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  • Title: Rapid large artery remodeling following the administration and withdrawal of calcium channel blockers in spontaneously hypertensive rats.
    Author: Vaja V, Ochodnicky P, Krenek P, Klimas J, Bajuszova Z, Kyselovic J.
    Journal: Eur J Pharmacol; 2009 Oct 01; 619(1-3):85-91. PubMed ID: 19683522.
    Abstract:
    Chronic treatment with several antihypertensive agents, including calcium channel blockers, may interfere with remodeling of large arteries and increased arterial stiffness. We hypothesize that even a short, seven-day administration of calcium channel blockers might alter an aortic remodeling in spontaneously hypertensive rat (SHR). Male SHR and normotensive WKY rats (n=14 each) were treated by either vehicle, vasculoselective calcium channel blocker nifedipine (1mg/kg/day) or cardiac/vascular calcium channel blockers diltiazem (5mg/kg/day) or verapamil (4 mg/kg/day, n=6 for each treatment) subcutaneously twice daily for seven days. Additional SHR rats were randomized for termination 24, 72 or 120 h (n=5 each) after the withdrawal of nifedipine. Systolic blood pressure was measured by tail cuff and thoracic aorta was collected for histomorphometric and functional analysis including acetylcholine-induced endothelium-dependent relaxation. Seven-day administration of diltiazem and nifedipine, but not verapamil decreased blood pressure in SHR. All drugs significantly attenuated abnormal aortic wall thickness, cross-sectional area and media-to-lumen ratio, but only nifedipine improved impaired endothelium-dependent relaxation. Following the withdrawal of nifedipine, all measured parameters returned back to control SHR values within 72 h. Seven-day treatment with distinct calcium channel blockers attenuates hypertensive remodeling of aorta, which might be, in case of nifedipine, reactivated even by a very short withdrawal of the drug. Therefore, vasculoprotection by calcium channel blockers is not restricted to a prolonged blood pressure modulation, but occurs rapidly. These findings could be relevant for an intervention in augmented vascular stiffness and related cardiovascular risk.
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