The Effect of Amethocaine on Acetylcholine‐induced Depolarization and Catecholamine Secretion in the Adrenal Chromaffin Cell

Douglas, W. W.; Kanno, Tomio

doi:10.1111/j.1476-5381.1967.tb02167.x

Cited by 32 publications

(9 citation statements)

References 23 publications

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“…We therefore investigated the effects of Ca channel blockers on this secretion to determine whether or not Ca entry through the specific channels is responsible for secretion (Douglas & Kanno, 1967;Jaanus, Miele & Rubin, 1967;Baker, Meves & Ridgway, 1973;Pinto & Trifar6, 1976).…”

Section: Perfusionmentioning

confidence: 99%

Exocytotic Secretion of Catecholamines From the Cat Adrenal Medulla by Sodium Deprivation: Involvement of Calcium Influx Mechanism

Nishimura

Sorimachi

Yamagami

1981

British J Pharmacology

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Cat adrenal glands were perfused with Ca‐deficient medium and secretion of catecholamines (CA) was induced by perfusion with Na‐free medium in which NaCl was replaced by an osmotically equivalent amount of sucrose. Release of CA and dopamine‐β‐hydroxylase (DBH), but not that of phenylethanolamine‐N‐methyltransferase, was concomitantly found in the effluents when the adrenals were stimulated, indicating that secretion was due to exocytosis. Secretion of CA induced by Na‐free (sucrose) medium was dependent on the concentration of Ca and was saturated at 0.5 mm of Ca. Sr or Ba substituted for Ca in maintaining secretion by Na‐free (sucrose) medium. The addition of Na, Li or alkali metal ions to Na‐free (sucrose) medium containing Ca reduced the response to a variable extent but this inhibition was reversed by raising the concentration of Ca in the Na‐free medium. All of the Na substitutes used induced secretion only when this medium contained Ca. However, different Na substitutes released different amounts of CA; sucrose was most effective, K, Tris and choline were moderately and Li least effective. Secretion of CA by Na‐free (sucrose) medium was strongly inhibited by D‐600, tetracaine or divalent cations such as Co, Ni, Zn and Mg. The inhibition by Co was partially reversed by raising the concentration of Ca in the Na‐free medium. Secretion of CA from bovine isolated chromaffin cells was induced by Na‐deficient (sucrose) medium and was dependent on the concentrations of ionized Ca involved. All the Na substitutes tested increased secretion of CA and 45Ca uptake, in a parallel fashion. A correlation between secretion and 45Ca uptake was found under various experimental manipulations which reduced secretion of CA. These results demonstrated that unlike the perfused bovine adrenals, the Ca influx mechanism is essential for secretion by Na deprivation in the perfused cat adrenals as it is in bovine isolated chromaffin cells. It is suggested that Na deprivation increases Ca entry through the Ca channels by eliminating the competition between Na and Ca, and possibly by activating Ca influx linked with Na efflux.

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Section: Perfusionmentioning

confidence: 99%

Exocytotic Secretion of Catecholamines From the Cat Adrenal Medulla by Sodium Deprivation: Involvement of Calcium Influx Mechanism

Nishimura

Sorimachi

Yamagami

1981

British J Pharmacology

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“…In one preparation the resting membrane potential 150 min after exposing the tissue to Ca-free solution was 14 mV, yet this cell still responded to addition of ACh to the tissue bath with a depolarization of 10 mV. D-600 (ac-isopropyl-cc-(N -methyl -N -homoveratryl) -y -aminopropyl -3,4,5 -trimethoxy -phenylacetonitril) (104 M), tetracaine (10-3 M) and La3+ (5 mM), substances that interfere with membrane Ca2+ currents in other tissues (Kohihardt, Bauer, Krause & Fleckenstein, 1972;Douglas & Kanno, 1967;Van Breemen & DeWeer, 1970) all caused some reduction in the mean amplitude of the 290 PANCREATIC MEMBRANE POTENTIALS ACh-induced depolarization (Fig. 7).…”

Section: The Importance Of Camentioning

confidence: 99%

Pancreatic acinar cells: ionic dependence of the membrane potential and acetylcholine‐induced depolarization

