TY - JOUR
T1 - Angiotensin II effect on 22Na+ transport in vascular smooth muscle cells
AU - Kuriyama, S.
AU - Nakamura, A.
AU - Hopp, L.
AU - Fine, B. P.
AU - Kino, M.
AU - Cragoe, E.
AU - Aviv, A.
PY - 1988
Y1 - 1988
N2 - It is well established that angiotensin II (AII) rapidly increases free cytosolic Ca2+ in vascular smooth muscle cells (VSMCs). Several studies have indicated that the hormone also plays a role in Na+-K+ regulation of these cells. In this study, we explored the mechanism of AII effect on 22Na+ transport in cultured rat VSMCs. The 22Na+ washout from these cells was described by three exponents with exponential factors k1>k2>k3. In 1.8 mM Ca2+ medium, AII (10-9-10-6M) increased (in a dose response manner) the k1 value, and consequently the initial washout rate constant (ki(e)) for the isotope. AII had no effect on ki(e) in Ca2+-deficient medium or in the presence of ouabain. Amiloride (10-3 M) and verapamil (10-5M) abolished the AII induced increase in ki(e). These findings are consistent with angiotensin II stimulation of an amiloride-sensitive Na+ transport, which is likely to represent the Na+/H+ antiport. In cultured VSMCs, the sustained stimulation by AII of this transport system requires the presence of extracellular Ca2+ and its influx into these cells.
AB - It is well established that angiotensin II (AII) rapidly increases free cytosolic Ca2+ in vascular smooth muscle cells (VSMCs). Several studies have indicated that the hormone also plays a role in Na+-K+ regulation of these cells. In this study, we explored the mechanism of AII effect on 22Na+ transport in cultured rat VSMCs. The 22Na+ washout from these cells was described by three exponents with exponential factors k1>k2>k3. In 1.8 mM Ca2+ medium, AII (10-9-10-6M) increased (in a dose response manner) the k1 value, and consequently the initial washout rate constant (ki(e)) for the isotope. AII had no effect on ki(e) in Ca2+-deficient medium or in the presence of ouabain. Amiloride (10-3 M) and verapamil (10-5M) abolished the AII induced increase in ki(e). These findings are consistent with angiotensin II stimulation of an amiloride-sensitive Na+ transport, which is likely to represent the Na+/H+ antiport. In cultured VSMCs, the sustained stimulation by AII of this transport system requires the presence of extracellular Ca2+ and its influx into these cells.
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U2 - 10.1097/00005344-198802000-00003
DO - 10.1097/00005344-198802000-00003
M3 - Article
C2 - 2452306
AN - SCOPUS:0023833249
SN - 0160-2446
VL - 11
SP - 139
EP - 146
JO - Journal of Cardiovascular Pharmacology
JF - Journal of Cardiovascular Pharmacology
IS - 2
ER -