scholarly journals Roles of extracellular ions and pH in 5-HT-induced sperm motility in marine bivalve

Reproduction ◽  
2014 ◽  
Vol 147 (3) ◽  
pp. 331-345 ◽  
Author(s):  
Sayyed Mohammad Hadi Alavi ◽  
Natsuki Matsumura ◽  
Kogiku Shiba ◽  
Naoki Itoh ◽  
Keisuke G Takahashi ◽  
...  
Keyword(s):  
Sperm Motility ◽  
Pacific Oyster ◽  
Manila Clam ◽  
Marine Bivalve ◽  
Channel Blockers ◽  
Inhibitory Effects ◽  
Patinopecten Yessoensis ◽  
Independent Mechanism ◽  
Intracellular Ca ◽  
Extracellular Ions

Factors that inhibit and stimulate the initiation of sperm motility were determined for Manila clam (Ruditapesphilippinarum), Pacific oyster (Crassostrea gigas), and Japanese scallop (Patinopecten yessoensis). Compared with artificial seawater (ASW), serotonin (5-hydroxytryptamine creatinine sulfate, 5-HT) could fully trigger sperm motility and increase sperm velocity and motility duration. Sperm motility was decreased in ASW at pH 6.5–7.0 and suppressed at pH 4.0. In Manila clam and Pacific oyster, 5-HT could overcome the inhibitory effects of acidic pH on sperm motility. In the presence of nigericin (a K+/H+exchanger), sperm motility was only triggered at pH 8.3. Testicular fluid K+concentrations were two- to fourfold higher than that in ASW. Sperm motility and velocity were decreased in ASW or 5-HT containing ≥40 mM K+or ≥2.5 mM 4-aminopyridine, suggesting K+efflux requirement to initiate motility. Sperm motility and velocity were reduced in ASW or 5-HT containing EGTA or W-7, suggesting that extracellular Ca2+is required for Ca2+/calmodulin-dependent flagellar beating. Ca2+influx occurs via Ca2+channels because sperm motility and velocity were decreased in both ASW and 5-HT containing T-type and L-type Ca2+channel blockers. 5-HT-dependent initiation of sperm motility was associated with intracellular Ca2+rise, which was comparable to that seen in ASW but was not observed in the presence of EGTA or a Ca2+channel blocker. Extracellular Na+is also essential for sperm motility initiation via regulation of Na+/Ca2+exchange. Overall, 5-HT-dependent initiation of sperm motility in marine bivalve mollusks is an osmolality-independent mechanism and regulated by extracellular pH, K+, Ca2+, and Na+.

Involvement of Na+/Ca2+ exchanger in catecholamine-induced increase in intracellular calcium in cardiomyocytes

2006 ◽  
Vol 290 (1) ◽  
pp. H373-H380 ◽  
Author(s):  
Harjot K. Saini ◽  
Onkar N. Tripathi ◽  
Shetuan Zhang ◽  
Vijayan Elimban ◽  
Naranjan S. Dhalla
Keyword(s):  
Purinergic Receptor ◽  
Cyclopiazonic Acid ◽  
Channel Blockers ◽  
Inhibitory Effects ◽  
Inotropic Action ◽  
Rat Cardiomyocytes ◽  
Isolated Hearts ◽  
Adrenoceptor Agonist ◽  
Significant Depression ◽  
Intracellular Ca

