Intracellular Cl- activity of canine submandibular gland cells: An in vitro observation.

Mori, Hirohiko; Murakami, Masataka; Nakahari, Takashi; Imai, Yusuke

doi:10.2170/jjphysiol.33.869

Cited by 8 publications

(3 citation statements)

References 5 publications

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“…In the following, we give specific figures for the concentrations in the basolateral extracellular space ([Na]1, [K]1, [Cl]1), in the intracellular compartment ([Na]i, [K]i, [Cl]i), and in the lumen ([Na]2, [K]2, [Cl]2), and for their respective potentials, V1, Vi and V2 which are consistent with available information (e.g. Poulsen & Oakley, 1979;Mori, Murakami, Nakahari & Imai, 1983;Sasaki et al 1983) and which yield fluxes in the directions shown in the Figure. For simplicity, only Na, K and Cl are considered.…”

Section: Ca-dependent Channels In Lacrimal Glandssupporting

confidence: 84%

Three types of calcium‐dependent channel in rat lacrimal glands.

Marty¹,

Tan²,

Trautmann³

1984

The Journal of Physiology

359

207

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SUMMARY1. Isolated cells from rat lacrimal glands were studied with patch-clamp techniques. Whole-cell and cell-attached recordings were obtained while the cells were stimulated by application of carbamylcholine or of the Ca ionophore, A23187. The results were compared with recordings of Ca-dependent channels obtained in isolated patches.2. Whole-cell recordings revealed two types of carbamylcholine-induced current. At low levels of stimulation, a specific class of Ca-dependent K channels was selectively activated ('BK channels'). With more intense stimulation an inward current, Ii, was obtained at the cell resting potential. Ii rose rather abruptly after a long delay. In several cells, Ii currents presented spontaneous oscillations.3

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Section: Ca-dependent Channels In Lacrimal Glandssupporting

confidence: 84%

Three types of calcium‐dependent channel in rat lacrimal glands.

Marty¹,

Tan²,

Trautmann³

1984

The Journal of Physiology

359

207

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“…The evidence includes the demonstration that secretion can be blocked by furosemide (Case et al, 1982(Case et al, , 1984Martinez and Cassity, 1985a;Novak et al, 1984;Novak and Young, 1986;, and by removal of extracellular C1 (Case et al, 1984;Lundberg, 1958;Murakami et al, 1986;Novak and Young, 1986;Martinez and Cassity, 1985b). Additional evidence includes the demonstration that the secretary system shows a marked preference for Br and Cl over other anions (Case et al, 1982(Case et al, , 1984Novak and Young, 1986), a preference that is characteristic of Na-K-2C1 symports (Ellory et al, 1982), that cytosolic Cl activity is above equilibrium both at rest and during stimulation (Lau and Case, 1986;Martinez and Cassity, 1985a;Mori et al, 1983;Poulsen and Kristensen, 1982), and that six C1 ions are transported per ATP molecule, indicative of a process coupling C1 and Na fluxes in a ratio of 2:1 (Smaje et al, 1986). In salivary glands, however, there is good evidence to show that secretion can persist, albeit at a reduced rate, even when symport activity has been halted, and it is thought that this residual secretion is due to the operation of a Na-H antiport, which concentrates HCO3 in the cytosol, and a Cl-HCO3 antiport, which allows the cytosolic HCO3 to exchange for interstitial C1 (Case et al, 1982(Case et al, , 1984Martinez and Cassity, 1985c;Novak and Young, 1986).…”

Section: Introductionmentioning

confidence: 99%

Effects of Ion Transport Inhibition on Rat Mandibular Gland Secretion

et al. 1987

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The effects of substituting gluconate for extracellular Cl, and of treatment with various ion transport blockers, on cytosol pH (pHi) and secretion by the acetylcholine stimulated rat mandibular gland were studied in vitro. Gluconate replacement increased pHi from 7.12 +/- 0.02 to 7.27 +/- 0.04, caused secretory rate to fall by 75%, and increased salivary HCO3 from 14 +/- 0.9 mmol/L to 67 +/- 1.5 mmol/L. Furosemide (1 mmol/L), which blocks Na-K-2Cl symports and Cl-HCO3 antiports, had effects similar to those of gluconate replacement, except that secretion was reduced only by 59%. Bumetanide (1 mmol/L), which blocks only Na-K-2Cl symports, caused a 67% reduction in secretion rate, but it had little effect on pHi and caused only a small rise in salivary HCO3 concentration. SITS (1 mmol/L), which blocks Cl-HCO3 antiports, increased pHi to 7.26 +/- 0.03 and induced a small rise in the secretory rate. Methazolamide and acetazolamide (1 mmol/L), both of which inhibit carbonic anhydrase and may also block anion channels, increased pHi to 7.43 +/- 0.02 and 7.20 +/- 0.03, respectively, but had no effect on secretory rate, and reduced salivary HCO3 slightly. Ba (3 mmol/L), tetraethylammonium (10 mmol/L), and decamethonium (5 mmol/L) all caused marked but reversible reductions in secretory rate, consistent with the known actions of these agents on K channels. Ba, however, also appeared to act as a Ca antagonist, an action that it seemed to share with Mn ions (5 mmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

