Analysis of angiotensin‐stimulated sodium transport in cultured smooth muscle cells from rat aorta
Analysis of angiotensin‐stimulated sodium transport in cultured smooth muscle cells from rat aorta
复制标题
大鼠主动脉培养平滑肌细胞中血管紧张素刺激的钠转运分析
DOI:
--
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发表时间:
1983
影响因子:
5.6
通讯作者:
T. Brock
中科院分区:
文献类型:
--
作者:
Jeffrey B. Smith;T. Brock
Angiotensin peptides (AI, AII, AIII) increased the rate of Na+ accumulation by smooth muscle cells (SMC) cultured from rat aorta. The stimulatory effect of All on Na+ uptake was observed which Na+ exodus via the Na+/K+ pump was blocked either by ouabain or by the removal of extracellular K+. All was at least ten times more potent than AIII and about 100 times more potent than AI in stimulating Na+ uptake. Saralasin had little effect on Na+ uptake by itself but almost completely blocked the increase caused by All. The stimulation of net Na+ entry by AI, but not AII, was prevented by protease inhibitors. The stimulation of Na+ uptake was almost completely blocked by amiloride. Tetrodotoxin, which prevented veratridine from increasing Na+ uptake, had no effect on the response to AII. Angiotensin increased the rate of ouabain‐sensitive 86Rb+ uptake (Na+/K+ pump activity) but had no effect on ouabain‐sensitive ATPase activity in frozen‐thawed SMC or in microsomal membranes isolated from cultured SMC. The stimulation of ouabain‐sensitive 86Rb+ uptake by All was blocked by saralasin. Omitting Na+ from the external medium prevented All from increasing 86Rb+ uptake. All had no effect on cell volume or cyclic AMP levels in the cultured SMC. These results suggest that angiotensin peptides activate an amiloride‐sensitive Na+ transporter which supplies the Na+ /K+ pump with more Na+, its rate‐limiting substrate.
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影响因子:
6.1
作者:
Brock,TA;Smith,JB
通讯作者:
Smith,JB
DOI:
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发表时间:
1981
期刊:
The Journal of pharmacology and experimental therapeutics
影响因子:
--
作者:
Webb,RC;Bohr,DF
通讯作者:
Bohr,DF
影响因子:
2.9
作者:
Schultz,GS;Galardy,RE;Jamieson,JD
通讯作者:
Jamieson,JD
DOI:
10.1159/000158360
发表时间:
1981
期刊:
Blood vessels
影响因子:
--
作者:
Zelcer,E;Sperelakis,N
通讯作者:
Sperelakis,N