The effect of nifedipine, a calcium channel blocker, on human spermatozoal functions

Kanwar, U.; Anand, Radhi; Sanyal, Sankar Nath

doi:10.1016/0010-7824(93)90135-t

Cited by 34 publications

(16 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It has long been known that the fertilization response is a Ca 21 -dependent process 179 and more specifically that voltage-gated Ca 21 channels are an important component of this response. 135 Evidence has been provided for roles for T-type and Ltype channels, [142][143][144]147,180 as well as sperm-specific channels (CatSper1 and 2) that resemble voltage-gated Ca 21 channels in their structure. 152,153 Greater definition of the roles of these channels and the design of specific antagonists might represent a valuable new tool for both human and animal fertility control.…”

Section: Discussionmentioning

confidence: 98%

Drug Targets in the Voltage-Gated Calcium Channel Family: Why Some Are and Some Are Not

Triggle

2003

ASSAY and Drug Development Technologies

View full text Add to dashboard Cite

The L-type calcium channel antagonists have been, and continue to be, a very successful group of therapeutic agents targeted at cardiovascular disorders, notably angina and hypertension. The discovery that the voltage-gated calcium channels are a large and widely distributed family with important roles in both the peripheral and central nervous systems has initiated a major search for drugs active at other calcium channel types directed at disorders of the central nervous system, including pain, epilepsy, and stroke. These efforts have not been therapeutically successful thus far, and small molecule equivalents of the L-type blockers nifedipine, diltiazem, and verapamil directed at non-L-type channels have not been found. The underlying reasons for this are discussed together with suggestions for new directions, including fertility control, oxygen-sensitive channels, and calcium channel activators.

show abstract

Section: Discussionmentioning

confidence: 98%

Drug Targets in the Voltage-Gated Calcium Channel Family: Why Some Are and Some Are Not

Triggle

2003

ASSAY and Drug Development Technologies

View full text Add to dashboard Cite

show abstract

“…2A). Nifedipine is known to selectively inhibit voltage-dependent L-type calcium channels at this concentration (21,31). This allowed ruling out the participation of voltage-gated channels in the recorded influx.…”

Section: C884 Trpv2 and Soce In Calcium Influx Disorder Of Dmd Myotubesmentioning

confidence: 99%

Involvement of TRPV2 and SOCE in calcium influx disorder in DMD primary human myotubes with a specific contribution of α₁-syntrophin and PLC/PKC in SOCE regulation

Harisseh

Chatelier

Magaud

et al. 2013

American Journal of Physiology-Cell Physiology

View full text Add to dashboard Cite

Harisseh R, Chatelier A, Magaud C, Déliot N, Constantin B. Involvement of TRPV2 and SOCE in calcium influx disorder in DMD primary human myotubes with a specific contribution of ␣ 1-syntrophin and PLC/PKC in SOCE regulation. Am J Physiol Cell Physiol 304: C881-C894, 2013. First published February 20, 2013 doi:10.1152/ajpcell.00182.2012.-Calcium homeostasis is critical for several vital functions in excitable and nonexcitable cells and has been shown to be impaired in many pathologies including Duchenne muscular dystrophy (DMD). Various studies using murine models showed the implication of calcium entry in the dystrophic phenotype. However, alteration of store-operated calcium entry (SOCE) and transient receptor potential vanilloid 2 (TRPV2)-dependant cation entry has not been investigated yet in human skeletal muscle cells. We pharmacologically characterized basal and storeoperated cation entries in primary cultures of myotubes prepared from muscle of normal and DMD patients and found, for the first time, an increased SOCE in DMD myotubes. Moreover, this increase cannot be explained by an over expression of the well-known SOCE actors: TRPC1/4, Orai1, and stromal interaction molecule 1 (STIM1) mRNA and proteins. Thus we investigated the modes of regulation of this cation entry. We firstly demonstrated the important role of the scaffolding protein ␣ 1-syntrophin, which regulates SOCE in primary human myotubes through its PDZ domain. We also studied the implication of phospholipase C (PLC) and protein kinase C (PKC) in SOCE and showed that their inhibition restores normal levels of SOCE in DMD human myotubes. In addition, the involvement of TRPV2 in calcium deregulation in DMD human myotubes was explored. We showed an abnormal elevation of TRPV2-dependant cation entry in dystrophic primary human myotubes compared with normal ones. These findings show that calcium homeostasis mishandling in DMD myotubes depends on SOCE under the influence of Ca 2ϩ /PLC/PKC pathway and ␣1-syntrophin regulation as well as on TRPV2-dependant cation influx. DMD; human primary myotubes; Ca 2ϩ /PLC/PKC; ␣1-syntrophin; TRPV2; SOCE CALCIUM HOMEOSTASIS IS BASED on strictly cohesive and regulated communication between internal and plasma membrane calcium channels and pumps and has been shown to be altered in several pathologies and particularly in dystrophinopathies including Duchenne muscular dystrophy (DMD; Ref. 5). DMD is characterized by an abnormally high concentration of intracellular ionized calcium (7), which is thought to contribute to the final muscle necrosis. DMD is an X-linked recessive genetic disorder that affects 1 male birth over 3,500 in the world. This disease is caused by mutations on the locus Xp21.2 of the gene encoding the subsarcolemmal dystrophin, resulting in the loss of this protein (57). In the absence of dystrophin, the transmembrane dystrophin glycoprotein complex components lose their localization at costamers. This disorganization is thought to be responsible for membrane instability and muscle damage and for ...