Although sarcolemmal (SL) Na+/Ca2+ exchanger is known to regulate the intracellular Ca2+ concentration ([Ca2+]i), its involvement in catecholamine-induced increase in [Ca2+]i is not fully understood. To gain some information in this regard, isolated rat cardiomyocytes were treated with different agents, which are known to modify Ca2+ movements, in the absence or presence of a β-adrenoceptor agonist, isoproterenol, and [Ca2+]i in cardiomyocytes was determined spectrofluorometrically with fura-2 AM. Treatment with isoproterenol did not alter [Ca2+]i in quiescent cardiomyocytes, whereas the ATP (purinergic receptor agonist)-induced increase in [Ca2+]i was significantly potentiated by isoproterenol. Unlike ryanodine and cyclopiazonic acid, which affect the sarcoplasmic reticulum function, SL L-type Ca2+ channel blockers verapamil and diltiazem, as well as a SL Ca2+-pump inhibitor, vanadate, caused a significant depression in the isoproterenol-induced increase in [Ca2+]i. The SL Na+/Ca2+ exchange blockers amiloride, Ni2+, and KB-R7943 also attenuated the isoproterenol-mediated increase in [Ca2+]i. Combination of KB-R7943 and verapamil showed additive inhibitory effects on the isoproterenol-induced increase in [Ca2+]i. The isoproterenol-induced increase in [Ca2+]i in KCl-depolarized cardiomyocytes was augmented by low Na+; this augmentation was significantly depressed by treatment with KB-R7943. The positive inotropic action of isoproterenol in isolated hearts was also reduced by KB-R7943. These data suggest that in addition to SL L-type Ca2+ channels, SL Na+/Ca2+ exchanger seems to play an important role in catecholamine-induced increase in [Ca2+]i in cardiomyocytes.

scholarly journals Localization of sperm intracellular Ca2+ keeps fertilizability in the newt vas deferens

Reproduction ◽  
2020 ◽  
Vol 159 (3) ◽  
pp. 339-349
Author(s):  
Nanae Makino ◽  
Nozomi Sato ◽  
Eriko Takayama-Watanabe ◽  
Akihiko Watanabe
Keyword(s):  
Sperm Motility ◽  
Salt Solution ◽  
Acrosome Reaction ◽  
Vas Deferens ◽  
Sperm Quality ◽  
Ethylene Glycol Tetraacetic Acid ◽  
Channel Blockers ◽  
Tetraacetic Acid ◽  
Intracellular Ca ◽  
Principal Piece

Sperm intracellular Ca2+ is crucial for the induction of sperm-egg interaction, but little is known about the significance of Ca2+ maintenance prior to induction. In sperm of the newt Cynops pyrrhogaster, intracellular Ca2+ is localized to the midpiece during storage in the vas deferens, while extracellular Ca2+ is influxed in modified Steinberg’s salt solution to promote a spontaneous acrosome reaction related to the decline of sperm quality. In the present study, sperm from the vas deferens were loaded with the Ca2+ indicator Fluo8H, and changes in Ca2+ localization in modified Steinberg’s salt solution were examined. Calcium ions expanded from the cytoplasmic area of the midpiece to the entire tail in most sperm during a 1-h incubation and localized to the principal piece in some sperm within 24 h. Similar changes in Ca2+ localization were observed in reconstructed vas deferens solution that included ions and pH at equivalent levels to those in the vas deferens fluid. Sperm with Ca2+ localization in the entire tail or the principal piece weakened or lost responsiveness to sperm motility-initiating substances, which trigger sperm motility for fertilization, but responded to a trigger for acrosome reaction. The change in Ca2+ localization was delayed and transiently reversed by ethylene glycol tetraacetic acid or a mixture of Ca2+ channel blockers including Ni2+ and diltiazem. These results suggest that C. pyrrhogaster sperm localize intracellular Ca2+ to the midpiece through Ca2+ transport in the vas deferens to allow for responses to sperm motility-initiating substances.

scholarly journals Human trabecular meshwork cell volume regulation

2002 ◽  
Vol 283 (1) ◽  
pp. C315-C326 ◽  
Author(s):  
Claire H. Mitchell ◽  
Johannes C. Fleischhauer ◽  
W. Daniel Stamer ◽  
K. Peterson-Yantorno ◽  
Mortimer M. Civan
Keyword(s):  
Cell Volume ◽  
Trabecular Meshwork ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Channel Blockers ◽  
Uptake Mechanism ◽  
Fluid Uptake ◽  
Intracellular Ca ◽  
Predominant Effect ◽  
Volume Decrease

