scholarly journals Adrenaline Stimulates Glucagon Secretion in Pancreatic A-Cells by Increasing the Ca2+ Current and the Number of Granules Close to the L-Type Ca2+ Channels

1997 ◽  
Vol 110 (3) ◽  
pp. 217-228 ◽  
Author(s):  
Jesper Gromada ◽  
Krister Bokvist ◽  
Wei-Guang Ding ◽  
Sebastian Barg ◽  
Karsten Buschard ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Adrenergic Receptors ◽  
Action Potentials ◽  
Glucagon Secretion ◽  
Stimulatory Action ◽  
Voltage Gated ◽  
A Cells ◽  
Β Adrenergic Receptors ◽  
Ca2 Channels ◽  
Stimulation Of

We have monitored electrical activity, voltage-gated Ca2+ currents, and exocytosis in single rat glucagon-secreting pancreatic A-cells. The A-cells were electrically excitable and generated spontaneous Na+- and Ca2+-dependent action potentials. Under basal conditions, exocytosis was tightly linked to Ca2+ influx through ω-conotoxin-GVIA–sensitive (N-type) Ca2+ channels. Stimulation of the A-cells with adrenaline (via β-adrenergic receptors) or forskolin produced a greater than fourfold PKA-dependent potentiation of depolarization-evoked exocytosis. This enhancement of exocytosis was due to a 50% enhancement of Ca2+ influx through L-type Ca2+ channels, an effect that accounted for <30% of the total stimulatory action. The remaining 70% of the stimulation was attributable to an acceleration of granule mobilization resulting in a fivefold increase in the number of readily releasable granules near the L-type Ca2+ channels.

α-Adrenergic receptor modulation of the intrathoracic efferent sympathetic nervous system regulating the canine heart

1989 ◽  
Vol 67 (10) ◽  
pp. 1199-1204 ◽  
Author(s):  
J. A. Armour
Keyword(s):  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Blocking Agent ◽  
Sympathetic Ganglia ◽  
Canine Heart ◽  
Receptor Modulation ◽  
Adrenergic Antagonist ◽  
Cervical Ganglia ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The augmentation of ventricular inotropism induced by electrical stimulation of acutely decentralized efferent sympathetic preganglionic axons was reduced, but still present, following administraiton of hexamethonium (10 mg/kg i.v.). While hexamethonium continued to be administered, the cardiac augmentations so induced were enhanced significantly following administration of the α-adrenergic receptor blocking agent, phentolamine myselate (1 mg/kg i.v.). Stimulation of the sympathetic efferent postganglionic axons in cardiopulmonary nerves induced cardiac augmentations that were unchanged following administration of these agents singly or together. The cardiac augmentations induced by stimulation of efferent preganglionic sympathetic axons were unchanged when phentolamine was administered alone. The augmentations of cardiac inotropism induced by efferent postganglionic sympathetic axonal stimulation were decreased following local administration of the β-adrenergic antagonist timolol into the ipsilateral stellate and middle cervical ganglia. Thereafter, these augmentations were unchanged following the subsequent intravenous administration of phentolamine. It is concluded that the activation of cardiac neurons in the stellate and middle cervical ganglia by stimulation of efferent preganglionic sympathetic axons can be modified by α-adrenergic receptors and that these effects are dependent upon β-adrenergic receptors, not nicotinic ones, in intrathoracic ganglia.Key words: α-adrenergic inotropism, sympathetic ganglia, hexamethonium, phentolamine.

Deoxyglucose and reduced glutathione mimic effects of hypoxia on K+ and Ca2+ conductances in pulmonary artery cells

1994 ◽  
Vol 267 (1) ◽  
pp. L52-L63 ◽  
Author(s):  
X. J. Yuan ◽  
M. L. Tod ◽  
L. J. Rubin ◽  
M. P. Blaustein
Keyword(s):  
Pulmonary Artery ◽  
Action Potentials ◽  
Reduced Glutathione ◽  
Metabolic Inhibitors ◽  
Common Mechanism ◽  
Pipette Solution ◽  
Voltage Gated ◽  
Kv Channels ◽  
Channel Inhibition ◽  
Ca2 Channels