show abstract

“…Calcium channel blockers : Nifedipine, Amlodipine, Verapamil and Diltiazem (Kanwar et al ., ; Benoff et al ., ; Brezina et al ., )…”

Section: Resultsmentioning

confidence: 99%

The impact of drugs on male fertility: a review

et al. 2017

View full text Add to dashboard Cite

Beside cytotoxic drugs, other drugs can impact men's fertility through various mechanisms. Via the modification of the hypothalamic-pituitary-gonadal axis hormones or by non-hormonal mechanisms, drugs may directly and indirectly induce sexual dysfunction and spermatogenesis impairment and alteration of epididymal maturation. This systematic literature review summarizes existing data about the negative impact and associations of pharmacological treatments on male fertility (excluding cytotoxic drugs), with a view to making these data more readily available for medical staff. In most cases, these effects on spermatogenesis/sperm maturation/sexual function are reversible after the discontinuation of the drug. When a reprotoxic treatment cannot be stopped and/or when the impact on semen parameters/sperm DNA is potentially irreversible (Sulfasalazine Azathioprine, Mycophenolate mofetil and Methotrexate), the cryopreservation of spermatozoa before treatment must be proposed. Deleterious impacts on fertility of drugs with very good or good level of evidence (Testosterone, Sulfasalazine, Anabolic steroids, Cyproterone acetate, Opioids, Tramadol, GhRH analogues and Sartan) are developed.

show abstract

The effect of nifedipine, a calcium channel blocker, on human spermatozoal functions

Cited by 34 publications

References 23 publications

Drug Targets in the Voltage-Gated Calcium Channel Family: Why Some Are and Some Are Not

Drug Targets in the Voltage-Gated Calcium Channel Family: Why Some Are and Some Are Not

Involvement of TRPV2 and SOCE in calcium influx disorder in DMD primary human myotubes with a specific contribution of α₁-syntrophin and PLC/PKC in SOCE regulation

The impact of drugs on male fertility: a review

Contact Info

Product

Resources

About

The effect of nifedipine, a calcium channel blocker, on human spermatozoal functions

Cited by 34 publications

References 23 publications

Drug Targets in the Voltage-Gated Calcium Channel Family: Why Some Are and Some Are Not

Drug Targets in the Voltage-Gated Calcium Channel Family: Why Some Are and Some Are Not

Involvement of TRPV2 and SOCE in calcium influx disorder in DMD primary human myotubes with a specific contribution of α1-syntrophin and PLC/PKC in SOCE regulation

The impact of drugs on male fertility: a review

Contact Info

Product

Resources

About

Involvement of TRPV2 and SOCE in calcium influx disorder in DMD primary human myotubes with a specific contribution of α₁-syntrophin and PLC/PKC in SOCE regulation