β-adrenergic mobilization of Ca2+ from an intracellular store in rat submandibular acini

1993 ◽  
Vol 293 (3) ◽  
pp. 691-695 ◽  
Author(s):  
C Lloyd Mills ◽  
M B Hallett ◽  
M A McPherson ◽  
R L Dormer
Keyword(s):  
Adrenergic Stimulation ◽  
Mucin Secretion ◽  
Beta Adrenergic ◽  
Intracellular Store ◽  
Submandibular Acini

Increases in cytoplasmic free Ca2+ concentration in rat submandibular acini were observed in response to isoprenaline (10 microM), noradrenaline (10 microM) and carbamoylcholine (10 microM). Noradrenaline and carbamoylcholine responses were decreased to 27% and 33% respectively in the absence of extracellular Ca2+, suggesting a major requirement for Ca2+ entry. beta-Adrenergic stimulation elicited a small (35-40 nM) free Ca2+ rise, approx. 75% of which was mobilized from an intracellular store. Results suggest that this Ca2+ rise is a key event in the physiological triggering of mucin secretion by exocytosis.

scholarly journals Adrenergic regulation of formation of inositol phosphates in rat submandibular acini

1987 ◽  
Vol 241 (3) ◽  
pp. 705-709 ◽  
Author(s):  
C Doughney ◽  
R L Dormer ◽  
M A McPherson
Keyword(s):  
Inositol Phosphates ◽  
Second Messengers ◽  
Inositol Polyphosphate ◽  
Adrenergic Stimulation ◽  
Mucin Secretion ◽  
Beta Adrenergic ◽  
Inositol Polyphosphates ◽  
Inositol Tetrakisphosphate ◽  
Submandibular Acini ◽  
Stimulation Of

Formation of inositol phosphates in response to adrenergic secretagogues was studied in rat submandibular acini labelled with myo-[2-3H]inositol. Noradrenaline rapidly (within 5 s) increased radioactivity incorporated into inositol 1,4,5-trisphosphate and inositol tetrakisphosphate, with less rapid (within 1 min) increases in inositol 1,3,4-trisphosphate being observed. Inositol polyphosphate formation was less sensitive to noradrenaline than was stimulation of mucin secretion and was mediated by stimulation of alpha- but not beta-adrenergic receptors. The beta-adrenergic agonist isoproterenol, which is a potent stimulator of mucin secretion [McPherson & Dormer (1984) Biochem. J. 224, 473-481] did not increase formation of inositol mono-, bis- or polyphosphates during a 15 min incubation. The results suggest that inositol phosphates do not mediate beta-adrenergic stimulation of mucin secretion in rat submandibular acini. In addition, rat submandibular acinar cells contain a Ca2+ pool which can be mobilized by isoproterenol [McPherson & Dormer (1984) Biochem. J. 224, 473-481], without involvement of inositol polyphosphates as second messengers.

Role of protein phosphorylation in regulating rat submandibular mucin secretion

1983 ◽  
Vol 245 (1) ◽  
pp. G44-G53 ◽  
Author(s):  
D. O. Quissell ◽  
L. M. Deisher ◽  
K. A. Barzen
Keyword(s):  
Plasma Membrane ◽  
Protein Phosphorylation ◽  
Adrenergic Receptor ◽  
Enzyme Analysis ◽  
Dibutyryl Camp ◽  
Adrenergic Stimulation ◽  
Mucin Secretion ◽  
Receptor Stimulation ◽  
Beta Adrenergic ◽  
Camp Stimulation

