the protein kinase C (PKC) inhibitor chelerythrine (50 µM) or calphostin C (1 µM). The above results allow us to conclude that strong intracellular Ca2+ buffering prevents the physiological actions of ANG II on cardiac ICa, which are also dependent on activation of PKC.

cardiac myocytes; perforated patch


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