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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Involvement of G-protein betagamma subunits on the influence of inhibitory alpha2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens.
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Involvement of G-protein betagamma subunits on the influence of inhibitory alpha2-autoreceptors on the angiotensin AT1-receptor modulation of noradrenaline release in the rat vas deferens.

机译：G蛋白betagamma亚基参与抑制α2自体受体对大鼠输精管中去甲肾上腺素释放的血管紧张素AT1受体调节的影响。

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摘要

The influence of alpha2-autoreceptors on the facilitation of [3H]-noradrenaline release mediated by angiotensin II was studied in prostatic portions of rat vas deferens preincubated with [3H]-noradrenaline. Angiotensin II enhanced tritium overflow evoked by trains of 100 pulses at 8 Hz, an effect that was attenuated by the AT1-receptor antagonist losartan (0.3-1 microM), at concentrations suggesting the involvement of the AT1B subtype. The effect of angiotensin II was also attenuated by inhibition of phospholipase C (PLC) and protein kinase C (PKC) indicating that prejunctional AT1-receptors are coupled to the PLC-PKC pathway. Angiotensin II (0.3-100 nM) enhanced tritium overflow more markedly, up to 64%, under conditions that favor alpha2-autoinhibition, observed when stimulation consisted of 100 pulses at 8 Hz, than under poor alpha2-autoinhibition conditions, only up to 14%, observed when alpha2-adrenoceptors were blocked with yohimbine (1 microM) or when stimulation consisted of 20 pulses at 50 Hz.Activation of PKC with 12-myristate 13-acetate (PMA, 0.1-3 microM) also enhanced tritium overflow more markedly under strong alpha2-autoinhibition conditions. Inhibition of Gi/o-proteins with pertussis toxin (8 microg/ml) or blockade of Gbetagamma subunits with the anti-betagamma peptide MPS-Phos (30 microM) attenuated the effects of angiotensin II and PMA. The results indicate that activation of AT1-receptors coupled to the PLC-PKC pathway enhances noradrenaline release, an effect that is markedly favoured by an ongoing activation of alpha2-autoreceptors. Interaction between alpha2-adrenoceptors and AT1-receptors seems to involve the betagamma subunits released from the Gi/o-proteins coupled to alpha2-adrenoceptors and protein kinase C activated by AT1-receptors.
机译：在预先孵育[3H]-去甲肾上腺素的大鼠输精管的前列腺中研究了α2-自身受体对血管紧张素II介导的[3H]-去甲肾上腺素释放促进的影响。血管紧张素II增强了by以100 Hz的脉冲在8 Hz时引起的overflow溢流，该浓度被AT1受体拮抗剂洛沙坦（0.3-1 microM）减弱，浓度暗示了AT1B亚型的参与。血管紧张素II的作用也通过抑制磷脂酶C（PLC）和蛋白激酶C（PKC）而减弱，表明结前AT1-受体与PLC-PKC途径偶联。血管紧张素II（0.3-100 nM）在有利于α2自抑制的条件下更明显地增强了overflow的溢出，高达64％，而在不良的α2自抑制条件下，当刺激由8 Hz的100个脉冲组成时，观察到的14只有14个当用育亨宾（1 microM）阻断α2-肾上腺素受体或在50 Hz刺激下包含20个脉冲时观察到的％，肉豆蔻酸12-肉豆蔻酸13-乙酸酯（PMA，0.1-3 microM）激活PKC也显着增强了tri的溢出在强α2自抑制条件下。用百日咳毒素（8 microg / ml）抑制Gi / o蛋白或用抗βγ肽MPS-Phos（30 microM）阻滞Gbetagamma亚基减弱了血管紧张素II和PMA的作用。结果表明，与PLC-PKC途径偶联的AT1受体的激活增强了去甲肾上腺素的释放，α2自体受体的持续激活明显促进了这种作用。 α2肾上腺素受体与AT1受体之间的相互作用似乎涉及从与α2肾上腺素受体和AT1受体激活的蛋白激酶C偶联的Gi / o蛋白释放的betagamma亚基。

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