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1999b). In that study, all dihydropyridines, except cilnidipine, showed a small inhibitory effect at a concentration of 1 μM. The N-type channel-blocking action of cilnidipine has also been confirmed in IMR-32 human neuroblastoma cells and PC12 pheochromocytoma of the rat adrenal medulla cells. , 2002). Dual L/N-Type Ca Channel Blocker: Cilnidipine as a New Type of Antihypertensive Drug 2+ Mode of action Pharmacology 1) Cardiovascular action 2) Anti-sympathetic action 3) Suppression of reninangiotensin-aldosterone system 4) Anti-oxidation 5) Others Antihypertensive action 1) Animal model 2) Human Actions in key organs 1) Kidney 2) Heart 3) Brain 33 Inhibition of L-type Ca2+ channels (vascular smooth muscle, in vitro); inhibition of N-type Ca2+ channels (sympathetic neuron, in vitro) Vascular relaxation (in vitro); hypotensive action (in vivo) Decrease of catecholamine release, tissue (kidney) norepinephrine level, (in vitro, in vivo); inhibition of sympathetic tachycardia and cold stress-induced vasoconstriction (in vivo); decrease in plasma/urinary norepinephrine, muscle sympathetic nerve activity, low frequency/high frequency ratio (LF/HF ratio), and plasma level of ß-thromboglobulin (clinical) Decrease in plasma level of angiotensin II and aldosterone (in vivo, clinical); inhibition of aldosterone production (adrenocortical cells, in vitro); inhibition of reflex aldosterone production, and angiotensin II-renin feedback (in vivo) Inhibition of NADPH oxidase-derived superoxide production (kidney, in vivo) Improvement of insulin resistance (in vivo); increases of nitric oxide production (in vitro); protection from retinal neuronal injury (in vivo); anti-nociception (in vivo) Antihypertensive action in spontaneously hypertensive rats, stroke-prone spontaneously hypertensive rat, renal hypertensive rats, DOCA-salt hypertensive rats, Otsuka Long-Evans Tokushima Fatty rat, Dahl salt sensitive rat and 2-kidney 1-clip hypertensive dogs (in vivo) Essential hypertension; severe hypertension; hypertension with chronic kidney disease, cerebrovascular disease or diabetes (clinical) Increase in renal blood flow; dilation of afferent and efferent arterioles; natriuresis; inhibition of renal nerve stimulationinduced antinatriuresis; suppression of albuminuria; glomerular hypertrophy and interstitial fibrosis; decrease in renal angiotensin II content (in vivo); decrease in albuminuria and urinary protein (clinical) Increase in coronary blood flow (in vitro, in vivo); suppression of vasopressin-induced ST depression; reduction of the myocardial infarct size and incidence of ventricular premature beats after ischemia-reperfusion; abbreviation of abnormally prolonged ventricular repolarization (in vivo); decrease in BNP, LV mass index, heart rate and cardiothoracic ratio (clinical) Downward shift of the lower limit of autoregulation for cerebral blood flow; reduction of the cerebral infarction size (in vivo); increase in cerebral blood flow (clinical) Table 1.

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