Ca2+ and cyclic nucleotide dependence of amylase release from isolated rat pancreatic acinar cells rendered permeable by intense electric fields

Knight, D. E.; Koh, Eio

doi:10.1016/0143-4160(84)90007-1

Cited by 67 publications

(20 citation statements)

References 43 publications

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“…4). This is similar to the K d of 2 M Ca 2+ that is found for enzyme release in these cells (Knight and Koh, 1984). Our K d value is also comparable to endocrine cells, such as chromaffin cells, where the calculated K d is 1.6 M (Augustine and Neher, 1992).…”

Section: Discussionsupporting

confidence: 71%

Exocytosis, dependent on Ca2+ release from Ca2+ stores, is regulated by Ca2+ microdomains

Low

Shukla

Behrendorff

et al. 2010

Journal of Cell Science

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dependence of exocytosis, (4) significant reduction in exocytosis in the prescence of cytosolic EGTA, (5) spatial exclusion of secretory granules from the cell membrane by the endoplasmic reticulum, and (6) inability of local Ca 2+ responses to trigger exocytosis. These results strongly indicate that the control of exocytosis, triggered by Ca 2+ release from stores, is through the regulation of cytosolic [Ca 2+ ] within a microdomain.

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Section: Discussionsupporting

confidence: 71%

Exocytosis, dependent on Ca2+ release from Ca2+ stores, is regulated by Ca2+ microdomains

Low

Shukla

Behrendorff

et al. 2010

Journal of Cell Science

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“…As shown in Fig. 4, this has been found experimentally for acinar cells (25,26) as well as for parathyroid cells (9,19). Further experiments are required to determine whether this hypothesis is correct.…”

Section: Possible Resolution Of the Parathyroid Paradoxsupporting

confidence: 49%

Regulation of Parathyroid Hormone Secretion*

1991

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Calcium is the most important physiological regulator of PTH secretion. Peak PTH secretion occurs at an intracellular calcium concentration of about 200 nM, regardless of the extracellular calcium concentration. We suggest, therefore, that intracellular calcium concentration is a regulator of PTH secretion that maintains calcium homeostasis. Other factors may be responsible for modulation of the intracellular calcium concentration, ultimately modulating PTH secretion. The "paradoxical" nature of the dependence of PTH secretion on the calcium concentration may be explained by considering PTH secretion to be unusual in a quantitative, rather than a qualitative, fashion. A possible mechanism for the control of PTH secretion by intracellular calcium, which involves calcium-activated potassium channels, is proposed. The parathyroid cell plasma membrane contains several sensors or channels by means of which the cell senses extracellular calcium. It is not clear whether these entities are coupled to each other or whether they function independently. Guanine nucleotide regulatory proteins are transducers of extracellular signals, including calcium. Several other second messengers that influence PTH secretion have also been described, but possible interactions between these messengers have not yet been determined.

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“…Phorbol esters enhance amylase release in a Ca2+-dependent manner in the acinar cells of exocrine pancreas (Knight & Koh, 1984;Kimura, Imamura, Eckhardt & Schulz, 1986). Phorbol esters may therefore have a dual effect on stimulus-secretion coupling in pancreatic acinar cells, one of which is desensitization (negative feedback) of receptor signalling, and the other enhancement of exocytosis acting rather directly on the exocytotic machinery (also see Nishizuka, 1988).…”

Section: Inositol Polyphosphates and The Increase In [Caa2+]mentioning

confidence: 99%

Activation and desensitization mechanisms of muscarinic current response in single pancreatic acinar cells of rats.

Maruyama

1989

The Journal of Physiology

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3. The sensitivity of 1P3 recovers after short-term administration of ACh (0 2 ,tM), and in turn, the ACh-induced response is augmented by the presence of internal IP3. These results suggest that a synergism between IP3 and another ACh-induced substance plays an important role in muscarinic Ca2+ signalling.4. ACh-induced responses are inhibited by pre-incubation (10 min) with an activator of protein kinase C, TPA (12-O-tetradecanoylphorbol-13-acetate, 16 nM), or augmented by pre-incubation (10 min) with an inhibitor, H-7 (1-(5-isoquinolinesulphonyl)-2-methylpiperazine, 10 /tM), whilst IP3-induced responses are unaffected by that with both agents. These results indicate that protein kinase C acts negatively on the signalling elements prior to the formation of IP3.5. The oscillatory responses, induced by cell dialysis with a nominally Ca2+-free (ca 1-10 /tM) solution containing GTPyS (100 aM), are unaffected by the pre-treatment with TPA or H-7. In addition, these responses and/or those triggered by shortterm stimulation with ACh and internal GTPyS are not influenced by external ACh. On the other hand, the oscillatory responses recorded in acinar cells pre-treated with H-7 are tightly controlled by external ACh. 6. Taken together these results suggest that activation of protein kinase C does not affect the activity of GTP-binding protein, but disconnects the link between the muscarinic ACh receptor and GTP-binding protein, or inhibits ACh binding to the receptor, in rat pancreatic acinar cells.

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Ca2+ and cyclic nucleotide dependence of amylase release from isolated rat pancreatic acinar cells rendered permeable by intense electric fields

Cited by 67 publications

References 43 publications

Exocytosis, dependent on Ca2+ release from Ca2+ stores, is regulated by Ca2+ microdomains

Exocytosis, dependent on Ca2+ release from Ca2+ stores, is regulated by Ca2+ microdomains

Regulation of Parathyroid Hormone Secretion*

Activation and desensitization mechanisms of muscarinic current response in single pancreatic acinar cells of rats.

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