Matsumura Y, Kawazoe S, Ichihara T, Shinyama H, Kageyama M, Morimoto S
Department of Pharmacology, Osaka University of Pharmaceutical Sciences, Japan.
Clin Exp Hypertens A. 1988;10(6):1305-7. doi: 10.1080/07300077.1988.11878926.
Stimulatory effects of extracellular high K+ in the presence of nifedipine (NIF) on renin release (RR) from kidney cortical slices were investigated. The stimulation was suppressed either by propranolol or by metoprolol but not by prazosin. High K+ plus NIF-induced increase in RR was attenuated by renal denervation. The enhancing effect was not observed when the slices were incubated in Ca2+-free buffer or in medium containing divalent cations such as Cd2+, Co2+ and Mn2+. These alterations in RR correlated with 3H-efflux from the slices preloaded with 3H-norepinephrine. We conclude that the high K+ plus NIF-induced increase in RR from the slices is mediated by norepinephrine (NE) derived from renal sympathetic nerves and that this neuronally released NE stimulates RR via the activation of beta-adrenoceptors.
研究了硝苯地平(NIF)存在时细胞外高钾对肾皮质切片肾素释放(RR)的刺激作用。普萘洛尔或美托洛尔可抑制该刺激作用,但哌唑嗪无此作用。肾去神经支配可减弱高钾加NIF诱导的RR增加。当切片在无钙缓冲液或含二价阳离子如镉离子、钴离子和锰离子的培养基中孵育时,未观察到增强作用。RR的这些变化与预先用3H-去甲肾上腺素加载的切片中的3H外流相关。我们得出结论,高钾加NIF诱导的切片RR增加是由肾交感神经释放的去甲肾上腺素(NE)介导的,并且这种神经元释放的NE通过激活β-肾上腺素能受体刺激RR。