AJP - Cell Physiology, Vol 263, Issue 4 C873-C878, Copyright © 1992 by American Physiological Society
Cellular mechanisms of vasopressin and endothelin to mobilize [Mg2+]i in vascular smooth muscle cells
K. Okada, S. Ishikawa and T. Saito
Department of Medicine, Jichi Medical School, Tochigi, Japan.
The present study was undertaken to examine the effects of arginine
vasopressin (AVP) and endothelin-1 (ET-1) on cytosolic free Mg2+ ([Mg2+]i)
in cultured rat vascular smooth muscle cells (VSMC). [Mg2+]i was measured
using the fluorescence indicator dye mag-fura-2. AVP and ET-1 at a
concentration of 1 x 10(-9) M or higher induced the mobilization of [Mg2+]i
and cytosolic free Ca2+ ([Ca2+]i) in a dose-dependent manner in rat VSMC.
Atrial natriuretic peptide and sodium nitroprusside producing cellular
guanosine 3',5'-cyclic monophosphate did not affect [Mg2+]i and [Ca2+]i. A
diterpene activator of adenylate cyclase, forskolin, also did not alter
[Mg2+]i and [Ca2+]i. The removal of extracellular Mg2+ enhanced the
AVP-mobilized [Ca2+]i and did not change the AVP-mobilized [Mg2+]i. The
Ca(2+)-free and nominally Mg2+/Ca(2+)-free states decreased the
AVP-mobilized [Mg2+]i and [Ca2+]i. The Na(+)-free state enhanced the
sustained, but not peak, level of the AVP-mobilized [Mg2+]i. These results
indicate that AVP and ET-1 mobilize [Mg2+]i mediated through their
intracellular second messenger [Ca2+]i and independent of extracellular
Mg2+. Also, an increase in [Mg2+]i is indicated to stimulate the Na(+)-Mg2+
exchange to increase cellular Mg2+ efflux.
