Angiotensin II-induced inhibition of calcium currents via G(q/11)-protein involving protein kinase C in hamster submandibular ganglion neurons.

Abstract

Angiotensin II (AngII) is one of the most important vasoconstrictive hormones but is also known to act as a neuromodulator and a neurotransmitter in the central and peripheral nervous systems. In a previous study, we have shown that AngII, mediated by AT(1) receptors, inhibits voltage-dependent calcium channel (VDCC) currents (I(Ca)) via G-proteins in submandibular ganglion (SMG) neurons. In this study, we further characterized the signal transduction of AngII-induced inhibition of I(Ca). Application of 1 microM AngII inhibited I(Ca) by 32.1+/-2.7% (mean+/-S.E.M., n=9). Intracellular dialysis of anti-G(q/11) antibodies attenuated these inhibition (8.8+/-1.3%, n=6). In addition, treatment of protein kinase C (PKC) activator and inhibitor also attenuated these inhibition (8.0+/-0.9 and 9.8+/-0.9%, n=6 and 9, respectively). We therefore conclude that AngII inhibits VDCC via G(q/11)-proteins involving in SMG neurons. In addition, such PKC-dependent pathways mediated mainly L-type VDCC inhibition.