Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells.
Atrial natriuretic peptide enhances activity of potassium conductance in adrenal glomerulosa cells.
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心房钠尿肽增强肾上腺肾小球细胞钾电导的活性。
DOI：
10.1152/ajpcell.1994.266.5.c1357
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Barrett,PQ
中科院分区：
文献类型：
--
作者：
Ganz,MB;Nee,JJ;Isales,CM;Barrett,PQ
肾上腺肾小球(AG)细胞分泌的醛固酮被心钠素(ANP)抑制。由于K+电导的改变可以调节醛固酮的分泌，因此我们研究了ANP对细胞内K+稳态的影响。用K(+)敏感染料--K(+)结合的苯并呋喃间苯二甲酸酯荧光分光光度法测定AG细胞内K+浓度([K+]i)。在无HCO3、N-2-hydroxyethylpiperazine-N‘-2-ethanesulfonic酸缓冲介质中，AG细胞[K+]i的静止值为12 0+/-1 2 mm(n=37)。AG细胞暴露于ANP后，[K+]i呈剂量依赖性一过性下降，从100 PM时的21+/-3.2%(n=7)下降到1微米时的31+/-2.3%(n=7)。在心钠素的持续存在下，[K+]i在90 S内迅速恢复到接近基础值。用电位敏感染料1-3(-sulfonatopropyl)-4-[beta-(-(di-n-butylamino)-6-naphthyl)vinyl]-甜菜碱测量膜电压时，膜电位也发生了相应的变化。用巴(0.5 mM)、四乙基铵(0.1 mM)、查氏毒素(100 NM)或乙二醇双(β-氨基乙醚)-N，N，N‘，N’-四乙酸(0.5 mM)预处理AG细胞后，ANP-C受体选择性激动剂ANP-(7-23)对ANP引起的[K+]i下降无明显影响，而cGMP(50微米)对[K+]i无明显影响。我们认为，ANP通过激活ANP A受体，通过钙离子激活的K(+)传导通路改变K+动态平衡，可能是最大的钾通道。
Aldosterone secretion from the adrenal glomerulosa (AG) cells is inhibited by atrial natriuretic peptide (ANP). Inasmuch as alterations in K+ conductance can modulate aldosterone secretion, the effect of ANP on intracellular K+ homeostasis was investigated. Intracellular K+ concentration ([K+]i) of AG cells was assessed by spectrofluorometry using the K(+)-sensitive dye, K(+)-binding benzofuran isophthalate. The resting value of [K+]i in AG cells was determined to be 120 +/- 1.2 mM (n = 37) in a HCO3-free, N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered medium. Exposure of AG cells to ANP led to a dose-dependent, transient decrease in [K+]i, from 21 +/- 3.2% (n = 7) at 100 pM to 31 +/- 2.3% at 1 microM (n = 7). In the continued presence of ANP, a rapid recovery to near basal values of [K+]i was attained within 90 s. Measurements of membrane voltage using the potential sensitive dye 1-3(-sulfonatopropyl)-4-[beta-(-(di-n-butylamino)-6-naphthyl)vinyl ]- pyridinium betaine documented an accompanying change in membrane potential. Pretreatment of AG cells with barium (0.5 mM), tetraethylammonium (0.1 mM), charybdotoxin (100 nM), or ethylene glycol-bis(beta-aminoethylether)-N,N,N',N'-tetraacetic acid (0.5 mM) blunted the ANP-induced decrease in [K+]i. ANP-(7-23), the ANP-C-receptor selective agonist, which does not elevate guanosine 3',5'-cyclic monophosphate (cGMP) did not alter [K+]i in contrast to cGMP (50 microM), which did. We conclude that ANP via the activation of the ANP A receptor alters K+ homeostasis through a Ca(2+)-activatable K(+)-conductive pathway likely to be the maxi-K channel.