Renal nerve stimulation causes alpha 1-adrenoceptor-mediated sodium retention but not alpha 2-adrenoceptor antagonism of vasopressin.

Renal nerve stimulation causes alpha 1-adrenoceptor-mediated sodium retention but not alpha 2-adrenoceptor antagonism of vasopressin.
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肾神经刺激引起α1-肾上腺素受体介导的钠潴留,但不引起加压素的α2-肾上腺素受体拮抗作用。

DOI:
10.1161/01.res.57.2.304
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发表时间:
1985
影响因子:
20.1
通讯作者:
Pettinger,WA
Pettinger,WA
中科院分区:
医学1区
文献类型:
--
作者:
Smyth,DD;Umemura,S;Pettinger,WA

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肾上腺素输注刺激肾α 2-肾上腺素能逆转环磷酸腺苷介导的抗利尿激素对钠和水排泄的影响。我们利用这种反应来确定肾神经刺激是否可以激活非再循环离体灌注大鼠肾脏中的α 2-肾上腺素受体(Krebs-Henseleit溶液;3.5 g/100 ml Ficoll; 1 g/100 ml白蛋白;36℃;心得安100 nM)。在prazosin (30 nM)阻断α 1-肾上腺素能受体的情况下,肾上腺素刺激α 2-肾上腺素能逆转环腺苷介导的抗利尿激素对钠(P < 0.05)和水(P < 0.05)排泄的影响。阈下(用于血管收缩)肾神经刺激(10 V; 1 msec; 0.65 +/- 0.10 Hz)未能改变加压素的作用。同样,高水平的肾神经刺激[加上吡唑嗪(100 nM)或苯氧苄胺(1.0 mg/kg / hr)阻断α 1-肾上腺素受体]不会激活与抗利尿激素作用相关的肾α 2-肾上腺素受体。在无加压素、无α 1-或α 2-肾上腺素受体阻断的情况下,同样水平的阈下肾神经刺激(0.85 +/- 0.14 Hz)可减少钠和水的排泄(P < 0.05)。α 1-肾上腺素受体阻断剂(普拉唑嗪30 nM)逆转了这种作用,但α 2-肾上腺素受体阻断剂(育亨宾300 nM)没有逆转这种作用,这表明肾神经刺激的这种作用是通过α 1-肾上腺素受体介导的。因此,大鼠肾脏的阈下肾神经刺激通过激活α 1-肾上腺素受体诱导钠和水潴留,如兔和狗的其他实验所示。(摘要删节250字)
Renal alpha 2-adrenoceptor stimulation by epinephrine infusion reverses cyclic adenosine monophosphate-mediated effects of vasopressin on sodium and water excretion. We used this response to determine whether renal nerve stimulation can activate renal alpha 2-adrenoceptors in the non-recirculating isolated perfused rat kidney (Krebs-Henseleit solution; 3.5 g/100 ml Ficoll; 1 g/100 ml albumin; 36 degrees C; propranolol 100 nM). In the presence of alpha 1-adrenoceptor blockade with prazosin (30 nM) alpha 2-adrenoceptor stimulation with epinephrine reversed the cyclic adenosine monophosphate-mediated effects of vasopressin on sodium (P less than 0.05) and water (P less than 0.05) excretion. Subthreshold (for vasoconstriction) renal nerve stimulation (10 V; 1 msec; 0.65 +/- 0.10 Hz) failed to alter the effect of vasopressin. Similarly, higher levels of renal nerve stimulation [plus prazosin (100 nM) or phenoxybenzamine (1.0 mg/kg per hr) to block alpha 1-adrenoceptors] did not activate renal alpha 2-adrenoceptors which are associated with the antagonism of the effects of vasopressin. The same level of subthreshold renal nerve stimulation (0.85 +/- 0.14 Hz) in the absence of vasopressin, and without alpha 1- or alpha 2-adrenoceptor blockade, decreased (P less than 0.05) sodium and water excretion. The reversal of this effect by alpha 1-adrenoceptor blockade (prazosin 30 nM) but not alpha 2-adrenoceptor blockade (yohimbine 300 nM) indicates that this effect of renal nerve stimulation is mediated through alpha 1-adrenoceptors. Thus, subthreshold renal nerve stimulation in the rat kidney induces sodium and water retention through activation of alpha 1-adrenoceptors, as shown by others in the rabbit and dog.(ABSTRACT TRUNCATED AT 250 WORDS)
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