多巴胺通过激活DA1受体抑制前列腺素F2α诱导的兔空肠动脉去极化。
Dopamine inhibits prostaglandin F2 alpha-induced depolarization of rabbit jejunal arteries via activation of DA1-receptors.
作者信息
Illes P, Nörenberg W
机构信息
Department of Pharmacology, University of Freiburg, Federal Republic of Germany.
出版信息
Naunyn Schmiedebergs Arch Pharmacol. 1989 Apr;339(4):483-5. doi: 10.1007/BF00736066.
In rabbit jejunal arteries, the membrane potential of single smooth muscle cells decreased on the application of noradrenaline 3 mumol/l. LY 171555 1 mumol/l did not change, whereas SKF 38393 10 mumol/l reversed the effect of noradrenaline. When prostaglandin F2 alpha (PGF2 alpha) was used to evoke depolarization in the presence of prazosin 0.1 mumol/l, rauwolscine 1 mumol/l and propranolol 1 mumol/l, both SKF 38393 10 mumol/l and dopamine 10 mumol/l repolarized the membrane. SCH 23390 1 mumol/l antagonized the effects of SKF 38393 10 mumol/l and dopamine 10 mumol/l. Thus, the change in membrane potential is mediated by a DA1-receptor.
在兔空肠动脉中，当施加3 μmol/L去甲肾上腺素时，单个平滑肌细胞的膜电位降低。1 μmol/L的LY 171555没有变化，而10 μmol/L的SKF 38393可逆转去甲肾上腺素的作用。当在存在0.1 μmol/L哌唑嗪、1 μmol/L育亨宾和1 μmol/L普萘洛尔的情况下使用前列腺素F2α（PGF2α）引起去极化时，10 μmol/L的SKF 38393和10 μmol/L的多巴胺均可使膜复极化。1 μmol/L的SCH 23390可拮抗10 μmol/L的SKF 38393和10 μmol/L的多巴胺的作用。因此，膜电位的变化是由DA1受体介导的。
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