Schwartz D D, Eikenburg D C
Department of Pharmacology, College of Medicine, University of Tennessee, Memphis 38163.
Life Sci. 1991;48(8):781-7. doi: 10.1016/0024-3205(91)90093-q.
The effects of synthetic atrial natriuretic factor (rANF(3-28)) on sympathetic neurotransmission in the isolated perfused rat kidney was examined. ANF (10(-10)-10(-7) M) had no significant effect on stimulus-induced (1 Hz, 2 min) overflow of endogenous norepinephrine (NE) from the rat kidney. ANF also failed to affect stimulus-induced overflow which was markedly enhanced as a result of prejunctional beta-adrenoceptor activation with isoproterenol (10(-6)M). However, over the same concentration range ANF markedly attenuated the vasoconstrictor response to nerve stimulation. In addition, ANF significantly reduced the renal vasoconstrictor responses to intra-arterial injections of NE and angiotensin II. These results suggest that, while ANF potently inhibits renal sympathetic neurotransmission by inhibition of vascular responsiveness to vasoconstrictor stimuli, ANF does not appear to have a prejunctional effect to alter NE release from renal sympathetic nerves.
研究了合成心房利钠因子（rANF(3 - 28)）对离体灌流大鼠肾脏交感神经传递的影响。心房利钠因子（10⁻¹⁰ - 10⁻⁷ M）对刺激诱导的（1赫兹，2分钟）大鼠肾脏内源性去甲肾上腺素（NE）溢出无显著影响。心房利钠因子也未能影响刺激诱导的溢出，而由于用异丙肾上腺素（10⁻⁶ M）激活突触前β - 肾上腺素能受体，刺激诱导的溢出显著增强。然而，在相同浓度范围内，心房利钠因子显著减弱了对神经刺激的血管收缩反应。此外，心房利钠因子显著降低了肾脏对动脉内注射去甲肾上腺素和血管紧张素II的血管收缩反应。这些结果表明，虽然心房利钠因子通过抑制血管对血管收缩刺激的反应性而有力地抑制肾脏交感神经传递，但心房利钠因子似乎没有突触前作用来改变肾脏交感神经释放去甲肾上腺素。
