Functional β2-adrenoceptors in rat left atria: effect of foot-shock stress

2017 ◽  
Vol 95 (9) ◽  
pp. 999-1008 ◽  
Author(s):  
André Luiz de Moura ◽  
Stephen Hyslop ◽  
Dora M. Grassi-Kassisse ◽  
Regina C. Spadari
Keyword(s):  
Receptor Antagonist ◽  
Adenylyl Cyclase ◽  
Left Atrial ◽  
Male Rats ◽  
Inotropic Response ◽  
Chronotropic Effect ◽  
Adenylyl Cyclase Activity ◽  
Altered Sensitivity ◽  
Right Atria ◽  
Shock Stress

Altered sensitivity to the chronotropic effect of catecholamines and a reduction in the β1/β2-adrenoceptor ratio have previously been reported in right atria of stressed rats, human failing heart, and aging. In this report, we investigated whether left atrial inotropism was affected by foot-shock stress. Male rats were submitted to 3 foot-shock sessions and the left atrial inotropic response, adenylyl cyclase activity, and β-adrenoceptor expression were investigated. Left atria of stressed rats were supersensitive to isoprenaline when compared with control rats and this effect was abolished by ICI118,551, a selective β2-receptor antagonist. Schild plot slopes for the antagonism between CGP20712A (a selective β1-receptor antagonist) and isoprenaline differed from unity in atria of stressed but not control rats. Atrial sensitivity to norepinephrine, as well as basal and forskolin- or isoprenaline-stimulated adenylyl cyclase activities were not altered by stress. The effect of isoprenaline on adenylyl cyclase stimulation was partially blocked by ICI118,551 in atrial membranes of stressed rats. These findings indicate that foot-shock stress equally affects inotropism and chronotropism and that β2-adrenoceptor upregulation contributes to the enhanced inotropic response to isoprenaline.

α1a-Adrenergic receptor mediated positive chronotropic effect in right atria isolated from rats

1994 ◽  
Vol 72 (12) ◽  
pp. 1574-1579 ◽  
Author(s):  
Anthony P. Williamson ◽  
Ernst Seifen ◽  
Jon P. Lindemann ◽  
Richard H. Kennedy
Keyword(s):  
Adrenergic Receptor ◽  
Response Curve ◽  
Male Rats ◽  
Chronotropic Effect ◽  
Rightward Shift ◽  
Spontaneous Rate ◽  
Negative Chronotropic Effect ◽  
Right Atria ◽  
Concentration Response Curve ◽  
Positive Chronotropic Effect

Experiments in right atria isolated from adult male rats were designed to determine which of the α1-adrenergic receptor (α1-AR) subtypes are involved in the positive chronotropic effect of phenylephrine, an α1-AR agonist. Chloroethylclonidine (CEC), an irreversible α1b-, α1c-, and α1d-AR antagonist, did not alter the efficacy or potency of phenylephrine; however, CEC did elicit a concentration-dependent negative chronotropic effect and reduce the absolute maximum spontaneous rate observed in the presence of phenylephrine. WB4101, a competitive α1a- and α1c-AR-selective antagonist, did not alter basal spontaneous rate or the efficacy of phenylephrine, but it did produce a significant rightward shift of the phenylephrine concentration–response curve. Phenoxybenzamine, an irreversible nonselective α-AR antagonist, elicited a concentration-dependent negative chronotropic effect, a significant rightward shift of the phenylephrine concentration–response curve, and a reduction in the efficacy of phenylephrine. The chronotropic action of the β-adrenergic agonist isoproterenol was not affected by CEC, WB4101, or phenoxybenzamine. These data suggest that the positive chronotropic effect of α1-adrenergic agonists in rat right atria is mediated via stimulation of α1a-ARs.Key words: α1-adrenergic receptor subtypes, chloroethylclonidine, WB4101, phenylephrine, right atria (rat).

Calcium Entry Attenuates Adenylyl Cyclase Activity

CHEST Journal ◽  
1995 ◽  
Vol 107 (5) ◽  
pp. 1420-1425 ◽  
Author(s):  
William B. Abernethy ◽  
John F. Butterworth ◽  
Richard C. Prielipp ◽  
Jian P. Leith ◽  
Gary P. Zaloga
Keyword(s):  
Adenylyl Cyclase ◽  
Calcium Entry ◽  
Cyclase Activity ◽  
Adenylyl Cyclase Activity

scholarly journals Spinal mechanisms contributing to the development of pain hypersensitivity induced by sphingolipids in the rat

2021 ◽  
Author(s):  
Hong Wei ◽  
Zuyue Chen ◽  
Ari Koivisto ◽  
Antti Pertovaara
Keyword(s):  
Amino Acid ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Gap Junction ◽  
Male Rats ◽  
Acid Oxidase ◽  
Amino Acid Oxidase ◽  
Mk 801 ◽  
Mechanical Hypersensitivity ◽  
Pain Hypersensitivity

