Renal disease constitutes an important determinant of cardiovascular disease. Although the mechanisms for the progression of renal impairment remain fully undetermined, available evidence indicate that renal glomerular hypertension is responsible in part for the development of renal injury. In renal disease, afferent arteriolar tone is reported to be reduced, while the augmented intrarenal angiotensin II serves to act as an efferent arteriolar constrictor, both of which result in an increase in glomerular capillary pressure. Angiotensin converting enzyme inhibitors (ACE-I) are established as the agent possessing both antihypertensive and renoprotective actions, which exert vasodilator action on efferent arterioles. Calcium antagonists are also reported to have salutary effect on renal disease, although their beneficial action varies depending on the antagonists used and the underlying disease. The use of calcium antagonists, however, is mandatory particularly under the circumstance where renal failure moderately to severely progresses and the ACE-I cannot be used.