Hypoxia-induced pulmonary vasoconstriction (HPV) is triggered by a rise in cytosolic Ca2+ concentration ([Ca2+]i) that is partially controlled by voltage-gated Ca2+ channels. Hypoxia inhibits voltage-gated K+ (KV) channels in pulmonary artery (PA) myocytes. This depolarizes the cells, opens voltage-gated Ca2+ channels, thereby increases [Ca2+]i, and initiates HPV. In intact animals and isolated perfused lungs, metabolic inhibitors and reducing agents augment HPV. We compared the effects of hypoxia with the glycolysis inhibitor, 2-deoxy-D-glucose (2-DOG), and the reducing agent, reduced glutathione (GSH), on voltage-gated steady-state K+ currents (IK,ss) and membrane potential (Em) in cultured rat pulmonary and mesenteric arterial (MA) smooth muscle cells. Bath application of 10 mM 2-DOG (glucose-free) or 5-10 mM GSH reversibly reduced IK,ss by 25-35% in PA myocytes, with 5 mM ATP present in the pipette solution. Neither hypoxia nor 2-DOG significantly affected IK,ss in MA myocytes, but GSH did reduce IK,ss in these cells. Furthermore, hypoxia, 2-DOG, and GSH depolarized PA cells in the absence as well as in the presence of external Ca2+. Hypoxia, 2-DOG, and GSH also evoked action potentials on the top of the steady depolarization in 36-50% of PA myocytes but not in any MA myocytes; removal of external Ca2+ abolished the action potentials without affecting the steady depolarization. These effects were comparable to those produced by 4-aminopyridine (5-10 mM), a blocker of KV channels. This implies that the action potentials are attributable to Ca2+ influx through voltage-gated Ca2+ channels opened by the steady depolarization due to KV channel inhibition. In the presence of 2-DOG or GSH, hypoxia had no further effect on IK,ss or Em in PA cells; this implies that hypoxia, 2-DOG, and GSH all block the same K+ channels. The data suggest that 1) the hypoxia-induced decrease of IK,ss and the resultant depolarization in PA myocytes may be related to a local decrease of intracellular ATP level and/or a change in redox status of the membrane or cytosol and 2) extracellular Ca(2+)-dependent action potentials may be responsible for at least part of the increase in [Ca2+]i during HPV. Similarities between the effects of hypoxia, 2-DOG, and GSH on IK,ss and Em in PA myocytes, along with the dissimilar responses of PA and MA myocytes, suggest that a common mechanism may underlie the responses of PA cells to these treatments.

Mechanism of sympathetic neural regulation of insulin, somatostatin, and glucagon secretion

1990 ◽  
Vol 258 (1) ◽  
pp. E220-E227 ◽  
Author(s):  
T. Kurose ◽  
Y. Seino ◽  
S. Nishi ◽  
K. Tsuji ◽  
T. Taminato ◽  
...  
Keyword(s):  
Glucagon Secretion ◽  
Fold Increase ◽  
Splanchnic Nerve ◽  
Stimulatory Action ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Adrenergic Mechanism ◽  
Adrenergic Activation ◽  
Splanchnic Nerve Stimulation ◽  
Stimulation Of

The effects of electrical stimulation of the left splanchnic nerve on insulin, somatostatin, and glucagon secretion from the isolated perfused rat pancreas were investigated. Electrical splanchnic nerve stimulation (SNS), performed by square-wave impulses, produced a 25% decrease in effluent flow and a 10-fold increase in perfusate norepinephrine. Both insulin and somatostatin output in the presence of 16.7 mM glucose were inhibited during SNS by 85 and 56% of the basal value, respectively. Glucagon output in the presence of 5.5 mM glucose was stimulated 20-fold by SNS. Perfusion with 10(-6) M propranolol further decreased insulin and somatostatin output during SNS, when expressed as the total decrement beneath basal during stimulation. The glucagon response to SNS tended to be enhanced, although not significantly, by simultaneous infusion of 10(-6) M propranolol. However, 10(-6) M phentolamine (Phe) attenuated the SNS-induced inhibition of insulin and somatostatin output by 50 and 40%, respectively. However, insulin output remained decreased after SNS with Phe. The SNS-induced glucagon response was completely abolished by 10(-6) M Phe alone or by 10(-6) M Phe plus 10(-6) M propranolol. With 10(-6) M Phe plus 10(-6) M propranolol, insulin and somatostatin output remained decreased after SNS. These results suggest that insulin and somatostatin secretions induced by glucose are inhibited during SNS through the alpha-adrenergic mechanism and also that the beta-adrenergic mechanism exerts a stimulatory action. SNS-induced glucagon secretion occurs mainly through alpha-adrenergic activation.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Membrane potential responses of paramecium caudatum to bitter substances: existence of multiple pathways for bitter responses

1998 ◽  
Vol 201 (1) ◽  
pp. 13-20
Author(s):  
K Oami
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Bathing Solution ◽  
Transduction Pathway ◽  
Paramecium Caudatum ◽  
External Application ◽  
Common Component ◽  
Voltage Gated ◽  
Mutant Cells ◽  
Ca2 Channels

