Alpha 2-receptors mediate catecholamine-stimulated acid secretion in Amphiuma jejunum

1988 ◽  
Vol 255 (5) ◽  
pp. G640-G646
Author(s):  
C. F. Hinton ◽  
J. F. White
Keyword(s):  
Acid Secretion ◽  
Basolateral Membrane ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Beta Adrenergic ◽  
Ussing Chambers ◽  
Adrenergic Antagonist ◽  
Half Maximal Effective Concentration ◽  
Uk 14,304 ◽  
Stimulation Of

The receptors mediating adrenergic stimulation of acid secretion by Amphiuma jejunum were characterized in this study using alpha- and beta-adrenergic agonists and antagonists. Isolated segments of jejunum were mounted in Ussing chambers and bathed in Cl- -free (SO4(2-] medium. Shortcircuit current (Isc) and acid secretion (JH) were recorded, the latter by measuring the rate of alkalinization of the serosal medium. The beta-adrenergic receptor antagonist, propranolol (10(-4) M), had no effect on the Isc and JH stimulated by norepinephrine (NE). The alpha 2-adrenergic agonists, clonidine and UK-14,304, mimicked the effect of NE, with effective concentrations providing 50% maximal delta Isc of 2.0 X 10(-7) and 9.0 X 10(-8) M, respectively. NE added subsequently produced no greater stimulation. In contrast, the alpha 1-adrenergic agonists, phenylephrine and methoxamine, produced little stimulation of JH and Isc; NE added subsequently stimulated the Isc. The alpha 1-adrenergic antagonist prazosin had no effect on the NE-induced Isc or JH, whereas the alpha 2-adrenergic antagonist yohimbine inhibited the NE-stimulated Isc with a half-maximal effective concentration of 3.5 X 10(-7) M. Yohimbine (10(-4) M) reduced the NE-stimulated Isc by 88%, whereas the spontaneous Isc was reduced by only 12%. These results demonstrate that alpha 2-adrenergic receptors on the basolateral membrane of Amphiuma enterocytes mediate NE-enhanced, but not spontaneous, intestinal acid secretion.

Effect of GRP on beta-adrenergic-stimulated gastrin and somatostatin release in the isolated rat stomach

1985 ◽  
Vol 249 (2) ◽  
pp. G197-G202 ◽  
Author(s):  
G. M. Short ◽  
G. M. Reel ◽  
J. W. Doyle ◽  
M. M. Wolfe
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Acid Output ◽  
Adrenergic Stimulation ◽  
Rat Stomach ◽  
Beta Adrenergic ◽  
Specific Antibodies ◽  
Gastrin Releasing Peptide ◽  
Isolated Rat ◽  
Stimulation Of

The present studies were directed toward examining the effects of gastrin-releasing peptide (GRP) on acid secretion and on beta-adrenergic-stimulated gastrin and somatostatin release using the isolated vascularly perfused rat stomach. Including pentagastrin in perfusion buffer increased acid output from 2.2 +/- 0.4 mueq H+/h during control perfusion to 18.8 +/- 1.8 mueq H+/h (P less than 0.01). No significant changes in acid secretion were detected when either GRP or specific antibodies to GRP were included in perfusate in the absence or presence of pentagastrin. Inclusion of 10(-9) M isoproterenol in the perfusate did not change acid output with respect to control; however, gastrin and somatostatin release into the portal venous effluent was significantly enhanced. Peak gastrin and somatostatin concentrations observed at 15 min were 753 +/- 43% (P less than 0.001) and 345 +/- 43% (P less than 0.01), respectively, of basal levels. When antibodies to GRP were included in perfusate containing isoproterenol, gastrin and somatostatin release into the portal venous effluent was significantly inhibited. The results of these studies indicate that GRP does not affect basal or pentagastrin-stimulated gastric acid secretion in the isolated perfused rat stomach. However, under the conditions of these experiments, beta-adrenergic stimulation of gastrin and somatostatin release appears to be mediated, at least in part, through GRP.

Alpha-adrenergic regulation of secretion by tracheal glands

1990 ◽  
Vol 259 (4) ◽  
pp. L198-L205 ◽  
Author(s):  
D. J. Culp ◽  
R. K. McBride ◽  
L. A. Graham ◽  
M. G. Marin
Keyword(s):  
Adrenergic Receptors ◽  
Specific Binding ◽  
Receptor Subtypes ◽  
Adrenergic Agonists ◽  
Beta Adrenergic ◽  
Adrenergic Regulation ◽  
Binding Characteristics ◽  
Low Concentrations ◽  
Adrenergic Antagonist ◽  
Uk 14,304

