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Article: cAMP- but not Ca 2+-regulated Cl - conductance is lacking in cystic fibrosis mice epididymides and seminal vesicles

TitlecAMP- but not Ca 2+-regulated Cl - conductance is lacking in cystic fibrosis mice epididymides and seminal vesicles
Authors
Issue Date1996
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/
Citation
American Journal Of Physiology - Cell Physiology, 1996, v. 271 n. 1 40-1, p. C188-C193 How to Cite?
AbstractCystic fibrosis (CF) reflects the loss of adenosine 3',5'-cyclic monophosphate (cAMP)-regulated Cl - secretion consequent to mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. In humans, but not mice, with CF, the disease is associated with male infertility. The present study investigated the relative magnitudes of the cAMP pathways and an alternative Ca 2+-regulated Cl - secretory pathway in primary cultures of the epididymides and the seminal vesicles of normal and CF mice. The basal equivalent short-circuit currents (I(eq)) of cultures derived from the epididymides and the seminal vesicles from the CF mice were lower (6.0 ± 0.6 and 4.0 ± 1.0 μA/cm 2, respectively) than those from normal mice (11.1 ± 1.0 and 6.6 ± 0.6 μA/cm 2, respectively). Forskolin induced significant I(eq) responses in both the epididymis (8.0 ± 0.7 μA/cm 2) and seminal vesicles (4.0 ± 0.5 μA/cm 2) from normal mice, whereas forskolin-induced changes in I(eq) in CF mouse epididymis and seminal vesicles were absent, consistent with defective cAMP-CFTR-mediated Cl - secretion in CF mice. I(eq) responses to agonists (ionomycin, ATP) that raise intracellular Ca 2+ (Ca(i)/ 2+) were larger than forskolin responses in normal animals (6.6 ± 0.9 and 13.4 ± 1.8 μA/cm 2, respectively) and were preserved in CF (6.5 ± 0.9 and 17.1 ± 1.0 μA/cm 2, respectively). We speculate that the fertility of male CF mice is maintained by persistent expression of the predominant alternative Ca 2+-mediated Cl - transport system in the epididymides and seminal vesicles.
Persistent Identifierhttp://hdl.handle.net/10722/162120
ISSN
2015 Impact Factor: 3.395
2015 SCImago Journal Rankings: 1.893
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, AYHen_US
dc.contributor.authorWong, PYDen_US
dc.contributor.authorYankaskas, JRen_US
dc.contributor.authorBoucher, RCen_US
dc.date.accessioned2012-09-05T05:17:27Z-
dc.date.available2012-09-05T05:17:27Z-
dc.date.issued1996en_US
dc.identifier.citationAmerican Journal Of Physiology - Cell Physiology, 1996, v. 271 n. 1 40-1, p. C188-C193en_US
dc.identifier.issn0363-6143en_US
dc.identifier.urihttp://hdl.handle.net/10722/162120-
dc.description.abstractCystic fibrosis (CF) reflects the loss of adenosine 3',5'-cyclic monophosphate (cAMP)-regulated Cl - secretion consequent to mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. In humans, but not mice, with CF, the disease is associated with male infertility. The present study investigated the relative magnitudes of the cAMP pathways and an alternative Ca 2+-regulated Cl - secretory pathway in primary cultures of the epididymides and the seminal vesicles of normal and CF mice. The basal equivalent short-circuit currents (I(eq)) of cultures derived from the epididymides and the seminal vesicles from the CF mice were lower (6.0 ± 0.6 and 4.0 ± 1.0 μA/cm 2, respectively) than those from normal mice (11.1 ± 1.0 and 6.6 ± 0.6 μA/cm 2, respectively). Forskolin induced significant I(eq) responses in both the epididymis (8.0 ± 0.7 μA/cm 2) and seminal vesicles (4.0 ± 0.5 μA/cm 2) from normal mice, whereas forskolin-induced changes in I(eq) in CF mouse epididymis and seminal vesicles were absent, consistent with defective cAMP-CFTR-mediated Cl - secretion in CF mice. I(eq) responses to agonists (ionomycin, ATP) that raise intracellular Ca 2+ (Ca(i)/ 2+) were larger than forskolin responses in normal animals (6.6 ± 0.9 and 13.4 ± 1.8 μA/cm 2, respectively) and were preserved in CF (6.5 ± 0.9 and 17.1 ± 1.0 μA/cm 2, respectively). We speculate that the fertility of male CF mice is maintained by persistent expression of the predominant alternative Ca 2+-mediated Cl - transport system in the epididymides and seminal vesicles.en_US
dc.languageengen_US
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpcell.physiology.org/en_US
dc.relation.ispartofAmerican Journal of Physiology - Cell Physiologyen_US
dc.subject.meshAdenosine Triphosphate - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCalcium - Physiologyen_US
dc.subject.meshChlorides - Physiologyen_US
dc.subject.meshCyclic Amp - Physiologyen_US
dc.subject.meshCystic Fibrosis - Physiopathologyen_US
dc.subject.meshElectric Conductivityen_US
dc.subject.meshEpididymis - Physiopathologyen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshIonomycin - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshReference Valuesen_US
dc.subject.meshSeminal Vesicles - Physiopathologyen_US
dc.titlecAMP- but not Ca 2+-regulated Cl - conductance is lacking in cystic fibrosis mice epididymides and seminal vesiclesen_US
dc.typeArticleen_US
dc.identifier.emailLeung, AYH:ayhleung@hku.hken_US
dc.identifier.authorityLeung, AYH=rp00265en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid8760045-
dc.identifier.scopuseid_2-s2.0-0029756171en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0029756171&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume271en_US
dc.identifier.issue1 40-1en_US
dc.identifier.spageC188en_US
dc.identifier.epageC193en_US
dc.identifier.isiWOS:A1996UX53400020-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLeung, AYH=7403012668en_US
dc.identifier.scopusauthoridWong, PYD=7403980262en_US
dc.identifier.scopusauthoridYankaskas, JR=7005074361en_US
dc.identifier.scopusauthoridBoucher, RC=7202772816en_US

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