Jpn. J. Pharmacol. 75 (1), 27-32 (1997)

Cilnidipine Attenuates Renal Nerve Stimulation-Induced Renal Vasoconstriction and Antinatriuresis in Anesthetized Dogs

Akira Takahara (1), Hideki Dohmoto (1), Hiroaki Hisa (2), Susumu Satoh (2) and Ryota Yoshimoto (1)

(1) Life Science Laboratories, Central Research Laboratories, Ajinomoto Co., Inc., 214 Maeda-cho, Totsuka-ku, Yokohama 244, Japan
(2) Department of Pharmacology, Pharmaceutical Institute, Tohoku University, Aobayama, Sendai 980-77, Japan

Abstract: 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 microg/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 microg/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.

Keywords: Cilnidipine, Renal nerve stimulation, Renal vasoconstriction, Antinatriuresis, Norepinephrine secretion rate

Copyrightę The Japanese Pharmacological Society 1997

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