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Comparative study on calcium channel antagonists in the human radial artery: clinical implications
1Cardiovascular Research Laboratory, Division of Cardiothoracic Surgery, Department of Surgery, University of Hong Kong, Grantham Hospital, Aberdeen, Hong Kong.
Insights
This study compared four calcium channel antagonists for their effectiveness in relaxing the human radial artery. Nifedipine and nicardipine showed the most potent antispastic effects, suggesting their suitability for clinical use.
Area of Science:
- Cardiovascular Pharmacology
- Vascular Smooth Muscle Physiology
Background:
- The radial artery is prone to spasms, necessitating effective antispastic treatments.
- Calcium channel antagonists are clinically employed to manage radial artery spasms.
Purpose of the Study:
- To compare the in vitro antispastic efficacy of four clinically used calcium channel antagonists: nicardipine, nifedipine, verapamil, and diltiazem.
- To determine the optimal calcium channel antagonist for treating radial artery spasms.
Main Methods:
- Segments of human radial artery from bypass surgery patients were studied in an organ bath.
- The relaxation effects of calcium channel antagonists were assessed in potassium-precontracted radial arteries.
- Inhibitory effects were evaluated at clinically relevant plasma concentrations and higher concentrations.
Main Results:
- All four calcium channel antagonists induced complete relaxation (97.8%-100%) of the radial artery.
- Nifedipine demonstrated higher sensitivity (P =.005) compared to nicardipine, verapamil, and diltiazem.
- Nicardipine and nifedipine significantly inhibited potassium-induced contractions at plasma concentrations, unlike verapamil and diltiazem.
Conclusions:
- While all tested calcium channel antagonists exhibit antispastic properties in the radial artery, varying sensitivities exist.
- Dihydropyridine derivatives, such as nifedipine and nicardipine, appear to be the most potent and are recommended for clinical application in managing radial artery spasms.
Objectives:
The radial artery is spastic, and calcium channel antagonists have been used clinically in the radial artery for their antispastic effects. To choose a proper calcium channel antagonist for such a purpose, we compared the in vitro antispastic effects of 4 clinically used calcium channel antagonists (nicardipine, nifedipine, verapamil, and diltiazem) in the human radial artery.
Methods:
Radial artery segments taken from patients undergoing coronary bypass operations were studied in the organ bath. The relaxation by the calcium channel antagonists was compared in the potassium-precontracted (25 mmol/L) radial artery. The inhibitory effect of the calcium channel antagonists at the clinically relevant plasma concentration and a higher concentration was also studied for the calcium channel antagonists.
Results:
All calcium channel antagonists induced a full relaxation (97.8%-100%, n = 5-7 for each), with higher sensitivity (P =.005, analysis of variance [ANOVA] among the calcium channel antagonists for the effective concentration of the constrictor [or dilator] agent that caused 50% of maximal contraction [or relaxation]) to nifedipine (-7.37 +/- 0. 20 log(10) M) than nicardipine (-6.43 +/- 0.39 log(10) M, P =.1), verapamil (-6.08 +/- 0.13 log(10) M, P =.03), and diltiazem (-5.87 +/- 0.07 log(10) M, P =.01). Pretreatment with the plasma concentration of the calcium channel antagonists (60 nmol/L for diltiazem and 20 nmol/L for the others) inhibited the potassium-induced contraction (n = 6 for each) by nicardipine (from 138.6% +/- 5.8% to 101.4% +/- 7.6%, P =.001) and nifedipine (to 87. 7% +/- 6.8%, P =.0003) but not by verapamil (to 140.3% +/- 15.2%, P =.9) or diltiazem (to 132.8% +/- 7.3%, P =.8), although at higher contractions (-4.5 log(10) M) all 4 calcium channel antagonists abolished the contraction.
Conclusions:
Although all calcium channel antagonists have antispastic effects in the radial artery, the vessel has different sensitivities to them. Dihydropyridine derivatives may be the most potent calcium channel antiagonists and therefore are recommended for the clinical use for this purpose.
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