The volume of certain subpopulations of trabecular meshwork (TM) cells may modify outflow resistance of aqueous humor, thereby altering intraocular pressure. This study examines the contribution that Na+/H+, Cl−/HCO[Formula: see text]exchange, and K+-Cl− efflux mechanisms have on the volume of TM cells. Volume, Cl− currents, and intracellular Ca2+ activity of cultured human TM cells were studied with calcein fluorescence, whole cell patch clamping, and fura 2 fluorescence, respectively. At physiological bicarbonate concentration, the selective Na+/H+ antiport inhibitor dimethylamiloride reduced isotonic cell volume. Hypotonicity triggered a regulatory volume decrease (RVD), which could be inhibited by the Cl− channel blocker 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB), the K+channel blockers Ba2+ and tetraethylammonium, and the K+-Cl− symport blocker [(dihydroindenyl)oxy]alkanoic acid. The fluid uptake mechanism in isotonic conditions was dependent on bicarbonate; at physiological levels, the Na+/H+ exchange inhibitor dimethylamiloride reduced cell volume, whereas at low levels the Na+-K+-2Cl− symport inhibitor bumetanide had the predominant effect. Patch-clamp measurements showed that hypotonicity activated an outwardly rectifying, NPPB-sensitive Cl− channel displaying the permeability ranking Cl− > methylsulfonate > aspartate. 2,3-Butanedione 2-monoxime antagonized actomyosin activity and both increased baseline [Ca2+] and abolished swelling-activated increase in [Ca2+], but it did not affect RVD. Results indicate that human TM cells display a Ca2+-independent RVD and that volume is regulated by swelling-activated K+ and Cl− channels, Na+/H+ antiports, and possibly K+-Cl− symports in addition to Na+-K+-2Cl− symports.

Differing temporal roles of Ca2+ and cAMP in nicotine-elicited elevation of tyrosine hydroxylase mRNA

1999 ◽  
Vol 276 (1) ◽  
pp. C54-C65 ◽  
Author(s):  
Volodia D. Gueorguiev ◽  
Richard J. Zeman ◽  
Bhargava Hiremagalur ◽  
Ana Menezes ◽  
Esther L. Sabban
Keyword(s):  
Gene Expression ◽  
Tyrosine Hydroxylase ◽  
Camp Response Element Binding ◽  
Second Phase ◽  
Channel Blockers ◽  
Nicotine Treatment ◽  
Transient Rise ◽  
Element Binding Protein ◽  
Intracellular Ca ◽  
Th Mrna

The involvement of cAMP- and Ca2+-mediated pathways in the activation of tyrosine hydroxylase (TH) gene expression by nicotine was examined in PC-12 cells. Extracellular Ca2+ and elevations in intracellular Ca2+ concentration ([Ca2+]i) were required for nicotine to increase TH mRNA. The nicotine-elicited rapid rise in [Ca2+]iwas inhibited by blockers of either L-type or N-type, and to a lesser extent P/Q-, but not T-type, voltage-gated Ca2+ channels. With continual nicotine treatment, [Ca2+]ireturned to basal levels within 3–4 min. After a lag of ∼5–10 min, there was a smaller elevation in [Ca2+]ithat persisted for 6 h and displayed different responsiveness to Ca2+ channel blockers. This second phase of elevated [Ca2+]iwas blocked by an inhibitor of store-operated Ca2+ channels, consistent with the observed generation of inositol trisphosphate. 1,2-Bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid-AM (BAPTA-AM), when added before or 2 h after nicotine, prevented elevation of TH mRNA. Nicotine treatment significantly raised cAMP levels. Addition of the adenylyl cyclase inhibitor 2′,5′-dideoxyadenosine (DDA) prevented the nicotine-elicited phosphorylation of cAMP response element binding protein. DDA also blocked the elevation of TH mRNA only when added after the initial transient rise in [Ca2+]iand not after 1 h. This study reveals that several temporal phases are involved in the induction of TH gene expression by nicotine, each of them with differing requirements for Ca2+ and cAMP.

