Open AccessAntireproductive effect of calcium channel blockers on male rats
Author(s) -
Morakinyo Ayodele O.,
Iranloye Bolanle O.,
Adegoke Olufeyisipe A.
Publication year - 2009
Publication title -
reproductive medicine and biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.005
H-Index - 22
eISSN - 1447-0578
pISSN - 1445-5781
DOI - 10.1007/s12522-009-0018-9
Subject(s) - diltiazem , nifedipine , verapamil , calcium channel , testosterone (patch) , epididymis , medicine , sperm , endocrinology , semen , sperm motility , pharmacology , calcium , andrology
Drugs have been shown to adversely affect male fertility and recently anti‐hypertensive drugs were added to the list. The anti‐fertility effects of nifedipine and similar calcium channel blockers are well‐illustrated in in vitro experiments but not in vivo. Purpose The present study was designed to experimentally elucidate the sub‐chronic effect of nifedipine, verapamil and diltiazem on sperm functions and reproductive hormone levels in vivo. Methods Male rats (150–200 g) were divided into four groups of ten rats each. Group 1 (control) received distilled water; Group 2 received nifedipine 0.57 mg/kg BW; Group 3 were given verapamil 3.40 mg/kg BW and Group 4 were given diltiazem 2.57 mg/kg BW. Each drug‐treated group had its own recovery group from which treatment was discontinued for 30 days before the animals were sacrificed. Blood samples were collected for hormonal assay of FSH, LH and testosterone. Semen evaluation was done and the testes, seminal vesicle, epididymis and prostate were removed, and weighed immediately. Results Nifedipine, verapamil and diltiazem significantly decreased ( P < 0.05) sperm count and motility in drug treated groups. The weight of the epididymis was significantly reduced ( P < 0.05) in the drug treated rats. Semen parameters and other associated changes were restored after 30 days of drug withdrawal. Conclusion Calcium channel blockers appear to have a reversible anti‐fertility effect on male rats which does not occur through inhibition of the pituitary‐gonadal axis.