Matthews¹,

Petersen²

1973

The Journal of Physiology

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1. Intracellular recordings of membrane potentials have been made in vitro from the exocrine acinar cells of the mouse pancreas using glass micro‐electrodes. 2. The mean membrane potential of the acinar cells during superfusion with Krebs‐Henseleit solution was −39·2 mV. Increasing [K]o tenfold decreased the membrane potential by 28 mV when [K]o was above 10 m M. This depolarization was not affected by atropine (1·4 × 10−6 M). Strophanthin‐G (10−3 M) slowly depolarized the cells at about 10 mV hr−1. 3. Brief exposure to acetylcholine (ACh), 5·5 × 10−5 M, or pancreozymin resulted in a short lasting depolarization of the acinar cells. Atropine (1·4 × 10−6 M) blocked the depolarizing action of ACh but not that of pancreozymin. Adrenaline (5·5 × 10−5 M) or cyclic AMP (10−3‐10−4 M) did not influence the membrane potential. 4. The amplitude of the ACh‐induced depolarization was not dependent on the presence of CO2/HCO3 in the bathing fluid, but it was closely dependent on the extracellular Na concentration. However, ACh was still able to evoke a small depolarization even after prolonged exposure of the tissue to a Na‐free solution. 5. During exposure of the tissue to a Ca‐free solution the resting membrane potential was decreased and the ACh‐induced depolarization was significantly reduced. Some substances which are known in other tissues to inhibit membrane Ca2+ currents, i.e. La3+, D‐600 and tetracaine, were able to reduce, but never abolish, the ACh‐induced depolarization. 6. These results suggest that the effect of ACh on the pancreatic acinar cell is to increase the permeability of the membrane to commonly occurring ions with a consequent Na‐influx and a small Ca‐influx.

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“…induced cell fusion [61] and secretory processes [22,67,71]. Concentrations of dibucaine or procaine, which reduce cell fusion induced by viruses [61], were found to inhibit Ca2+-induced fusion of vesicles ( Table 3).…”

Section: Ejfect Of Various Agentsmentioning

confidence: 94%

Fusion of secretory vesicles isolated from rat liver

Gratzl

Dahl

1978

J. Membrain Biol.

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Summary. Secretory vesicles isolated from rat liver were found to fuse after exposure to Ca 2 +. Vesicle fusion is characterized by the occurrence of twinned vesicles with a continuous cleavage plane between two vesicles in freeze-fracture electron microscopy. The number of fused vesicles increases with increasing Ca 2 +-concentrations and is half maximal around 10 -6 M. Other divalent cations (Ba 2+, Sr 2+, and Mg 2+) were ineffective. Mg 2+ inhibits Ca2+-induced fusion. Therefore, the fusion of secretory vesicles in vitro is Ca z+ specific and exhibits properties similar to the exocytotic process of various secretory cells.Various substances affecting secretion in vivo (microtubular inhibitors, local anesthetics, ionophores) were tested for their effect on membrane fusion in our system.The fusion of isolated secretory vesicles from liver was found to differ from that of pure phospholipid membranes in its temperature dependence, in its much lower requirement for Ca 2+, and in its Cag+-specificity. Chemical and enzymatic modifications of the vesicle membrane indicate that glycoproteins may account for these differences.Membrane fusion is an essential event in a variety of cell functions such as cell fusion, uptake of extracellular material (endocytosis) and release of cell products (exocytosis). Elucidation of the molecular mechanism of membrane fusion has been hampered by the lack of suitable systems for studying this process. Studies with intact cells have not yielded data which lead to ready interpretation concerning subcellular processes. On the other hand, studies with artificial membranes may be only tangentially related to the fusion of biological membranes.Recently our group investigated the fusion of isolated biological membranes [16,17,31,33,69,74]. We observed that Ca 2+ specifically induces the fusion of isolated secretory vesicles in a buffered sucrose medium.Intervesicular fusion of secretory vesicles, as well as the interaction between the cell membrane and the vesicle membrane, was observed in a variety of secretory cells [2,3,6,18,29,39,53,65]. Douglas [20] showed that in "compound exocytosis" by mast cells an external stimulus initiates fusion between secretory vesicle membranes and the

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The Effect of Amethocaine on Acetylcholine‐induced Depolarization and Catecholamine Secretion in the Adrenal Chromaffin Cell

Cited by 32 publications

References 23 publications

Exocytotic Secretion of Catecholamines From the Cat Adrenal Medulla by Sodium Deprivation: Involvement of Calcium Influx Mechanism

Exocytotic Secretion of Catecholamines From the Cat Adrenal Medulla by Sodium Deprivation: Involvement of Calcium Influx Mechanism

Pancreatic acinar cells: ionic dependence of the membrane potential and acetylcholine‐induced depolarization

Fusion of secretory vesicles isolated from rat liver

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