Dihydropyridine-sensitive cell volume regulation in proximal tubule: the calcium window

1990 ◽  
Vol 259 (6) ◽  
pp. F950-F960 ◽  
Author(s):  
N. A. McCarty ◽  
R. G. O'Neil
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Regulatory Volume Decrease ◽  
Cell Volume Regulation ◽  
Cell Swelling ◽  
Channel Blockers ◽  
Ca Channel ◽  
Hypotonic Solution ◽  
Dependent Manner ◽  
Intracellular Ca

The mechanism underlying the activation of hypotonic cell volume regulation was studied in rabbit proximal straight tubule (PST). When isolated non-perfused tubules were exposed to hypotonic solution, cells swelled rapidly and then underwent a regulatory volume decrease (RVD). The extent of regulation after swelling was highly dependent on extracellular Ca concentration ([Ca2+]o), with a half-maximal inhibition (K1/2) for [Ca2+]o of approximately 100 microM. RVD was blocked by the Ca-channel blockers verapamil, lanthanum, and the dihydropyridines (DHP) nifedipine and nitrendipine, implicating voltage-activated Ca channels in the RVD response. Using the fura-2 fluorescence-ratio technique, we observed that cell swelling caused a sustained rise in intracellular Ca ([Ca2+]i) only when [Ca2+]o was normal (1 mM) but not when [Ca2+]o was low (1-10 microM). Furthermore, external Ca was required early on during swelling to induce RVD. If RVD was initially blocked by reducing [Ca2+]o or by addition of verapamil during hypotonic swelling, volume regulation could only be restored by subsequently inducing Ca entry within the first 1 min or less of exposure to hypotonic solution. These data indicate a "calcium window" of less than 1 min, during which RVD is sensitive to Ca, and that part of the Ca-dependent mechanism responsible for achieving RVD undergoes inactivation after swelling. It is concluded that RVD in rabbit PST is modulated by Ca via a DHP-sensitive mechanism in a time-dependent manner.

α1-Adrenoceptor-induced Mg2+ extrusion from rat hepatocytes occurs via Na+-dependent transport mechanism

2001 ◽  
Vol 280 (6) ◽  
pp. G1145-G1156 ◽  
Author(s):  
Theresa E. Fagan ◽  
Andrea Romani
Keyword(s):  
Adrenergic Receptor ◽  
Chelating Agent ◽  
Rat Hepatocytes ◽  
Channel Blockers ◽  
Inositol Trisphosphate Receptor ◽  
Intracellular Ca ◽  
A Cell ◽  
Dependent Transport ◽  
Trisphosphate Receptor ◽  
Stimulation Of

The stimulation of the α1-adrenergic receptor by phenylephrine results in a sizable extrusion of Mg2+ from liver cells. Phenylephrine-induced Mg2+ extrusion is almost completely abolished by the removal of extracellular Ca2+ or in the presence of SKF-96365, an inhibitor of capacitative Ca2+entry. In contrast, Mg2+ extrusion is only partially inhibited by the Ca2+-channel blockers verapamil, nifedipine, or (+)BAY-K8644. Furthermore, Mg2+ extrusion is almost completely prevented by TMB-8 (a cell-permeant inhibitor of the inositol trisphosphate receptor), 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid (an intracellular Ca2+-chelating agent), or W-7 (a calmodulin inhibitor) Thapsigargin can mimic the effect of phenylephrine, and the coaddition of thapsigargin and phenylephrine does not result in an enlarged extrusion of Mg2+ from the hepatocytes. Regardless of the agonist used, Mg2+ extrusion is inhibited by >90% when hepatocytes are incubated in the presence of physiological Ca2+ but in the absence of extracellular Na+. Together, these data suggest that the stimulation of the hepatic α1-adrenergic receptor by phenylephrine results in an extrusion of Mg2+ through a Na+-dependent pathway and a Na+-independent pathway, both activated by changes in cellular Ca2+.

