Takahara A, Dohmoto H, Hisa H, Satoh S, Yoshimoto R
Life Science Laboratories, Ajinomoto Co., Inc., Yokohama, Japan.
Jpn J Pharmacol. 1997 Sep;75(1):27-32. doi: 10.1254/jjp.75.27.
We examined the effects of cilnidipine, which is an L- and N-type Ca2+ channel blocker, on adrenergically regulated renal functions in anesthetized dogs. Renal nerve stimulation (RNS) at high frequency (3-7 Hz) decreased renal blood flow (RBF) without changes in systemic blood pressure. The RBF response was inhibited by intrarenal arterial (i.r.a.) infusion of cilnidipine at 0.1-0.3 microgram/kg/min. Low-frequency RNS (0.5-1 Hz) reduced absolute and fractional urinary sodium excretion. These responses were attenuated during i.r.a. infusion of cilnidipine at 0.3 microgram/kg/min. An increase in norepinephrine secretion rate induced by low-frequency RNS was also attenuated during cilnidipine infusion. These results suggest that cilnidipine can suppress norepinephrine release from the renal nerve endings and thereby interfere with the neural control of renal functions.
我们研究了西尼地平(一种L型和N型钙通道阻滞剂)对麻醉犬肾上腺素能调节的肾功能的影响。高频(3 - 7Hz)肾神经刺激(RNS)可降低肾血流量(RBF),而全身血压无变化。肾内动脉(i.r.a.)以0.1 - 0.3微克/千克/分钟的速度输注西尼地平可抑制RBF反应。低频RNS(0.5 - 1Hz)可降低尿钠排泄绝对值和分数排泄率。在i.r.a.以0.3微克/千克/分钟的速度输注西尼地平期间,这些反应减弱。在输注西尼地平期间,低频RNS诱导的去甲肾上腺素分泌率增加也减弱。这些结果表明,西尼地平可抑制肾神经末梢去甲肾上腺素的释放,从而干扰肾功能的神经控制。