scholarly journals Stimulation of β-adrenergic receptors plays a protective role via increased expression of RAF-1 and PDX-1 in hyperglycemic rat pancreatic islet (RIN-m5F) cells

2017 ◽  
Vol 2 ◽  
pp. 470-480 ◽  
Author(s):  
Sher Zaman Safi ◽  
Rajes Qvist ◽  
Gracie Ong ◽  
Hamed Karimian ◽  
Muhammad Imran ◽  
...  
1989 ◽  
Vol 67 (10) ◽  
pp. 1199-1204 ◽  
Author(s):  
J. A. Armour

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.


1999 ◽  
Vol 27 (Supplement) ◽  
pp. A70
Author(s):  
Walter H Newman ◽  
Manuel R Castresana ◽  
Zhongbiao Wang ◽  
Martin L Dalton ◽  
Debra J Warejcka

1986 ◽  
Vol 111 (2) ◽  
pp. 263-270 ◽  
Author(s):  
J. M. Fyles ◽  
M. A. Cawthorne ◽  
S. L. Howell

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


1969 ◽  
Vol 47 (5) ◽  
pp. 415-419 ◽  
Author(s):  
C. V. Greenway ◽  
Anne E. Lawson

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.


2021 ◽  
Author(s):  
Marion Barthé ◽  
Flora Lefebvre ◽  
Emilie Langlois ◽  
Florence Lefebvre ◽  
Patrick Lechêne ◽  
...  

AbstractMembrane proteins are present in both cardiac T-tubule (TTM) and outer surface membrane (OSM), although at a different density. Classical pharmacology does not allow to explore the function of a membrane protein separately in OSM vs. TTM. Here, we developed a technology based on size exclusion to explore the function of β-adrenergic receptors (β-ARs) located in the OSM. We synthetized a PEG-Iso molecule by covalent linking between isoprenaline (Iso) and a 5000 Da PolyEthylene-Glycol (PEG). Using confocal microscopy, we show that PEGylation constrains molecules outside the T-tubule network. PEG-Iso produced similar effects as Iso on Ica,L, sarcomere shortening and Ca2+ transients. However, PEG-Iso increased [cAMP]i with a lower efficacy than Iso, produced a much lower stimulation of nuclear PKA activity than Iso but a larger stimulation of cytosolic PKA at equivalent levels of [cAMP]i. Our results show that activation of OSM β-ARs is sufficient to activate cytosolic PKA and excitation-contraction coupling, but insufficient to activate nuclear PKA or nuclear protein phosphorylation for which additional activation of TTM β-ARs is needed.


1997 ◽  
Vol 110 (3) ◽  
pp. 217-228 ◽  
Author(s):  
Jesper Gromada ◽  
Krister Bokvist ◽  
Wei-Guang Ding ◽  
Sebastian Barg ◽  
Karsten Buschard ◽  
...  

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.


1993 ◽  
Vol 4 (3) ◽  
pp. 531-535
Author(s):  
Eleni Kousvelari ◽  
Chih-Ko Yeh

Stimulation of β-adrenergic receptors by isoproterenol or addition of 8-BrcAMP rapidly and transiently induces the expression of the protooncogenes, c-fos, and jun B, but not that of c-jun in A5 cells. These results indicate that different intracellular pathways may operate within the same cell for the induction of this group of early response genes. The inducibility of c-fos and jun B genes by either isoproterenol of 8-BrcAMP is transcriptionally regulated and accompanied by increases in their respective products. Furthermore, both c-fos and jun B mRNA levels are elevated at G0/G 1 phase of the A5 cell cycle and are inducible by isoproterenol or 8-BrcAMP at the different phases of the cell cycle. These data further suggest a possible role of c-fos and jun B in A5 cell cycle.


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