Parathyroid cells express dihydropyridine-sensitive cation currents and L-type calcium channel subunits

2001 ◽  
Vol 281 (1) ◽  
pp. E180-E189 ◽  
Author(s):  
Wenhan Chang ◽  
Stacy A. Pratt ◽  
Tsui-Hua Chen ◽  
Chia-Ling Tu ◽  
Gabor Mikala ◽  
...  
Keyword(s):  
Parathyroid Hormone ◽  
Northern Blot ◽  
Northern Blot Analysis ◽  
Inhibitory Effects ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Alternatively Spliced ◽  
Induced Changes ◽  
Spliced Variant ◽  
Cdna Fragments

Parathyroid cells express Ca2+-conducting currents that are activated by raising the extracellular Ca2+ concentration ([Ca2+]o). We investigated the sensitivity of these currents to dihydropyridines, the expression of voltage-dependent Ca2+ channel (VDCC) subunits, and the effects of dihydropyridines on the intracellular free [Ca2+] ([Ca2+]i) and secretion in these cells. Dihydropyridine channel antagonists dose dependently suppressed Ca2+-conducting currents, and agonists partially reversed the inhibitory effects of the antagonists in these cells. From a bovine parathyroid cDNA library, we isolated cDNA fragments encoding parts of an α1S- and a β3-subunit of L-type Ca2+ channels. The α1S-subunit cDNA from the parathyroid represents an alternatively spliced variant lacking exon 29 of the corresponding gene. Northern blot analysis and immunocytochemistry confirmed the presence of transcripts and proteins for α1- and β3-subunits in the parathyroid gland. The addition of dihydropyridines had no significant effects on high [Ca2+]o-induced changes in [Ca2+]i and parathyroid hormone (PTH) release. Thus our studies indicate that parathyroid cells express alternatively spliced L-type Ca2+ channel subunits, which do not modulate acute intracellular Ca2+ responses or changes in PTH release.

Comparative Effects of Bupivacaine and Ropivacaine on Intracellular Calcium Transients and Tension in Ferret Ventricular Muscle

2004 ◽  
Vol 101 (4) ◽  
pp. 888-894 ◽  
Author(s):  
Yasushi Mio ◽  
Norio Fukuda ◽  
Yoichiro Kusakari ◽  
Yoshikiyo Amaki ◽  
Yasumasa Tanifuji ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Bay K 8644 ◽  
Clinical Settings ◽  
Ca Channel ◽  
Dependent Manner ◽  
Inhibitory Effects ◽  
Concentration Dependent Manner ◽  
Intracellular Ca ◽  
Slope Difference ◽  
The Relationship

Background Recent evidence suggests that ropivacaine exerts markedly less cardiotoxicity compared with bupivacaine; however, the mechanisms are not fully understood at the molecular level. Methods Isolated ferret ventricular papillary muscles were microinjected with the Ca-binding photoprotein aequorin, and intracellular Ca transients and tension were simultaneously measured during twitch in the absence and presence of bupivacaine or ropivacaine. Results Bupivacaine and ropivacaine (10, 30, and 100 microm) reduced peak systolic [Ca]i and tension in a concentration-dependent manner. The effects were significantly greater for bupivacaine, particularly on tension (approximately twofold). The percentage reduction of tension was linearly correlated with that of [Ca]i for both anesthetics, with the slope of the relationship being approximately equal to 1.0 for ropivacaine and approximately equal to 1.3 for bupivacaine (slope difference, P < 0.05), suggesting that the cardiodepressant effect of ropivacaine results predominantly from inhibition of Ca transients, whereas bupivacaine suppresses Ca transients and the reaction beyond Ca transients, i.e., myofibrillar activation, as well. BAY K 8644, a Ca channel opener, abolished the inhibitory effects of ropivacaine on Ca transients and tension, whereas BAY K 8644 only partially inhibited the effects of bupivacaine, particularly the effects on tension. Conclusion The cardiodepressant effect of bupivacaine is approximately twofold greater than that of ropivacaine. Bupivacaine suppresses Ca transients more markedly than does ropivacaine and reduces myofibrillar activation, which may at least in part underlie the greater inhibitory effect of bupivacaine on cardiac contractions. These results suggest that ropivacaine has a more favorable profile as a local anesthetic in the clinical settings.

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