Isradipine

Abstract

Isradipine is a potent dihydropyridine calcium channel blocker. It is highly selective for vascular smooth muscle, with very few negative inotropic or chronotropic effects. It may have minor depressant effects on the sinoatrial node, hence reducing the incidence of reflex tachycardia. The drug is extensively metabolized in the liver, with several pharmacologically inactive metabolites. As the elimination half-life is about 9 h the drug is usually given twice daily, but a once-daily modified release form is under investigation. Isradipine is effective monotherapy in essential hypertension, and has been successfully combined with pindolol and captopril. On the basis of more limited evidence it also appears to be beneficial in stable angina and in congestive cardiac failure. A trial is also under way to assess its antiatherogenic properties. Adverse effects are those predicted for a vasodilator calcium antagonist, and may be less frequent than for equivalent doses of nifedipine. This needs to be confirmed by more extensive clinical experience. Overall, isradipine can be considered favourably in essential hypertensives where a calcium channel blocker is indicated, particularly if it is desirable to avoid myocardial depression or to minimize reflex tachycardia. Its role in other cardiovascular disease awaits further evaluation.

Deletion of the Distal C Terminus of CaV1.2 Channels Leads to Loss of β-Adrenergic Regulation and Heart Failure in Vivo

“…Human hypertension is treated with dihydropyridine calcium channel blockers, which preferentially inhibit Ca V 1.2 channels in vascular smooth muscle cells in vivo (27,28). The calcium channel antagonist isradipine (1 and 3 mg/kg) reduced the heart to body weight ratio significantly and increased survival of DCT Ϫ/Ϫ embryos assayed at E18 (Fig.…”

“…Hypertension in humans is effectively treated with the calcium channel blocker isradipine and the angiotensin-converting enzyme inhibitor captopril (27,28,47). In addition, pulmonary hypertension in humans is effectively treated with tadalafil (48).…”

Atypical KCNQ1/Kv7 channel function in a neonatal diabetes patient: Hypersecretion preceded the failure of pancreatic β-cells

“…These observations suggest that β-cells with impaired KCNQ1 channels can accumulate abnormally elevated cytosolic Ca 2+ levels under high glucose concentrations. Notably, isradipine, an L-type Ca 2+ channel blocker, 48 could counteract this accumulation ( Figure S3 G). The similar level of Ca 2+ influx between UC-SC islets treated with Chromanol-293B and mutant SC islets under high glucose conditions suggests that the effect of the KCNQ1 R397W mutation on channel activity may not be directly additive to the effects of Chromanol-293B.…”