Pregnancy following discontinuation of a calcium channel blocker in the male partner

1995 ◽  
Vol 10 (3) ◽  
pp. 599-606 ◽  
Author(s):  
Avner Hershlag ◽  
George W. Cooper ◽  
Susan Benoff

Abstract The fertility potential of human sperm populations can be assessed by the presence of head-directed mannose ligand receptors (mannose-specific lectin) and the occurrence of spontaneous acrosome reactions after incubation under capacitating conditions in vitro. We have reported previously on the interaction between anti-hypertensive medications and their effects on these parameters of male fertility potential. In this report we document the effects of cessation of calcium ion channel blocker medication on male fertility. Motile spermatozoa from a 30 year old infertile patient on a calcium ion channel blocker as anti-hypertensive treatment had subnormal expression of mannose-specific lectin and did not exhibit spontaneous acrosome reactions. Three months following discontinuation of the medications, complete recovery of both the expression of head-directed mannose ligand receptors and the acrosome reaction was documented, though sperm motility and morphology remained unchanged. The couple had 2 years of infertility and previously failed to conceive through seven cycles of Pergonal/intra-uterine insemination. Conception occurred on the second Pergonal/intra-uterine insemination cycle after the husband discontinued calcium ion channel blocker medication. Calcium ion channel blockers may adversely affect sperm fertilizing potential. Discontinuation of such medications enhances the chances for conception.

1999 ◽  
Vol 11 (1) ◽  
pp. 1 ◽  
Author(s):  
D. P. Evenson

An important goal of modern analyses of semen is to elucidate the molecular traits of mammalian sperm chromatin structural abnormalities, defined here as ‘uncompensable’, that lead to abnormalities in fertility, pronuclear formation, early embryo quality and pregnancy outcome. Sperm with uncompensable nuclear abnormalities are able to fertilize oocytes both in vivo and in vitro; however, due to the uncompensable trait(s), the embryo development may be abnormal. Uncompensable nuclear traits can be experimentally induced in bull sperm by a mild thermal insult to the testis. Sperm nuclear morphology abnormalities seen in ejaculates 11-days post stress are likely related to molecular changes in chromatin observed 3-days post stress by the flow cytometric sperm chromatin structure assay (SCSA). The SCSA measures the susceptibility of sperm nuclear DNA to denaturation in situ. This susceptibility has been correlated with the presence of DNA strand breaks that may be derived in part by oxidative stress and possibly by a unique, abortive apoptotic mechanism. The extent of DNA denaturation is not significantly related to the level of disulfide bonding between the chromatin protamines. The use of human sperm with uncompensable nuclear traits for artificial reproductive techniques is also discussed. The goal of this research is to remove from semen doses those sperm with uncompensable nuclear traits and thereby increase male fertility potential. Extra key words: male fertility potential, sperm chromatin structure assay (SCSA).


2010 ◽  
Vol 298 (5) ◽  
pp. R1217-R1224 ◽  
Author(s):  
Thijs W. H. Flinsenberg ◽  
Saskia van der Sterren ◽  
Anne N. H. van Cleef ◽  
Marijn J. Schuurman ◽  
Pia Ågren ◽  
...  