Abstract Background Earlier studies show that endogenous sphingolipids can induce pain hypersensitivity, activation of spinal astrocytes, release of proinflammatory cytokines and activation of TRPM3 channel. Here we studied whether the development of pain hypersensitivity induced by sphingolipids in the spinal cord can be prevented by pharmacological inhibition of potential downstream mechanisms that we hypothesized to include TRPM3, σ1 and NMDA receptors, gap junctions and D-amino acid oxidase. Methods Experiments were performed in adult male rats with a chronic intrathecal catheter for spinal drug administrations. Mechanical nociception was assessed with monofilaments and heat nociception with radiant heat. N,N-dimethylsphingosine (DMS) was administered to induce pain hypersensitivity. Ononetin, isosakuranetin, naringenin (TRPM3 antagonists), BD-1047 (σ1 receptor antagonist), carbenoxolone (a gap junction decoupler), MK-801 (NMDA receptor antagonist) and AS-057278 (inhibitor of D-amino acid oxidase, DAAO) were used to prevent the DMS-induced hypersensitivity, and pregnenolone sulphate (TRPM3 agonist) to recapitulate hypersensitivity. Results DMS alone produced within 15 min a dose-related mechanical hypersensitivity that lasted at least 24 h, without effect on heat nociception. Preemptive treatments with ononetin, isosakuranetin, naringenin, BD-1047, carbenoxolone, MK-801 or AS-057278 attenuated the development of the DMS-induced hypersensitivity, but had no effects when administered alone. Pregnenolone sulphate (TRPM3 agonist) alone induced a dose-related mechanical hypersensitivity that was prevented by ononetin, isosakuranetin and naringenin. Conclusions Among spinal pronociceptive mechanisms activated by DMS are TRPM3, gap junction coupling, the σ1 and NMDA receptors, and DAAO.

scholarly journals The Capacity to Secrete Insulin Is Dose-Dependent to Extremely High Glucose Concentrations: A Key Role for Adenylyl Cyclase

Metabolites ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 401
Author(s):  
Katherine M. Gerber ◽  
Nicholas B. Whitticar ◽  
Daniel R. Rochester ◽  
Kathryn L. Corbin ◽  
William J. Koch ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Adenylyl Cyclase ◽  
Human Islets ◽  
Adenylyl Cyclase Activity ◽  
World Record ◽  
Glucokinase Activator ◽  
Amplifying Pathway ◽  
Dose Dependent ◽  
Adenylyl Cyclase Inhibitor ◽  
Cyclase Activator

Insulin secretion is widely thought to be maximally stimulated in glucose concentrations of 16.7-to-30 mM (300-to-540 mg/dL). However, insulin secretion is seldom tested in hyperglycemia exceeding these levels despite the Guinness World Record being 147.6 mM (2656 mg/dL). We investigated how islets respond to 1-h exposure to glucose approaching this record. Insulin secretion from human islets at 12 mM glucose intervals dose-dependently increased until at least 72 mM glucose. Murine islets in 84 mM glucose secreted nearly double the insulin as in 24 mM (p < 0.001). Intracellular calcium was maximally stimulated in 24 mM glucose despite a further doubling of insulin secretion in higher glucose, implying that insulin secretion above 24 mM occurs through amplifying pathway(s). Increased osmolarity of 425-mOsm had no effect on insulin secretion (1-h exposure) or viability (48-h exposure) in murine islets. Murine islets in 24 mM glucose treated with a glucokinase activator secreted as much insulin as islets in 84 mM glucose, indicating that glycolytic capacity exists above 24 mM. Using an incretin mimetic and an adenylyl cyclase activator in 24 mM glucose enhanced insulin secretion above that observed in 84 mM glucose while adenylyl cyclase inhibitor reduced stimulatory effects. These results highlight the underestimated ability of islets to secrete insulin proportionally to extreme hyperglycemia through adenylyl cyclase activity.

scholarly journals Calcium-Stimulated Adenylyl Cyclase Activity Is Critical for Hippocampus-Dependent Long-Term Memory and Late Phase LTP

Neuron ◽  
1999 ◽  
Vol 23 (4) ◽  
pp. 787-798 ◽  
Author(s):  
Scott T Wong ◽  
Jaime Athos ◽  
Xavier A Figueroa ◽  
Victor V Pineda ◽  
Michele L Schaefer ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Late Phase ◽  
Cyclase Activity ◽  
Long Term Memory ◽  
Adenylyl Cyclase Activity ◽  
Term Memory

A fluorimetric assay for real-time monitoring of adenylyl cyclase activity based on terbium norfloxacin

2008 ◽  
Vol 381 (1) ◽  
pp. 86-93 ◽  
Author(s):  
Corinna M. Spangler ◽  
Christian Spangler ◽  
Martin Göttle ◽  
Yuequan Shen ◽  
Wei-Jen Tang ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Real Time ◽  
Cyclase Activity ◽  
Real Time Monitoring ◽  
Adenylyl Cyclase Activity ◽  
Fluorimetric Assay

scholarly journals κ-Opioid receptor-transfected cell lines: modulation of adenylyl cyclase activity following acute and chronic opioid treatments

FEBS Letters ◽  
1995 ◽  
Vol 361 (1) ◽  
pp. 70-74 ◽  
Author(s):  
Tomer Avidor-Reiss ◽  
Renata Zippel ◽  
Rivka Levy ◽  
Danielle Saya ◽  
Vittoria Ezra ◽  
...  
Keyword(s):  
Adenylyl Cyclase ◽  
Opioid Receptor ◽  
Cell Lines ◽  
Cyclase Activity ◽  
Adenylyl Cyclase Activity
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