The purpose of the present study was to begin to characterize, pharmacologically, the alpha-adrenergic regulation of glycoconjugate secretion from airway glands. Using isolated gland cells from cat trachea, we determined the binding characteristics of [3H]dihydroergocryptine ([3H]DHE), an alpha-adrenergic antagonist, with equal affinities for alpha 1- and alpha 2-adrenergic receptors. Specific binding of [3H]DHE to gland cell homogenates was saturable, of high affinity (KDapp = 4.2 nM) and inhibited with greater efficacy by epinephrine much greater than isoproterenol. Competition experiments with alpha 1- and alpha 2-adrenergic selective antagonists (prazosin and yohimbine, respectively) demonstrated high- and low-affinity sites for each antagonist, indicating the presence of both receptor subtypes. In studies of glycoconjugate secretion by cat tracheal explants, secretion was stimulated by adrenergic agonists with the rank potency: norepinephrine greater than or equal to phenylephrine greater than epinephrine much greater than clonidine. alpha-Adrenergic-stimulated secretion (epinephrine + propranolol) was inhibited by low concentrations of prazosin, but was unaffected by 100 nM yohimbine. The alpha 2-adrenergic agonists, clonidine and UK-14,304, each markedly inhibited beta-adrenergic-stimulated secretion. Collectively, these results demonstrate alpha 1-adrenergic regulation of glandular glycoconjugate secretion and suggest alpha 2-adrenergic receptors may modulate beta-adrenergic-stimulated secretion.

Adrenergic Stimulation of Regional Plasminogen Activator Release in Rabbits

1992 ◽  
Vol 68 (05) ◽  
pp. 545-549 ◽  
Author(s):  
W L Chandler ◽  
S C Loo ◽  
D Mornin
Keyword(s):  
Lower Extremity ◽  
Plasminogen Activator ◽  
Beta Blocker ◽  
Time Course ◽  
Vascular System ◽  
Adrenergic Stimulation ◽  
Epinephrine Administration ◽  
Adrenergic Antagonist ◽  
Vascular Beds ◽  
Stimulation Of

SummaryThe purpose of this study was to determine whether different regions of the rabbit vascular system show variations in the rate of plasminogen activator (PA) secretion. To start, we evaluated the time course, dose response and adrenergic specificity of PA release. Infusion of 1 µg/kg of epinephrine stimulated a 116 ± 60% (SD) increase in PA activity that peaked 30 to 60 s after epinephrine administration. Infusion of 1 µg/kg of norepinephrine, isoproterenol and phenylephrine had no effect on PA activity. Pretreatment with phentolamine, an alpha adrenergic antagonist, blocked the release of PA by epinephrine while pretreatment with the beta blocker propranolol had no effect. This suggests that PA release in the rabbit was mediated by some form of alpha receptor.Significant arterio-venous differences in basal PA activity were found across the pulmonary and splanchnic vascular beds but not the lower extremity/pelvic bed. After stimulation with epinephrine, PA activity increased 46% across the splanchnic bed while no change was seen across the lower extremity/pelvic bed. We conclude that several vascular beds contribute to circulating PA activity in the rabbit, and that these beds secrete PA at different rates under both basal and stimulated conditions.

ANTAGONISM BETWEEN INSULIN AND SELECTIVE ADRENERGIC AGONISTS ON THE GLYCOGEN SYNTHETASE AND PHOSPHORYLASE SYSTEMS OF THE ISOLATED RAT DIAPHRAGM

1975 ◽  
Vol 78 (2) ◽  
pp. 392-400
Author(s):  
Arne T. Hostmark ◽  
Ole Grønnerød ◽  
Robert S. Horn
Keyword(s):  
Glycogen Metabolism ◽  
Rat Diaphragm ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Insulin Effect ◽  
Glycogen Synthetase ◽  
Adrenergic Antagonists ◽  
Fasted Rats ◽  
Isolated Rat ◽  
Stimulation Of

ABSTRACT The antagonism between insulin and selective adrenergic stimulation on the converting systems for glycogen synthetase and phosphorylase has been investigated in the isolated rat diaphragm. Insulin significantly inhibited stimulation by terbutaline and noradrenaline of phosphorylase b to a conversion as well as stimulation of glycogen synthetase I to D conversion by these agents. The inhibition by insulin was stronger on the synthetase system than on the phosphorylase system. The insulin effect was not dependent upon the presence of glucose. In diaphragms from 24 h fasted rats the response of the phosphorylase system to both agonists decreased. Inhibition by insulin of terbutaline stimulated phosphorylase conversion was maintained upon fasting while no effect of insulin against stimulation by noradrenaline could be obtained in diaphragms from fasted rats. The effects of fasting and insulin were not influenced by beta adrenergic antagonists (practolol and butoxamine). The results indicate a difference in sensitivity of the synthetase and phosphorylase systems to insulin and suggest that noradrenaline and terbutaline influence glycogen metabolism by differing mechanisms.

