Influence of Acetazolamide on Aqp1 Gene Expression in Testis and on Sperm Count/Motility in Epididymis of Rats

Yu, Huidong; Sun, Bin; Bai, Qiufang; Koide, S. S.; Li, X.-J.

doi:10.1080/01485010290031592

Cited by 10 publications

(3 citation statements)

References 33 publications

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“…Although the cause of decreased motility is not clear, an earlier study showed that AQP1 is involved in sperm motility and density. 16 However AQP1 is expressed in the epithelium of the efferent duct but it is not expressed in sperm. 17 Sperm maturation depends on the changing microenvironment within the various regions of the epididymis.…”

Section: Aquaporin-7 In Human Testis and Ejaculated Spermmentioning

confidence: 99%

Localization of Aquaporin-7 in Human Testis and Ejaculated Sperm: Possible Involvement in Maintenance of Sperm Quality

et al. 2004

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Section: Aquaporin-7 In Human Testis and Ejaculated Spermmentioning

confidence: 99%

Localization of Aquaporin-7 in Human Testis and Ejaculated Sperm: Possible Involvement in Maintenance of Sperm Quality

et al. 2004

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“…Chronic administration of acetazolamide markedly alters CP function and structure [60], including the apical microvilli which contain the AQP1 channels. In the kidney, and in the testis (another barrier tissue), acetazolamide down-regulates AQP1 expression [61-64], possibly by way of pH i change. With regard to fluid transfer in the kidney, the crucial importance of Na + -H + antiport exchange (via NHE3) and pH i stability for maintaining intact AQP2 and NKCC2 systems is revealed in NHE3-knockout analyses [39].…”

Section: Csf Formationmentioning

confidence: 99%

Multiplicity of cerebrospinal fluid functions: New challenges in health and disease

Johanson

Duncan

Klinge

et al. 2008

Fluids Barriers CNS

696

704

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This review integrates eight aspects of cerebrospinal fluid (CSF) circulatory dynamics: formation rate, pressure, flow, volume, turnover rate, composition, recycling and reabsorption. Novel ways to modulate CSF formation emanate from recent analyses of choroid plexus transcription factors (E2F5), ion transporters (NaHCO3 cotransport), transport enzymes (isoforms of carbonic anhydrase), aquaporin 1 regulation, and plasticity of receptors for fluid-regulating neuropeptides. A greater appreciation of CSF pressure (CSFP) is being generated by fresh insights on peptidergic regulatory servomechanisms, the role of dysfunctional ependyma and circumventricular organs in causing congenital hydrocephalus, and the clinical use of algorithms to delineate CSFP waveforms for diagnostic and prognostic utility. Increasing attention focuses on CSF flow: how it impacts cerebral metabolism and hemodynamics, neural stem cell progression in the subventricular zone, and catabolite/peptide clearance from the CNS. The pathophysiological significance of changes in CSF volume is assessed from the respective viewpoints of hemodynamics (choroid plexus blood flow and pulsatility), hydrodynamics (choroidal hypo- and hypersecretion) and neuroendocrine factors (i.e., coordinated regulation by atrial natriuretic peptide, arginine vasopressin and basic fibroblast growth factor). In aging, normal pressure hydrocephalus and Alzheimer's disease, the expanding CSF space reduces the CSF turnover rate, thus compromising the CSF sink action to clear harmful metabolites (e.g., amyloid) from the CNS. Dwindling CSF dynamics greatly harms the interstitial environment of neurons. Accordingly the altered CSF composition in neurodegenerative diseases and senescence, because of adverse effects on neural processes and cognition, needs more effective clinical management. CSF recycling between subarachnoid space, brain and ventricles promotes interstitial fluid (ISF) convection with both trophic and excretory benefits. Finally, CSF reabsorption via multiple pathways (olfactory and spinal arachnoidal bulk flow) is likely complemented by fluid clearance across capillary walls (aquaporin 4) and arachnoid villi when CSFP and fluid retention are markedly elevated. A model is presented that links CSF and ISF homeostasis to coordinated fluxes of water and solutes at both the blood-CSF and blood-brain transport interfaces.Outline1 Overview2 CSF formation2.1 Transcription factors2.2 Ion transporters2.3 Enzymes that modulate transport2.4 Aquaporins or water channels2.5 Receptors for neuropeptides3 CSF pressure3.1 Servomechanism regulatory hypothesis3.2 Ontogeny of CSF pressure generation3.3 Congenital hydrocephalus and periventricular regions3.4 Brain response to elevated CSF pressure3.5 Advances in measuring CSF waveforms4 CSF flow4.1 CSF flow and brain metabolism4.2 Flow effects on fetal germinal matrix4.3 Decreasing CSF flow in aging CNS4.4 Refinement of non-invasive flow measurements5 CSF volume5.1 Hemodynamic factors5.2 Hydrodynamic factors5.3 Neuroendocrine factors6 CS...

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“…Inhibition of CA activity with acetazolamide (ACTZ) inhibited acidification of epididymal fluid [6,7], decreased fluid secretion in the testis, and impaired sperm function [8,9]. In rabbits, CA activity in the uterus is related to plasma progesterone levels [10,11].…”

Section: Introductionmentioning

confidence: 99%

Carbonic Anhydrase Regulate Endometrial Gland Development in the Neonatal Uterus1

Hu¹,

Spencer²

2005

Biology of Reproduction

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Carbonic anhydrases (CAs) are zinc metalloenyzmes that catalyze the reversible conversion of carbon dioxide to carbonic acid and are involved in respiration, calcification, acid-base balance, and formation of fluids. Transcriptional profiling of the developing neonatal mouse uterus detected expression of Car1, Car2, Car11, and Car13 between Postnatal Days (PNDs) 3 and 18. In the neonatal mouse uterus, Car2 and Car11 mRNAs were predominantly localized in endometrial epithelial and stromal cells, respectively, whereas Car13 mRNA was detected in both epithelia and stroma. CAR2 protein was detected primarily in the endometrial epithelia and from PND 3 to PND 18 in the uteri of neonatal mice. To determine whether CA regulated uterine development, neonatal mice were treated s.c. with acetazolamide, a CA inhibitor, from PND 3 to PND 18. Treatment with acetazolamide decreased CA activity in the uterus and the number of endometrial glands without apparent effects on differentiation of the stroma or myometrium. In the neonatal sheep uterus, CA2 mRNA was initially expressed at birth (PND 0) in the endometrial luminal epithelium and was predominantly expressed in the developing glandular epithelium from PND 7 to PND 56. These results support the hypothesis that CA has a functional role in endometrial gland development during postnatal uterine morphogenesis.

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Influence of Acetazolamide on Aqp1 Gene Expression in Testis and on Sperm Count/Motility in Epididymis of Rats

Cited by 10 publications

References 33 publications

Localization of Aquaporin-7 in Human Testis and Ejaculated Sperm: Possible Involvement in Maintenance of Sperm Quality

Localization of Aquaporin-7 in Human Testis and Ejaculated Sperm: Possible Involvement in Maintenance of Sperm Quality

Multiplicity of cerebrospinal fluid functions: New challenges in health and disease

Carbonic Anhydrase Regulate Endometrial Gland Development in the Neonatal Uterus1

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