Characterization of α- and β-Adrenergic Agonist Stimulation of Adenylate Cyclase Activity in Human Epidermal Keratinocytes In Vitro

Many studies previously have shown that the B-adrenergic agonist isoproterenol and the a-adrenergic agonist norepinephrine will stimulate secretion by the adult rat submandibular (SMG) and parotid glands. Recent data from several laboratories indicates that adrenergic agonists bind to specific receptors on the secretory cell surface and stimulate membrane associated adenylate cyclase activity which generates cyclic AMP. The production of cyclic AMP apparently initiates a cascade of events which culminates in exocytosis. During recent studies in our laboratory it was observed that the adenylate cyclase activity in plasma membrane fractions derived from the prenatal and early neonatal rat submandibular gland was retractile to stimulation by isoproterenol but was stimulated by norepinephrine. In addition, in vitro secretion studies indicated that these prenatal and neonatal glands would not secrete peroxidase in response to isoproterenol but would secrete in response to norepinephrine. In contrast to these in vitro observations, it has been shown that the injection of isoproterenol into the living newborn rat results in secretion of peroxidase by the SMG (1).

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Stimulation of Adenylate Cyclase Activity in Rat Thymocytes in Vitro by 3,5,3′-Triiodothyronine*

Endocrinology ◽

10.1210/endo-116-5-2036 ◽

1985 ◽

Vol 116 (5) ◽

pp. 2036-2043 ◽

Cited By ~ 14

Author(s):

JOSEPH SEGAL ◽

CHRISTOPHER BUCKLEY ◽

SIDNEY H. INGBAR

Keyword(s):

Adenylate Cyclase ◽

Cyclase Activity ◽

Adenylate Cyclase Activity ◽

Stimulation Of

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Partial and full dopamine D1 receptor agonists in mice and rats: relation between behavioural effects and stimulation of adenylate cyclase activity in vitro

European Journal of Pharmacology ◽

10.1016/0014-2999(92)90690-6 ◽

1992 ◽

Vol 213 (2) ◽

pp. 259-267 ◽

Cited By ~ 106

Author(s):

Jørn Arnt ◽

John Hyttel ◽

Connie Sánchez

Keyword(s):

Adenylate Cyclase ◽

Dopamine D1 Receptor ◽

D1 Receptor ◽

Cyclase Activity ◽

Adenylate Cyclase Activity ◽

Receptor Agonists ◽

Behavioural Effects ◽

Stimulation Of

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Adenylate cyclase activity of human nasal polyps during stimulation of serotonin biosynthesis in vitro

Bulletin of Experimental Biology and Medicine ◽

10.1007/bf00797558 ◽

1976 ◽

Vol 81 (4) ◽

pp. 524-526

Author(s):

L. S. Malykhina ◽

G. A. Stepanova ◽

G. N. Popova ◽

N. A. Fedorov

Keyword(s):

Adenylate Cyclase ◽

Nasal Polyps ◽

Cyclase Activity ◽

Adenylate Cyclase Activity ◽

Serotonin Biosynthesis ◽

Stimulation Of

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Antisecretory effects of berberine in rat ileum

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1981.241.3.g253 ◽

1981 ◽

Vol 241 (3) ◽

pp. G253-G258 ◽

Cited By ~ 1

Author(s):

Y. H. Tai ◽

J. F. Feser ◽

W. G. Marnane ◽

J. F. Desjeux

Keyword(s):

Cyclic Amp ◽

Adenylate Cyclase ◽

Short Circuit ◽

Short Circuit Current ◽

Cyclase Activity ◽

Adenylate Cyclase Activity ◽

Rat Ileum ◽

Ion Secretion ◽

Stimulation Of

The in vitro antisecretory effects of the alkaloid berberine (1.0 mM) on intestinal ion secretion and mucosal adenylate cyclase and Na-K-ATPase activities were studied in the rat ileum. Mucosal berberine did not alter the individual basal net ion fluxes and basal adenylate cyclase activity but decreased short-circuit current (Isc) and increased the net absorption of chloride plus bicarbonate. In the cholera toxin-treated tissue, mucosal berberine stimulated absorption of Na and Cl and inhibited the increased adenylate cyclase activity but did not change the specific Na-K-ATPase activity, whereas serosal berberine stimulated Na secretion and decreased Isc. Mucosal berberine also decreased Isc, increased Cl permeability, and reversed the ion secretion induced by dibutyryl cyclic AMP, the heat-stable enterotoxin of Escherichia coli, and methylprednisolone administration. The antisecretory effects of mucosal berberine may be explained by stimulation of a Na-Cl-coupled absorptive transport process. The mechanism of action of serosal berberine remains to be elucidated. However, it is clear that mucosal berberine affects intestinal ion transport by mechanisms different from stimulation of the Na pump and probably at a step distal to the production or degradation of cyclic AMP or cyclic GMP.