The membrane potential responses of Paramecium caudatum to the external application of bitter substances were examined by employing conventional electrophysiological techniques. Mutant cells defective in voltage-gated Ca2+ channels were used to record the potential responses in the absence of contamination by Ca2+ action potentials. The cells produced a transient depolarization followed by a transient hyperpolarization in response to a rapid whole-cell application of chloroquine, strychnine nitrate or brucine. Of these chemicals, chloroquine was the most potent. Cells produced a simple depolarization in response to a localized application of test chemicals to the anterior region, whereas they produced a transient hyperpolarization in response to an application to the posterior region. Membrane potential responses to an application of chloroquine declined with repeated application. The presence of chloroquine in the external bathing solution strongly inhibited the membrane potential responses to an application of brucine or strychnine. However, the presence of chloroquine did not affect the membrane potential responses to an application of quinine. It is suggested that chloroquine, strychnine and brucine share a common component of their transduction pathways, but that the transduction pathway for quinine is different.

STIMULATION OF β-ADRENERGIC RECEPTORS INHIBITS TUMOR NECROSIS FACTOR ALPHA RELEASE FROM THE ISOLATED RAT HEART

1999 ◽  
Vol 27 (Supplement) ◽  
pp. A70
Author(s):  
Walter H Newman ◽  
Manuel R Castresana ◽  
Zhongbiao Wang ◽  
Martin L Dalton ◽  
Debra J Warejcka
Keyword(s):  
Tumor Necrosis Factor ◽  
Adrenergic Receptors ◽  
Tumor Necrosis ◽  
Isolated Rat Heart ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Β Adrenergic Receptors ◽  
Necrosis Factor ◽  
Isolated Rat ◽  
Stimulation Of

The characteristics of β-adrenergic binding sites on pancreatic islets of Langerhans

1986 ◽  
Vol 111 (2) ◽  
pp. 263-270 ◽  
Author(s):  
J. M. Fyles ◽  
M. A. Cawthorne ◽  
S. L. Howell
Keyword(s):  
Insulin Secretion ◽  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Islets Of Langerhans ◽  
Binding Sites ◽  
Adrenergic Receptors ◽  
Islet Cells ◽  
Pancreatic Islets Of Langerhans ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

ABSTRACT The sympathetic nervous system is believed to play a part in the control of insulin release from the pancreatic islets of Langerhans. Stimulation of α-adrenoceptors is thought to inhibit the release of insulin whereas stimulation of β-adrenoceptors enhances insulin release. The present experiments were conducted to establish the existence of β-adrenergic receptors on guinea-pig and rat islet cells and to quantify them using the selective β-adrenergic ligands [3H]dihydroalprenolol (DHA) and [125I]cyanoiodopindolol (CYP). Guinea-pig islets had 62 fmol β-adrenoceptors/mg protein using [3H]DHA, corresponding to 43 700 binding sites/cell and 25 fmol β-adrenoceptors/mg protein using [125I]CYP, corresponding to 17 400 sites/cell. Rat islet cells were found to have 4·6 fmol β-adrenoceptors/mg protein using [125I]CYP, corresponding to 7200 sites/cell. Adenylate cyclase activation exhibited a positive dose–response relationship when exposed to the β-adrenoceptor agonist isoprenaline, with a maximum response (190 ± 21% above basal) at 10 μmol isoprenaline/l. This response was abolished with 1 μmol/l of the β-adrenergic antagonist 1-alprenolol. Insulin secretion in the presence of 10 mmol glucose/l, but in the absence of the α-adrenoceptor blocker phentolamine, was not affected by 10 μmol isoprenaline/l. However, perifusion experiments showed that secretion of insulin from isolated rat islets in the presence of 10 mmol glucose/l was significantly increased (332%) by 10 μmol isoprenaline/l in the presence of 10 μmol phentolamine/l. These results suggest that binding of selective radio-labelled ligands occurs to β-adrenergic receptors on the B cell surface of the islets of Langerhans, and that these receptors are functionally coupled to insulin secretion through modulation of adenylate cyclase activity. J. Endocr. (1986) 111, 263–270

ACTIVATION OF HYPOTHALAMIC NEURONAL ACTIVITY BY THE ELECTROLYTIC DEPOSITION OF IRON INTO THE PREOPTIC AREA

1978 ◽  
Vol 79 (1) ◽  
pp. 107-NP ◽  
Author(s):  
P. VAN DER SCHOOT ◽  
D. W. LINCOLN ◽  
J. S. CLARK
Keyword(s):  
Electrical Activity ◽  
Action Potentials ◽  
Preoptic Area ◽  
Slow Wave Sleep ◽  
Platinum Electrode ◽  
Electrophysiological Recording ◽  
Electrolytic Deposition ◽  
Steel Electrode ◽  
Electrolytic Lesions ◽  
Stimulation Of

