Okada K, Ishikawa S, Saito T
Department of Medicine, Jichi Medical School, Tochigi, Japan.
Biochem Biophys Res Commun. 1990 Nov 30;173(1):224-30. doi: 10.1016/s0006-291x(05)81045-9.
The effect of arginine vasopressin (AVP) on Na+ kinetics was examined in cultured rat vascular smooth muscle cells (VSMC) and rat renal papillary collecting tubule cells (RPCT) by the direct measurement of intracellular sodium concentration [(Na+]i) using fluorescence dye; SBFI. AVP increased [Na+]i in a dose-dependent manner at a concentration of 10(-9) M or higher in rat VSMC but did not affect [Na+]i in rat RPCT. The calcium (Ca2+)-free solution completely blocked the increasing effect of AVP on [Na+]i in rat VSMC. A Ca2+ ionophore, ionomycin (1-2 x 10(-6) M) increased [Na+]i both in rat VSMC and RPCT. The Ca2(+)-free solution abolished the ionomycin-increased [Na+]i both in rat VSMC and RPCT. These results therefore indicate that after binding the V1 receptor AVP increases [Na+]i mediated through an increase in cellular Ca2+ uptake in VSMC.
通过使用荧光染料SBFI直接测量细胞内钠浓度[（Na +）i]，研究了精氨酸加压素（AVP）对培养的大鼠血管平滑肌细胞（VSMC）和大鼠肾乳头集合管细胞（RPCT）中Na +动力学的影响。在大鼠VSMC中，AVP在浓度为10（-9）M或更高时以剂量依赖性方式增加[Na +] i，但不影响大鼠RPCT中的[Na +] i。无钙溶液完全阻断了AVP对大鼠VSMC中[Na +] i的增加作用。钙（Ca2 +）离子载体离子霉素（1-2×10（-6）M）在大鼠VSMC和RPCT中均增加了[Na +] i。无Ca2（+）溶液消除了离子霉素在大鼠VSMC和RPCT中增加的[Na +] i。因此，这些结果表明，在结合V1受体后，AVP通过增加VSMC中细胞Ca2 +摄取来增加[Na +] i。
