101. Angiotensin II stimulates cardiac L-type [Ca.sup.2+] current by a [Ca.sup.2+] - and protein kinase C-dependent mechanism
- Author
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AIELLO, E. A. and CINGOLANI, H. E.
- Subjects
Angiotensin II receptor blockers -- Research ,Protein kinases -- Research ,Muscle cells -- Research ,Heart muscle -- Research ,Biological sciences - Abstract
Aiello, E. A., and H. E. Cingolani. Angiotensin II stimulates cardiac L-type [Ca.sup.2+] current by a [Ca.sup.2+] - and protein kinase C-dependent mechanism. Am J Physiol Heart Circ Physiol 280: H1528-H1536, 2001.--Angiotensin II (ANG II) evokes positive inotropic responses in various species. However, the effects of this peptide on L-type [Ca.sup.2+] currents ([I.sub.Ca]) are still controversial. We report in this study that the effects of ANG II on [I.sub.Ca] 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 [micro]M) 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 [+ or -] 6% increase in [I.sub.Ca] (-2.2 [+ or -] 0.3 in control and -3.9 [+ or -] 0.6 pA/pF in ANG II, n = 8, P [is less than] 0.05). When WC was used in cells dialyzed with low [Ca.sup.2+] buffer capacity (EGTA 0.1 mM), ANG II was able to induce an increase in [I.sub.Ca] (-3.5 [+ or -] 0.3 in control vs. -4.8 [+ or -] 0.4 pA/pF in ANG II, n = 13, P [is less than] 0.05). This increase was prevented when the cells were also dialyzed with the protein kinase C (PKC) inhibitor chelerythrine (50 [micro]M) or calphostin C (1 [micro]M). The above results allow us to conclude that strong intracellular [Ca.sup.2+] buffering prevents the physiological actions of ANG II on cardiac [I.sub.ca], which are also dependent on activation of PKC. cardiac myocytes; perforated patch
- Published
- 2001