Changes in brain activity after electrochemical stimulation of the preoptic area of prooestrous rats were studied by the measurement of the electro-encephalogram (EEG) of the frontal cortex and the recording of single neurones in the anterior hypothalamus. All rats were anaesthetized with urethane between 10.00 and 12.00 h to allow prolonged electrophysiological recording and to block the spontaneous surge of LH during the afternoon. Electrochemical stimulation was applied, between 12.00 and 14.00 h, as an anodal current through an implanted steel electrode; this caused the electrolytic deposition of iron and evoked the release of LH and ovulation. Electrochemical stimulation of the preoptic area changed the cortical EEG, either immediately or after a delay of a few minutes, from a labile pattern with alternate periods of arousal and slow-wave sleep, to a stage of continuous arousal which persisted for the remainder of the recording period (2–3 h). Conversely, the EEG pattern of the cortex was not disturbed by electrolytic lesions placed in the preoptic area through a platinum electrode. Electrochemical stimulation of the arcuate region of the hypothalamus, the lateral septal area, the medial amygdaloid complex and the anterior parts of the thalamus caused no obvious change in the EEG patterns. Ipsilateral anterior hypothalamic neurones, about 1 mm caudal to the focus of electrochemical stimulation, displayed an immediate decrease in electrical activity after application of the current. After 10–20 min however, the rates of discharge of action potentials in 9 out of the 16 neurones under consideration increased progressively from 0·5 to 15–25 action potentials/s and these rates were maintained until the recordings were lost after 90–230 min. No such acceleration in electrical activity was observed in neurones on the contralateral side. Iron deposited during electrochemical stimulation was precipitated as sulphide and stained by Timm's method. There was a central damaged area of radius 0·6 mm surrounded by an 'undamaged' area with considerable infiltration of iron, up to a distance of 1·7 mm from the electrode tip. Cells within the area of infiltration did not stain for iron 10 min after electrochemical stimulation, but after 30 min, neural elements in this peripheral zone were stained in a manner similar to the Golgi method. The concentrations of LH in the plasma remained unchanged in all rats for 10–15 min after electrochemical stimulation. Thereafter, the concentrations increased progressively and approximately in parallel to the changes in action potential activity until, after 2 h, the individual concentrations of 300–600 ng LH/ml were more than six times the values obtained before stimulation. Bilateral electrochemical stimulation resulted in appreciably higher concentrations of LH and produced values close to those observed during the pro-oestrous surge of the hormone. Electrochemical stimulation during the afternoon of the day before pro-oestrus consistently advanced ovulation; this response occurred irrespective of whether the resultant lesions were large or small. The production of a large lesion during the afternoon of the day before pro-oestrus without concomitant deposition of iron by the use of a platinum electrode appeared to block the surge of LH on the subsequent day and the preovulatory follicles became atretic. These results suggest that the ovulatory response to electrochemical stimulation is related primarily to an increase in the electrical activity of the hypothalamus and not to the destruction of brain tissue.

β-Adrenergic receptors in the hepatic arterial bed of the anesthetized cat

1969 ◽  
Vol 47 (5) ◽  
pp. 415-419 ◽  
Author(s):  
C. V. Greenway ◽  
Anne E. Lawson
Keyword(s):  
Adrenergic Receptors ◽  
Electromagnetic Flowmeter ◽  
Sympathetic Nerves ◽  
Arterial Blood Flow ◽  
Arterial Infusion ◽  
Arterial Blood ◽  
Basal Tone ◽  
Β Receptor ◽  
Β Adrenergic Receptors ◽  
Stimulation Of

The hepatic arterial blood flow of cats anesthetized with pentobarbital was recorded with an electromagnetic flowmeter. Administration of isoprenaline by close arterial infusion caused a vasodilatation which was blocked after propranolol. Adrenaline caused a variable change but after propranolol it consistently produced vasoconstriction, and after phenoxybenzamine, vasodilatation. One hour after phenoxybenzamine, stimulation of the sympathetic nerves caused a marked vasodilatation which was blocked by propranolol. It is concluded that both α and β adrenergic receptors are present in the hepatic arterial bed. However, β receptor responses may be difficult to elicit if the basal tone of the vascular bed is already reduced by prior procedures.

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