Dispersed rat parotid acinar cells. II. Characterization of adrenergic receptors

Mangos, J. A.; McSherry, NR; Barber, T.; Arvanitakis, SN; Wagner, Virginia L.

doi:10.1152/ajplegacy.1975.229.3.560

Cited by 59 publications

(17 citation statements)

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“…The concentration of terbutaline needed to produce half maximal stimulation (EC50) was 0.8 ,M, a value which is a little lower than the range of 2-12 ,tM described in other cell systems (42,43). The decrease in stimulation seen at the highest concentrations (termed "autoinhibition") of terbutaline has been observed with various 8-adrpnergic agonists; autoinhibition may be a result of cqmpetitive inhibition by the D-isomer at high concentrations, but other explanations (44) (42,46,48). Phentolamine, even at high concentrations, did not inhibit the release induced by terbutaline (Fig.…”

Section: Methodsmentioning

confidence: 90%

Pulmonary Alveolar Type II Cells Isolated from Rats

Dobbs¹,

Mason²

1979

J. Clin. Invest.

329

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Section: Methodsmentioning

confidence: 90%

Pulmonary Alveolar Type II Cells Isolated from Rats

Dobbs¹,

Mason²

1979

J. Clin. Invest.

329

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“…Secretion ofamylase is also elevated by these agonists, albeit weakly in comparison with f-adrenergic agonists (Babad et al, 1967;Mangos et al, 1975;Kanagasuntheram & Randle, 1976). These effects are dependent on extracellular Ca2+ and are believed to be initiated by a rise in intracellular free Ca2+ Kanagasuntheram & Randle, 1976).…”

mentioning

confidence: 98%

“…Activation of the fl-adrenergic receptor stimulates adenylate cyclase Wojcik et al, 1975) and induces a rapid and copious release of amylase (Bdolah et al, 1964;Butcher et al, 1975;Mangos et al, 1975). Moreover, the incorporation of radioactively labelled amino acids into trichloroacetic acid-insoluble proteins and amylase is also increased 4-6h after fl-adrenergic stimulation (Lillie & Han, 1973;Johnson & Sreebny, 1973).…”

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confidence: 99%

Calcium-dependent inhibition of protein synthesis in rat parotid gland

Kanagasuntheram¹,

Lim²

1978

Biochemical Journal

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1. Protein synthesis in the rat parotid gland in vitro was studied by measuring the incorporation of [3H]phenylalanine into trichloroacetic acid-insoluble proteins. In the unstimulated gland, the rate of incorporation was deperndent on the phenylalanine concentration in the medium and proceeded linearly for up to 3 h. 2. Adrenaline, carbamoylcholine, phenylephrine and ionophore A23187 inhibited the incorporation of [3H]phenylalanine into acid-insoluble protein; isoprenaline, dibutyryl cyclic AMP and 8-bromo-cyclic GMP were inactive. 3. Inhibition by adrenaline and carbamoylcholine but not by ionophore A23187 required extracellular Ca2+. 4. Both adrenaline and carbamoylcholine increased the magnitude of the acid-soluble [3H]phenylalanine pool at 10pM extracellular phenylalanine, but had no effect if the phenylalanine concentration was increased to 200pM. 5. There was no correlation between cellular ATP content and the observed inhibition of protein synthesis. 6. Our results suggest that both a-adrenergic and cholinergic receptors may play a role in the regulation of protein synthesis in the rat parotid gland, and that their effects are mediated by a rise in intracellular free Ca2+.

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“…The transmitters, acetylcholine (ACh) and noradrenaline, interact with cholinergic, a-and /J-adrenergic receptors on the acinar cells. The actions of these transmitters on K transport have been extensively studied in salivary glands in vivo (Burgen, 1956) and in vitro (Batzri, Selinger, Schramm & Robinovitch, 1973;Bogart & Picarelli, 1978;Butcher, McBride & Rudich, 1976;Butcher, Rudich, Emler & Nemerovsky, 1976;Marier, Putney & Van de Walle, 1978; Mangos, McSherry, Barber, Arvanitakis & Wagner, 1975;Martinez, Quissell & Giles, 1976;Petersen, 1970aPetersen, , b, 1971aPutney, 1976Putney, , 1977Poulsen & Oakley, 1978;Quissell, 1980).…”

mentioning

confidence: 99%

Activation of potassium transport induced by secretagogues in superfused submaxillary gland segments of rat and mouse.

Katoh¹,

Nakasato²,

Nishiyama³

et al. 1983

The Journal of Physiology

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In order to investigate the actions of acetylcholine (ACh), catecholamines and substance P on K transport in the submaxillary gland, measurements of net K flux to and from the gland tissue using flame photometry, Na efflux from the tissue using radioactive 22Na, and membrane potential and input resistance using micro‐electrodes were carried out on isolated superfused segments of rat and mouse submaxillary glands. ACh (5.5 X 10(‐8) to 5.5 X 10(‐4) M), phenylephrine (5 X 10(‐7) to 5 X 10(‐4) M) or substance P (10(‐9) to 10(‐5) M) stimulation for 5 min induced a transient K release followed by a small K uptake after the cessation of stimulation. The K release was markedly enhanced by the simultaneous addition of ouabain (10(‐3) M). On the other hand, isoprenaline (2.5 X 10(‐9) to 2.5 X 10(‐5) M) induced a transient K uptake without any preceding K release. The K uptake was completely blocked by the addition of ouabain. Noradrenaline induced only K uptake at a low concentration (3 X 10(‐7) M), but induced transient K release followed by marked K uptake at higher concentrations (3 X 10(‐6) to 3 X 10(‐4) M). The K release induced by noradrenaline was suppressed by the addition of phentolamine (10(‐5) M), while the K uptake was suppressed by propranolol (5 X 10(‐6) M). The K release induced by ACh, phenylephrine, noradrenaline or substance P was severely reduced by Ca omission from the superfusing solution and restored by the re‐admission of Ca. The isoprenaline‐ or noradrenaline‐induced K uptake was, however, little affected by Ca omission. Application of isoprenaline (2.5 X 10(‐6) M) induced an increase in 22 Na efflux. The increase in 22Na efflux was completely abolished in the presence of ouabain. Local application to the tissue bath of isoprenaline (4.7 X 10(‐13) to 4.7 X 10(‐12) mole) or noradrenaline (5.7 X 10(‐12) to 5.7 X 10(‐11) mole) in the presence of phentolamine (10(‐5) M) induced membrane hyperpolarization without any appreciable change in input resistance. The hyperpolarization was abolished in the presence of ouabain (10(‐3) M) or propranolol (5 X 10(‐6) M) or in a K‐free or low Na solution. Higher doses of both agonists, however, induced depolarization or biphasic responses (initial depolarization followed by hyperpolarization). The depolarizations were accompanied by a moderate reduction in input resistance. It is concluded that in the rat and mouse submaxillary gland acinar cells cholinergic, alpha‐adrenergic or substance P stimulation causes K release (and perhaps Na uptake) resulting in activation of the Na‐K pump, while beta‐adrenergic receptor stimulation might directly activate the Na‐K pump resulting in K uptake, or might cause Na uptake resulting in activation of the Na‐K pump.

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Dispersed rat parotid acinar cells. II. Characterization of adrenergic receptors

Cited by 59 publications

References 0 publications

Pulmonary Alveolar Type II Cells Isolated from Rats

Pulmonary Alveolar Type II Cells Isolated from Rats

Calcium-dependent inhibition of protein synthesis in rat parotid gland

Activation of potassium transport induced by secretagogues in superfused submaxillary gland segments of rat and mouse.

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