The possible involvement of protein phosphorylation during beta-adrenergic receptor stimulation in rat submandibular gland was investigated in vitro using a dispersed cell preparation. (-)-Isoproterenol, a beta-adrenergic agonist, or dibutyryl cAMP stimulation was associated with an enhanced phosphorylation of three protein bands having apparent molecular weights of 34,000, 26,000, and 21,000, respectively. (-)-Propranolol, a beta-adrenergic antagonist, inhibited the phosphorylation of the three proteins during beta-adrenergic stimulation but not during dibutyryl cAMP stimulation. The three proteins were not fragments of a higher-molecular-weight protein. Subcellular fractionation using differential centrifugation, fractionation in an aqueous two-phase polymer system, and discontinuous sucrose gradient ultracentrifugation coupled with marker enzyme analysis indicated that all three proteins were enriched in the same subfractions: a heavy plasma membrane fraction and a fraction containing plasma membrane and Golgi membrane material. The extent of protein phosphorylation for all three proteins increased as a function of time and dose after beta-adrenergic stimulation. After 20 min of maximal beta-adrenergic stimulation, the addition of a beta-adrenergic blocker caused a time-dependent decrease in the 32P content of all three proteins. Pure cholinergic or pure alpha-adrenergic receptor stimulation had no effect on the 32P content of the three proteins. These data are consistent with a role for cAMP-mediated protein phosphorylation during mucin secretion from rat submandibular cells.

Compounds that increase cAMP prevent ischemia-reperfusion pulmonary capillary injury

1992 ◽  
Vol 72 (2) ◽  
pp. 492-497 ◽  
Author(s):  
W. K. Adkins ◽  
J. W. Barnard ◽  
S. May ◽  
A. F. Seibert ◽  
J. Haynes ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Vascular Permeability ◽  
Vascular Resistance ◽  
Capillary Permeability ◽  
Ischemia Reperfusion ◽  
Receptor Activation ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Beta Receptor ◽  
Pulmonary Capillary

This study evaluated the physiological effects of compounds that increase adenosine 3′,5′-cyclic monophosphate (cAMP) on changes in pulmonary capillary permeability and vascular resistance induced by ischemia-reperfusion (I-R) in isolated blood-perfused rabbit lungs. cAMP was elevated by 1) beta-adrenergic stimulation with isoproterenol (ISO, 10(-5) M), 2) post-beta-receptor stimulation of adenylate cyclase with forskolin (FSK, 10(-5) M), 3) and dibutyryl cAMP (DBcAMP, 1 mM), a cAMP analogue. Vascular permeability was assessed by determining the capillary filtration coefficient (Kf,c), and capillary pressure was measured using the double occlusion technique. The total, arterial, and venous vascular resistances were calculated from measured pulmonary arterial, venous, and capillary pressures and blood flow. Reperfusion after 2 h of ischemia significantly (P less than 0.05) increased Kf,c (from 0.115 +/- 0.028 to 0.224 +/- 0.040 ml.min-1.cmH2O-1.100 g-1). These I-R-induced changes in capillary permeability were prevented when ISO, FSK, or DBcAMP was added to the perfusate at reperfusion (0.110 +/- 0.022 and 0.103 +/- 0.021, 0.123 +/- 0.029 and 0.164 +/- 0.024, and 0.153 +/- 0.030 and 0.170 +/- 0.027 ml.min-1.cmH2O-1.100 g-1, respectively). I-R significantly increased total, arterial, and venous vascular resistances. These increases in vascular resistance were also blocked by ISO, FSK, and DBcAMP. These data suggest that beta-adrenergic stimulation, post-beta-receptor activation of adenylate cyclase, and DBcAMP prevent the changes in pulmonary vascular permeability and vascular resistances caused by I-R in isolated rabbit lungs through a mechanism involving an increase in intracellular levels of cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Different effects of alpha- and beta-adrenergic stimulation on cytosolic pH and myofilament responsiveness to Ca2+ in cardiac myocytes.