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.

scholarly journals Adrenergic stimulation of substrate utilization by cardiac myocytes isolated from rainbow trout

1991 ◽  
Vol 159 (1) ◽  
pp. 185-202 ◽  
Author(s):  
C. L. Milligan
Keyword(s):  
Rainbow Trout ◽  
Lactate Dehydrogenase ◽  
Cardiac Myocytes ◽  
Trypan Blue ◽  
Glycogen Content ◽  
Substrate Utilization ◽  
Co2 Production ◽  
Adrenergic Agonists ◽  
Adrenergic Stimulation ◽  
Stimulation Of

A method is described for the isolation of calcium-tolerant myocytes from adult rainbow trout. Isolated myocytes remain viable for at least 4 h in suspension as indicated by (1) maintenance of ATP, phosphocreatine (PCr) and glycogen levels; (2) maintenance of the integrity of cell membranes, shown by low rates of leakage of lactate dehydrogenase (LDH) to the medium and exclusion of Trypan Blue; (3) the ability to metabolize substrates; and (4) sensitivity to adrenergic agonists. CO2 production from both glucose and lactate was sensitive to adrenergic stimulation, with the following order of potency: isoproterenol greater than noradrenaline much greater than adrenaline greater than phenylephrine, which indicates the presence of beta 1-adrenoceptors. Myocytes isolated from trout acclimated to 20 degrees C in the summer were more sensitive to beta-adrenergic stimulation than myocytes isolated from trout acclimated to 9 degrees C in either summer or winter. In the absence of exogenous fuel, there was a net reduction in myocyte glycogen content and glycogenolysis was further stimulated by 10(−7) mmol l-1 noradrenaline. However, in the presence of exogenous fuel (either 5 mmol l-1 lactate or 5 mmol l-1 glucose), glycogen was ‘spared’ and noradrenaline-stimulated glycogenolysis was apparently inhibited.

Modulation of lung liquid clearance by isoproterenol in rat lungs

1998 ◽  
Vol 274 (5) ◽  
pp. L694-L701 ◽  
Author(s):  
F. Saldías ◽  
E. Lecuona ◽  
E. Friedman ◽  
M. L. Barnard ◽  
K. M. Ridge ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Basolateral Membrane ◽  
Alveolar Type ◽  
Type Ii Cells ◽  
Type Ii ◽  
Adrenergic Stimulation ◽  
Alveolar Type Ii Cells ◽  
Rat Lungs ◽  
Lung Liquid ◽  
Stimulation Of

β-Adrenergic agonists have been reported to increase lung liquid clearance by stimulating active Na+ transport across the alveolar epithelium. We studied mechanisms by which β-adrenergic isoproterenol (Iso) increases lung liquid clearance in isolated perfused fluid-filled rat lungs. Iso perfused through the pulmonary circulation at concentrations of 10−4 to 10−8 M increased lung liquid clearance compared with that of control lungs ( P < 0.01). The increase in lung liquid clearance was inhibited by the β-antagonist propranolol (10−5 M), the Na+-channel blocker amiloride (10−4 M), and the antagonist of Na-K-ATPase, ouabain (5 × 10−4 M). Colchicine, which inhibits cell microtubular transport of ion-transporting proteins to the plasma membrane, blocked the stimulatory effects of Iso on active Na+ transport, whereas the isomer lumicolchicine, which does not affect cell microtubular transport, did not inhibit Na+ transport. In parallel with these changes, the Na-K-ATPase α1-subunit protein abundance and activity increased in alveolar type II cells stimulated by 10−6 M Iso. Colchicine blocked the stimulatory effect of Iso and the recruitment of Na-K-ATPase α1-protein to the basolateral membrane of alveolar type II cells. Accordingly, Iso increased active Na+ transport and lung liquid clearance by stimulation of β-adrenergic receptors and probably by upregulation of apical Na+ channels and basolateral Na-K-ATPase mechanisms. Recruitment from intracellular pools and microtubular transport of Na+pumps to the plasma membrane participate in β-adrenergic stimulation of lung liquid clearance in rat lungs.

beta-Adrenergic stimulation of respiratory ciliary activity

1980 ◽  
Vol 48 (5) ◽  
pp. 868-871 ◽  
Author(s):  
P. Verdugo ◽  
N. T. Johnson ◽  
P. Y. Tam
Keyword(s):  
Respiratory Epithelium ◽  
Ciliary Activity ◽  
Ciliated Cells ◽  
Adrenergic Stimulation ◽  
Laser Scattering ◽  
Beta Adrenergic ◽  
Ciliary Beating ◽  
Stimulation Of

We investigated the effect of isoproterenol on ciliary activity using a mucus-free preparation of cultured ciliated cells of the rabbit trachea. The frequency of ciliary beating was monitored by dynamic laser-scattering spectroscopy. The results demonstrated that isoproterenol directly stimulates the activity of ciliated cells of the respiratory epithelium and that this effect is beta-adrenergic specific inasmuch as the observed stimulation can be blocked by propranolol.

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