The antihypertensive effect of nitrendipine cannot be explained only by its reduction of the increased peripheral vascular resistance. In contrast to the antihypertensive vasodilators, nitrendipine improves impaired renal function and prevents generalized vasculopathy in hypertensive animals. Chronic treatment with nitrendipine prevents spontaneous (Okamoto rats) and salt-induced (Dahl rats) hypertension and cardiac hypertrophy. In rats with established hypertension, nitrendipine normalizes blood pressure, reduces cardiac hypertrophy, and improves renal ischaemia. In salt-induced malignant hypertension in stroke-prone spontaneously hypertensive rats, nitrendipine only slightly reduces blood pressure but dramatically improves survival and prevents vascular lesions in the heart, brain, and kidneys. Nitrendipine reduces the intracellular availability of calcium ions in vascular smooth muscle responsible for the increased peripheral and renovascular resistance in hypertension. Moreover, in preventing the deleterious calcium overload, nitrendipine preserves tissue integrity and increases life span in malignant hypertension.

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