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Mechanism of inhibition by methacholine of norepinephrine-stimulated ANP secretion

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1988.255.6.h1429 ◽

1988 ◽

Vol 255 (6) ◽

pp. H1429-H1433 ◽

Cited By ~ 2

Author(s):

R. J. Schiebinger

Keyword(s):

Adenylate Cyclase ◽

Cyclase Activity ◽

Adenylate Cyclase Activity ◽

Base Line ◽

Adrenergic Agonist ◽

Beta Adrenergic ◽

Mechanism Of Inhibition ◽

Beta Adrenergic Agonist ◽

Alpha Adrenergic Agonist

We have previously reported that methacholine inhibits norepinephrine-stimulated immunoreactive atrial natriuretic peptide (ANP-IR) secretion by 65% in vitro. In the present study, we examined the mechanism by which methacholine inhibits norepinephrine-stimulated secretion using isolated, paced rat left atria superfused in vitro. Norepinephrine has beta- and alpha-adrenergic properties, both of which stimulate ANP secretion. Thus we separately examined the effect of 10 microM methacholine on ANP-IR secretion stimulated by the beta-adrenergic agonist isoproterenol (0.1 microM) and by the alpha-adrenergic agonist phenylephrine (10 microM). Methacholine lowered isoproterenol-stimulated ANP-IR secretion to base line but did not inhibit phenylephrine-stimulated ANP-IR secretion. Atria were superfused with 0.5 mM dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) to determine whether inhibition of isoproterenol-stimulated secretion by methacholine occurred by a reduction in adenylate cyclase activity or at a point distal to cAMP. Methacholine inhibited dibutyryl cAMP-stimulated ANP-IR secretion by 50%. This inhibition could not be reversed by 20 microM isobutylmethylxanthine. We conclude that 1) methacholine completely blocks isoproterenol-stimulated ANP-IR secretion; 2) inhibition appears to be primarily due to a decrease in adenylate cyclase activity; however, inhibition occurs at a point(s) distal to cAMP production; 3) methacholine does not inhibit phenylephrine-stimulated ANP-IR secretion; and 4) inhibition by methacholine of norepinephrine-stimulated ANP-IR secretion reflects a block in beta-adrenergic activity.

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A possible role of adenylate cyclase in the longterm dietary regulation of insulin secretion from rat islets of Langerhans

Biochemical Journal ◽

10.1042/bj1360343 ◽

1973 ◽

Vol 136 (2) ◽

pp. 343-349 ◽

Cited By ~ 32

Author(s):

Simon L. Howell ◽

Irene C. Green ◽

William Montague

Keyword(s):

Insulin Secretion ◽

Adenylate Cyclase ◽

Islets Of Langerhans ◽

Glucose Concentration ◽

Cyclase Activity ◽

Adenylate Cyclase Activity ◽

Maximal Response ◽

Long Term Effects ◽

Stimulation Of

1. Adenylate cyclase activity and patterns of insulin release in response to various concentrations of glucose were determined in islets of Langerhans isolated from starving, fed, or glucose-loaded rats. 2. Basal and glucagon-stimulated activities of adenylate cyclase were lower in islets from starved than from fed rats. The minimum glucose concentration required for stimulation of insulin secretion was higher, whereas the maximum secretory response to glucose was lower, in islets from starved than from fed rats. 3. Adenylate cyclase activity in islets of Langerhans obtained from fed rats loaded with glucose by intermittent intravenous or intraperitoneal injections over 5h was significantly higher than that seen in islets from normal fed rats. Islets obtained from glucose-loaded rats required a lower glucose concentration for stimulation of insulin secretion and attained a higher maximal response to glucose stimulation than those derived from fed rats. 4. Incubation in vitro of islets isolated from normal fed rats, for periods of 1 to 24h in the presence of high concentrations of glucose resulted in an activation of adenylate cyclase that occurred progressively from 2 to 7h and which was maintained during 24h of incubation. The increase of adenylate cyclase activity in isolated islets incubated for 4h in the presence of glucose was not prevented by addition of cycloheximide or actinomycin D. Galactose or 2-deoxyglucose was ineffective in increasing adenylate cyclase activity, and pyruvate (20mm) was less effective than glucose. 5. It is suggested that glucose or a glucose metabolite may exert long-term effects on islet cell adenylate cyclase.

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