Sex hormones have an important influence on cardiovascular physiology and pathophysiology and sex differences in vascular reactivity have been widely demonstrated. In the present study we hypothesized 1) the presence of sexual dimorphism in chicken ductus arteriosus (DA) responsiveness to contractile and relaxant stimuli and 2) that estrogens are vasoactive in the chicken DA. In vitro contractions (assessed with a wire myograph) induced by normoxia, KCl, 4-aminopyridine, norepinephrine, phenylephrine, U46619, or endothelin-1, as well as relaxations induced by ACh, sodium nitroprusside, BAY 41–2272, PGE2, isoproterenol, forskolin,Y-27632, and hydroxyfasudil were not significantly different between males and females. The estrogen 17β-estradiol elicited concentration-dependent relaxation of KCl-, phenylephrine-, and oxygen-induced active tone in male and female chicken DA. The stereoisomer 17α-estradiol showed lesser relaxant effects, and the selective estrogen receptor (ER) agonists 4,4′,4′′-(4-propyl-[1H]pyrazole-1,3,5-triyl)tris-phenol (ERα) and 2,3-bis(4-hydroxyphenyl)-propionitrile (ERβ) did not show any effect. There were no sex differences in the responses to estrogen. Endothelium removal or the presence of the soluble guanylate cyclase inhibitor ODQ, the K+ channel blockers tetraethylammonium, glibenclamide, and charybdotoxin, or the ER antagonist fulvestrant did not modify 17β-estradiol-induced relaxation. CaCl2 (30 μM–10 mM) induced concentration-dependent contraction in DA rings depolarized by 62.5 mM KCl or stimulated with 21% O2 in Ca2+-free medium. Preincubation with 17β-estradiol or the L-type Ca2+ channel blocker nifedipine produced an inhibition of CaCl2-induced contractions. In conclusion, there are no sex-related differences in chicken DA reactivity. The estrogen 17β-estradiol induces an endothelium-independent relaxation of chicken DA that is not mediated by ER activation. This relaxant effect is, at least partially, due to inhibition of Ca2+ entry from extracellular space.


1991 ◽  
Vol 155 (1) ◽  
pp. 275-290
Author(s):  
R. Krattenmacher ◽  
R. Voigt ◽  
M. Heinz ◽  
W. Clauss

Electrogenic ion transport through the colon epithelium of the African clawed toad (Xenopus laevis) was investigated with electrophysiological methods in vitro. Interest was focused on a previously described phenomenon, that removal of Ca2+ from the mucosal Ringer's solution increases electrogenic sodium absorption. Our results clearly show that Ca2+ removal reveals an apical ion channel that is not a specific Na+ channel, but a non-selective cation channel with an ‘apparent’ ion selectivity of the order K+ greater than Na+ = Rb+ greater than Cs+ greater than Li+. This Ca2(+)-sensitive current increased linearly with the mucosal pH, and could be inhibited by other divalent cations (Mg2+, Ba2+) and the organic ion channel blockers quinidine and verapamil. The mucosal Ca2+ concentration that induced a half-maximal inhibition of the Ca2(+)-sensitive current was about 1 mumol l-1 and was independent of the mucosal pH. Owing to the high Ca2+ sensitivity, a regulation of the channel conductivity by extracellular Ca2+ is ruled out. It is concluded that this channel, which is almost identical to similar channels found in amphibian skin and bladder, acts as a pathway for cation absorbing or secreting processes. Possibly the binding of extracellular Ca2+ is related to selectivity changes of the Ca2(+)-sensitive ion channel.


1983 ◽  
Vol 61 (9) ◽  
pp. 1057-1062 ◽  
Author(s):  
M. A. Young ◽  
G. F. Merrill

The calcium channel blocker nifedipine attenuates the coronary response to adenosine infusion and reactive hyperemia in dogs. Other evidence indicates adenosine may dilate vascular smooth muscle with a mechanism similar to the calcium channel blockers. In isolated rabbit femoral arterial rings, we studied the interaction of adenosine and nifedipine in mediating vascular relaxation. We also compared the actions of adenosine and nifedipine in relaxing norepinephrine- and K+-stimulated tension, and Ca2+-free contractions in an effort to elucidate differences in the specificity of the two agents. Nifedipine (10–25 μg/L) was without effect on adenosine-mediated relaxation of femoral arteries. Adenosine exhibited a greater ability to relax NE-induced contractions and contractions in Ca2+-free medium than did nifedipine. Conversely, nifedipine attenuated K+-induced contractions more effectively than adenosine. These results suggest that adenosine and nifedipine have different cellular actions and that part of adenosine-mediated relaxation may operate intracellularly. Furthermore, the negative interaction of nifedipine and adenosine in vivo suggests that these agents might act differently in an in vitro setting.


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