Nilvadipine: Difference between revisions
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'''Nilvadipine''' is prescribed for patients with both [[hypertension]] and chronic major cerebral artery [[occlusion]]. In hypertensive patients with high risk of [[atherosclerosis]], nilvadipine may protect [[LDL cholesterol]] from in vivo [[oxidation]]. Nilvadipine reduces [[infarction]] foci, improves cerebral microcirculation, but does not affect the systemic arterial blood pressure. Pathohistochemical studies have revealed that the volume of the infarction in the middle cerebral artery occlusion model could be decreased by nilvadipine. Although it is a [[dihydropyridine]] derivative, nilvadipine has several kinetic, dynamic, and therapeutic effects that are different from even those of the other voltage-dependent Ca2+ channel blockers belonging to the same class. Nilvadipine could easily be transmitted to the [[central nervous system]]. Moreover, vascular smooth muscles contracted by [[potassium]] were reported to be inhibited by nilvadipine. It antagonizes both L- and T-type Ca2+ channels and exerts an antioxidant effect that is reported to be greater than the effects of [[nimodipine]], [[nicardipine]], and [[amlodipine]]. It has also been reported that nilvadipine (but not amlodipine) increased striatal [[dopamine]] and DOPAC contents and protected against motor deficits in mice. | '''Nilvadipine''' is prescribed for patients with both [[hypertension]] and chronic major cerebral artery [[occlusion]]. In hypertensive patients with high risk of [[atherosclerosis]], nilvadipine may protect [[LDL cholesterol]] from in vivo [[oxidation]]. Nilvadipine reduces [[infarction]] foci, improves cerebral microcirculation, but does not affect the systemic arterial blood pressure. Pathohistochemical studies have revealed that the volume of the infarction in the middle cerebral artery occlusion model could be decreased by nilvadipine. Although it is a [[dihydropyridine]] derivative, nilvadipine has several kinetic, dynamic, and therapeutic effects that are different from even those of the other voltage-dependent Ca2+ channel blockers belonging to the same class. Nilvadipine could easily be transmitted to the [[central nervous system]]. Moreover, vascular smooth muscles contracted by [[potassium]] were reported to be inhibited by nilvadipine. It antagonizes both L- and T-type Ca2+ channels and exerts an antioxidant effect that is reported to be greater than the effects of [[nimodipine]], [[nicardipine]], and [[amlodipine]]. It has also been reported that nilvadipine (but not amlodipine) increased striatal [[dopamine]] and DOPAC contents and protected against motor deficits in mice. | ||
Revision as of 14:58, 23 July 2014
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1], Sheng Shi, M.D. [2]
Nilvadipine is prescribed for patients with both hypertension and chronic major cerebral artery occlusion. In hypertensive patients with high risk of atherosclerosis, nilvadipine may protect LDL cholesterol from in vivo oxidation. Nilvadipine reduces infarction foci, improves cerebral microcirculation, but does not affect the systemic arterial blood pressure. Pathohistochemical studies have revealed that the volume of the infarction in the middle cerebral artery occlusion model could be decreased by nilvadipine. Although it is a dihydropyridine derivative, nilvadipine has several kinetic, dynamic, and therapeutic effects that are different from even those of the other voltage-dependent Ca2+ channel blockers belonging to the same class. Nilvadipine could easily be transmitted to the central nervous system. Moreover, vascular smooth muscles contracted by potassium were reported to be inhibited by nilvadipine. It antagonizes both L- and T-type Ca2+ channels and exerts an antioxidant effect that is reported to be greater than the effects of nimodipine, nicardipine, and amlodipine. It has also been reported that nilvadipine (but not amlodipine) increased striatal dopamine and DOPAC contents and protected against motor deficits in mice.
Currently Nilvadipine is tested in clinical trial as a possible treatment for Alzheimer's Disease in Ireland by the Roskamp Institute, Florida, USA and Trinity College, Ireland. More information can be found here.