1992 ◽  
Vol 71 (4) ◽  
pp. 870-882 ◽  
Author(s):  
G Gambassi ◽  
H A Spurgeon ◽  
E G Lakatta ◽  
P S Blank ◽  
M C Capogrossi
Keyword(s):  
Cardiac Myocytes ◽  
Adrenergic Stimulation ◽  
Cytosolic Ph ◽  
Beta Adrenergic

Relation between contractile function and regulatory cardiac proteins in hypertrophied hearts

1996 ◽  
Vol 270 (6) ◽  
pp. H2021-H2028 ◽  
Author(s):  
B. Stein ◽  
S. Bartel ◽  
U. Kirchhefer ◽  
S. Kokott ◽  
E. G. Krause ◽  
...  
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Troponin I ◽  
Contractile Function ◽  
Papillary Muscles ◽  
Camp Accumulation ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
C Protein ◽  
Camp Formation ◽  
Phosphate Incorporation

The aim of this study was to examine the mechanism(s) underlying the reduced isoproterenol-induced positive inotropic and lusitropic effects in hypertrophied hearts. Chronic beta-adrenergic stimulation (2.4 mg isoproterenol.kg-1. day-1 for 4 days) induced cardiac hypertrophy by 33 +/- 2% in rats. A parallel downregulation of phospholamban (PLB) and sarcoplasmic reticulum Ca2(+)-ATPase (SERCA2) protein expression by 49 and 40%, respectively, was observed, whereas troponin I (TNI) and C protein remained unchanged. In papillary muscles from chronically beta-adrenergically stimulated rats, the isoproterenol-induced positive inotropic and lusitropic effects, as well as adenosine 3',5'-cyclic monophosphate (cAMP) accumulation, were attenuated compared with those in control animals. Acute exposure to isoproterenol induced phosphate incorporation into PLB, TNI, and C protein of 48 +/- 4.6, 55 +/- 5.0, and 27 +/- 4.9 pmol/mg homogenate protein, respectively, in control animals. In the hypertrophied hearts, phosphate incorporation into PLB was reduced by 76%, whereas phosphate incorporation into TNI or C protein remained unchanged. In conclusion, chronic beta-adrenergic stimulation reduced the isoproterenol-stimulated positive inotropic and lusitropic effects in papillary muscles, which were accompanied by 1) diminished cAMP formation, 2) attenuation of cAMP-mediated PLB phosphorylation, and 3) downregulation of PLB and SERCA2 protein.

Changes in vascular responsiveness following chronic exposure to cold in the rat

1983 ◽  
Vol 55 (3) ◽  
pp. 823-829 ◽  
Author(s):  
B. A. Bryar ◽  
M. J. Fregly ◽  
F. P. Field
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscles ◽  
Aortic Tissue ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Aortic Smooth Muscle ◽  
Beta Adrenergic Agonists ◽  
Adrenergic Antagonist ◽  
Vascular Responsiveness ◽  
High Concentrations

The responsiveness of smooth muscle from rings of aortic tissue of cold-acclimated (CA, 6 degrees C, 5-15 wk) rats to both alpha- and beta-adrenergic agonists and KCl was tested and compared with that of warm-adapted (25 degrees C) controls. alpha-Adrenergic stimulation, induced by low doses (10(-8)-10(-7) M) of phenylephrine and norepinephrine in the presence and absence of the beta-adrenergic antagonist, propranolol, resulted in the development of less active tension by aortic smooth muscle from CA rats than from controls. Similar results were observed with the weakly alpha 1-adrenergic agonistic activities of tyramine, clonidine, and high concentrations of isoproterenol (10(-6)-10(-4) M). There was also a significant reduction in the tension developed by smooth muscles of the aortas from CA rats when depolarized with KCl in concentrations ranging from 8 to 20 mM. In contrast, aortic smooth muscle, contracted to 75% of maximum with KCl, showed an enhanced relaxation to the beta-adrenergic agonist, isoproterenol, in CA rats. These studies suggest that acclimation of rats to cold results in both a decrease in alpha-adrenergic responsiveness and an increase in beta-adrenergic responsiveness in vascular smooth muscle as well as a change in the biochemical events that couple activation of adrenergic receptors to changes in vasomotor tone.

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