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“…5A and B). The time between the break-in artifact and the peak of the transient ranged from 0-8 to 2-0 s, and the transient amplitude varied from 100 to 600 pA. Acinar cells from exocrine glands have a rather large internal Cl-concentration (Mori, Murakami, Nakahari & Imai, 1983;Saito, Ozawa, Hayashi & Nishiyama, 1985) such that at -60 mV, a substantial (approximately 25 mV) driving force exists for Cl-exit. (For the short times considered here ionic exchange between pipette and cell compartments may be neglected.)…”

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confidence: 99%

The initiation of calcium release following muscarinic stimulation in rat lacrimal glands.

Marty

Tan

1989

The Journal of Physiology

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SUMMARY1. Acinar cells were isolated from rat lacrimal glands, and the Ca2+ release response of these cells was studied using two experimental approaches. In one approach, changes in Ca2+ concentration, Ca2+, were monitored by measuring Ca2+_ dependent Cl-currents using tight-seal whole-cell recording. Alternatively, such changes were measured as a fluorescence signal in cells loaded with Fura-2.2. Following bath application of ACh (0-5 ,tM), the cell current recorded at -60 mV was unchanged for ca 0-8 s, then rose in a biphasic manner. The initial phase of the current rise ('hump') took different appearances depending on the cell studied, and it sometimes stood out from the main part of the response as a partially isolated transient.3. In cells which had been loaded with Fura-2, Ca?+ was found to rise abruptly following a silent period. The delay was larger if ACh (0-2-0-5 /tM) was applied in a depolarizing isotonic K+ saline than if it was applied in the normal saline. In addition, the maximum of the Cai2 response was reduced with depolarizing stimulating solutions. This indicates that membrane potential modulates the Ca1 response.4. Responses to 5 /iM-ACh, a saturating agonist concentration, were almost identical in K+ saline and in normal saline.5. If the cell potential was hyperpolarized, the delay of the ACh-induced current became shorter.6. Breaking into an acinar cell with a pipette containing an elevated Ca2+ concentration (0-1-1 mM) led to a transient activation of Ca2+-induced currents during the first seconds of whole-cell recording. These transients were obtained more reliably if the transition to the whole-cell mode was achieved by applying a sharp pulse of potential ('zapping') rather than by applying suction to the pipette compartment. At -60 mV, the transients elicited with the former method by 0 5 mM-Ca2+ had a time-to-peak near 0-6 s and an amplitude varying between 10 and 600 pA. With 041 mM-Ca2+, similar transients were also observed, but a number of cells failed to respond. Calcium-induced transients were blocked if cells were previously loaded with 50 /LM-Ruthenium Red. IMS 7589A. MARTY AND Y. P. TAN 7. Performing the same experiments with inositol trisphosphate (InsP3, 20 /tM) in the pipette solutions also led to early transient Ca2+-induced currents. Amplitudes, times-to-peak and 20-80 % transition times were similar for 0 5 mM-Ca2' and 20 /tMInsP3 stimulations.8. Calcium-or InsP3-induced transients were similar to 'humps' (point 2 above) and to rapid transients which were observed in certain cells upon application of a low ACh concentration (0-1 /LM). These results suggest a role of these transients in shaping the ACh-induced currents.9. The results indicate that Ca2+-induced Ca2+ release plays a key role in the initiation of the ACh-induced response. It is suggested that the silent lag period is due to the accumulation of active phospholipase C molecules up to the point where Ca2+_ induced Ca2+ release is initiated. It is finally proposed that the lag is determined by the occupancy of ...

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Intracellular Cl- activity of canine submandibular gland cells: An in vitro observation.

Cited by 8 publications

References 5 publications

Three types of calcium‐dependent channel in rat lacrimal glands.

Three types of calcium‐dependent channel in rat lacrimal glands.

Effects of Ion Transport Inhibition on Rat Mandibular Gland Secretion

The initiation of calcium release following muscarinic stimulation in rat lacrimal glands.

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