Calcium Channel Blocker

Abstract. Concerns regarding the safety of nifedipine emerged in 1995 with the report of an increased risk of myocardial infarction associated with adult patients receiving short-acting calcium channel blockers. There have been few case reports of adverse events in children ...

Based on the body of evidence implicating ocular blood flow disturbances in the pathogenesis of glaucoma, there is great interest in the investigation of the effects of antiglaucoma drugs and systemic medications on the various ocular vascular beds. The primary aim of this article was to review the current data available on the effects of antiglaucoma drugs and systemic medications on ocular blood flow. We performed a literature search in November 2002, which consisted of a textword search in MEDLINE for the years 1968–2002. The results of this review suggest that there is a severe lack of well-designed long-term studies investigating the effects of antiglaucoma and systemic medications on ocular blood flow in glaucomatous patients. However, among the 136 articles dealing with the effect of antiglaucoma drugs on ocular blood flow, only 36 (26.5%) investigated the effects of medications on glaucoma patients. Among these 36 articles, only 3 (8.3%) were long-term studies, and only 16 (...

The synergistic protective effect of Nicorandil (KATP channel opener) and Amlodipine (calcium channel blocker) on heart tissue antioxidant defense system and lipid profile were examined on isoproterenol induced myocardial infarction in rats. The rats given isoproterenol (150 mg kg−1 daily, i.p.) for 2 days showed significant changes in antioxidant defense system and lipid profile levels. Pretreatment with Nicorandil (2.5 mg kg−1 daily, p.o.) and Amlodipine (5.0 mg kg−1 daily, p.o.) for 3 days significantly prevented these alterations and restored the enzyme activities to near normal. These findings indicate the synergistic protective effect of Nicorandil and Amlodipine on tissue defense system and lipid metabolism during isoproterenol induced cardiac damage.

Chickpea (Cicer arietinum L.) is sensitive to chilling stress (< 15 °C). In the present study, hydroponically grown 14-day-old chickpea seedlings were subjected to temperatures ranging from 1 to 7 °C. Chilling injury was observed as electrolyte leakage (EL) and 2,3,5-triphenyltetrazolium (TTC) reduction activity. LT50 was noticed at 4 °C. Relative growth rate of the roots ceased at this temperature. Acclimation for 6 days at 10/7 °C lowered the LT50 by 2 °C. The growth rate of roots increased by 35% in cold-acclimated (CA) seedlings. Abscisic acid (ABA) content increased in cold-acclimated (CA) seedlings to 92 ng g−1 fw in comparison to 61 ng g−1 fw in non-acclimated (NA) seedlings. NA seedlings subjected to 4 °C in the presence of 1 μM Ca2+ (as CaCl2; Ca) or 0.1 μM abscisic acid (ABA) showed cold acclimation like response in terms of root growth, EL, TTC reduction, accumulation of cryoprotective solutes like total soluble carbohydrates, sucrose, glucose, fructose, trehalose and proline. Relatively, the increase was more in carbohydrates than proline. The oxidative damage as generation of lipid peroxides (malondialdehyde) and hydrogen peroxide (H2O2) was lesser in Ca or ABA treated NA and CA seedlings. Conversely, CA and NA seedlings growing in the presence of 10 μM verapamil (calcium channel blocker) or fluridone (ABA biosynthesis inhibitor) showed substantial decrease in root growth, EL, TTC reduction, accumulation of solutes and increase in MDA and H2O2 content providing an indirect evidence that acclimation confers cold tolerance by involvement of cellular calcium and ABA. The beneficial effects of acclimation could not be fully substituted by either Ca or ABA. Calcium appeared to alleviate the chilling-induced primary effects like membrane damage through more effective diminution of oxidative damage while ABA probably acted through modulation of solute levels. The recovery process was facilitated more with calcium as compared to ABA treatment.

Both intracellular calcium ions and neural input are important in esophageal smooth muscle contraction. The aim of this study was to compare the effects of well-tolerated doses of the calcium-channel blocker, nifedipine (20 mg sublingually/buccally) with the anticholinergic, propantheline bromide (15 mg orally) and the combination of these two agents on esophageal motor function. Seven healthy volunteers underwent manometric evaluation after nifedipine, propantheline bromide, the combination, and placebo on different days. Lower esophageal sphincter pressure decreased significantly (P less than 0.05 vs basal and placebo) by 32% after nifedipine, but fell only 21% after propantheline bromide. After the combination lower esophageal sphincter pressure fell by 45% (P less than 0.05 vs basal and placebo and nifedipine alone). Contraction amplitude in the body of the esophagus decreased significantly (P less than 0.05 vs basal and placebo) by 26% after propantheline bromide, but fell only 11% after nifedipine. The combination led to a decrease of 37% in contraction amplitude, but this was not significantly different from that obtained with propantheline bromide alone. No drug or combination had any effect on other manometric parameters. These data show that in the normal subjects studied with the above doses: (1) nifedipine has a greater effect than propantheline bromide on the lower esophageal sphincter; (2) propantheline bromide has a greater effect than nifedipine on esophageal contraction amplitude; and (3) the combination of nifedipine and propantheline bromide has an enhanced effect on both lower esophageal sphincter pressure and esophageal contraction amplitude.