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

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 fre quency (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 ƒÊg/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 ƒÊg/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.

Vasodilatory Effect of Cilnidipine, an L-type and N-type Calcium Channel Blocker, on Rat Kidney Glomerular Arterioles

“…32) In the present study, the dilatation of the efferent arterioles by cilnidipine was abolished after pretreatment with ω-conotoxin, which is a specific blocker of N-type calcium channels. This suggests that dilation of the efferent arterioles was dependent on the inhibition of norepinephrine release from the renal sympathetic nerve terminals in the glomeruli.…”

Comparison between Cilnidipine and Amlodipine Besilate with Respect to Proteinuria in Hypertensive Patients with Renal Diseases

“…The uptake of tritium-labeled norepinephrine has been shown to be most intense in the afferent arterioles, followed by the efferent arterioles, interlobular arteries, cortical capillaries, and arcuate arteries (18). In another study, an L-type CCB, nifedipine, failed to suppress the norepinephrine release by electric stimulation of the renal nerve, whereas cilnidipine suppressed its release (19), indicating that unlike nifedipine, cilnidipine has N-type calcium channel antagonistic action.…”

Comparison of Efficacy of Amlodipine and Cilnidipine on Left Ventricular Hypertrophy amongst Hypertensive Patients

“…The finding can be explained by, N-type Ca2+ channel blockade of Cilnidipine inhibit catecholamine release from the sympathetic nerve ending and adrenal gland [29,30], leading to suppression of the renin-angiotensin-aldosterone system [51], and suppression of aldosterone secretion from adrenocortical cells [52]. In contrast, Amlodipine might have activated the renin-angiotensinaldosterone system by increasing the sympathetic tone as well as by increase renin synthesis by JG cells [27,53,54].…”

“…However, the blockade of T-and N-type calcium channels did not affect calcium influx in these cells [28]. Cilnidipine, an L/N type CCB, has been reported to suppress the SNS over-activation associated with RAAS activation by blocking N-type calcium channels and to inhibit renin transcription in juxtaglomerular cells [29][30][31][32]. So Cilnidipine could attenuate the SNS and RAAS activation induced by its own blockade of L-type calcium channels.…”