scholarly journals Adrenergic Modulation With Photochromic Ligands

2020 ◽  
Author(s):  
Davia Prischich ◽  
Alexandre M. J. Gomila ◽  
Santiago Milla‐Navarro ◽  
Gemma Sangüesa ◽  
Rebeca Diez‐Alarcia ◽  
...  
Keyword(s):  
Adrenergic Modulation

Adrenergic modulation of Ca2+ homeostasis in isolated fish hepatocytes

1992 ◽  
Vol 88 (2) ◽  
pp. 267-276 ◽  
Author(s):  
J. Zhang ◽  
M. Désilets ◽  
T.W. Moon
Keyword(s):  
Adrenergic Modulation

Myocardial Performance and Adrenergic Modulation of Cyclic AMP Following Endotoxin Administration

1986 ◽  
pp. 171-185
Author(s):  
Raymond E. Shepherd ◽  
Charles H. Lang ◽  
Brent A. Brumfield ◽  
Norman W. Robie ◽  
Karen R. DuSapin ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Myocardial Performance ◽  
Endotoxin Administration ◽  
Adrenergic Modulation

Beta-adrenergic modulation of Na-K pump activity in young and adult canine cardiac Purkinje fibers

1996 ◽  
Vol 271 (2) ◽  
pp. H706-H712
Author(s):  
F. Charpentier ◽  
M. J. Legato ◽  
S. F. Steinberg ◽  
I. S. Cohen ◽  
M. R. Rosen
Keyword(s):  
Cell Surface ◽  
Volume Ratio ◽  
Beta Adrenergic ◽  
Purkinje Fibers ◽  
Age Related ◽  
Cardiac Purkinje Fibers ◽  
Adrenergic Modulation ◽  
Pump Activity ◽  
The Difference ◽  
Beta Adrenergic Agonist

We used standard microelectrode techniques to study the developmental changes and beta-adrenergic modulation of membrane potential and of Na-K pump activity in adult (> 1 yr of age) and neonatal (2-10 days) canine Purkinje fibers. Isoproterenol (10(-7) M) increased the rate of development and magnitude of pacing-induced hyperpolarization of adult fibers driven at a 1-s cycle length. This effect of isoproterenol was attenuated by treating dogs with pertussis toxin (PTX), (30 micrograms/kg). Other adult and neonatal fibers were superfused with a Tyrode solution containing Ba2+ 0.2 mM, Cs+ 2 mM, and 10(-6) M verapamil, thus leading to depolarization and cessation of spontaneous activity. The Na-K pump was studied by alternating solutions containing [K] at 0 mM (inhibiting the pump) and 4 mM (reactivating the pump). Although the kinetics of the Na-K pump appeared faster in neonatal fibers than in adult fibers, measurement of cell surface-to-volume ratio compensated for the difference. We therefore conclude that 1) the apparent age-related changes in Na-K pump activity in canine Purkinje fibers in fact reflect cell surface-to-volume ratio and, 2) the beta-adrenergic agonist-induced hyperpolarization in adults requires the presence of a PTX-sensitive G protein for its occurrence.

Modulation of K channels by coexpressed human alpha1C-adrenoceptor in Xenopus oocytes

1997 ◽  
Vol 272 (3) ◽  
pp. H1275-H1286
Author(s):  
G. N. Tseng ◽  
J. A. Yao ◽  
J. Tseng-Crank
Keyword(s):  
Protein Kinase ◽  
Model System ◽  
K Channel ◽  
K Channels ◽  
Channel Modulation ◽  
Channel Function ◽  
Adrenergic Modulation ◽  
Intracellular Ca ◽  
Dependent Protein ◽  
Multiple Receptor

alpha1-Adrenoceptors participate in the regulation of inotropy and chronotropy in the heart. Modulation of cardiac K-channel function plays an important role in these alpha1-adrenergic functions. Studies of the mechanisms of K-channel modulation by alpha1-adrenoceptors are hampered by the coexistence of multiple receptor and channel subtypes in the heart. We therefore used a model system of coexpressing a specific receptor (human alpha1c-adrenoceptor) and a K-channel clone (hIsK, rKv1.2, or rKv1.4) in oocytes. alpha1c-Adrenoceptor stimulation caused a rapid upregulation of hIsK by elevating the intracellular Ca concentration. At least part of this effect was due to an activation of calmodulin and Ca/calmodulin-dependent protein kinase II. On the other hand, alpha1c-adrenoceptor stimulation caused a slow downregulation of rKv1.2 and rKvl.4 by activating protein kinase C. The differential modulation of K channels by alpha1c-adrenoceptors demonstrated in our experiments corroborates the complexity of alpha1-adrenergic functions in the heart. Our results indicate that the oocyte model system can be a useful approach in studying alpha1-adrenergic modulation of ion-channel function and signal transduction.

Mechanism of action of cholecystokinin octapeptide on cat lower esophageal sphincter

1992 ◽  
Vol 263 (3) ◽  
pp. G419-G425 ◽  
Author(s):  
A. M. Salapatek ◽  
T. Hynna-Liepert ◽  
N. E. Diamant
Keyword(s):  
Lower Esophageal Sphincter ◽  
Mechanism Of Action ◽  
Trimethylammonium Chloride ◽  
Cholinergic Mechanism ◽  
Cholecystokinin Octapeptide ◽  
Inhibitory Mechanisms ◽  
Adrenergic Modulation ◽  
Ketamine Anesthesia ◽  
Esophageal Sphincter

In five cats we examined 1) the role of a cholinergic mechanism in cholecystokinin octapeptide (CCK-OP) excitation of the lower esophageal sphincter (LES) and 2) the interaction between CCK-OP-induced excitation and inhibition of the LES. Under ketamine anesthesia, LES pressure was monitored with a sleeve catheter. With CCK-OP, LES excitation was seen in four of five cats, and inhibition was seen in three of five cats. (4-Hydroxy-2-butynyl)trimethylammonium chloride (McNeil-A343) produced similar responses in the same cats but was less potent than CCK-OP. Atropine and/or hexamethonium reduced the response to CCK-OP. Pirenzepine had no effect on any CCK-OP response but reduced relaxation and enhanced excitation produced by McNeil-A343. Phentolamine increased CCK-OP-induced relaxation. In conclusion, CCK-OP can produce LES contraction through a preganglionic cholinergic mechanism involving a nicotinic synapse; however, induction of relaxation occurs predominantly at a postganglionic site involving adrenergic modulation. There is animal-to-animal variability in the balance of excitatory and inhibitory mechanisms to the LES, which determines the effect of a drug capable of activating both mechanisms.

beta-Adrenergic modulation of Ba2+ currents and K+ contractures in frog slow skeletal muscle fibers

1997 ◽  
Vol 272 (1) ◽  
pp. C77-C81 ◽  
Author(s):  
M. Huerta ◽  
X. Trujillo ◽  
C. Vasquez
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fibers ◽  
Isometric Tension ◽  
External Application ◽  
Beta Adrenergic ◽  
Cyclic Monophosphate ◽  
Slow Skeletal Muscle ◽  
Skeletal Muscle Fibers ◽  
Adrenergic Modulation ◽  
Ca2 Channels

beta-Adrenergic modulation of the Ba2+ current (IBa) and K+ contracture in slow skeletal muscle fibers of the frog (Rana pipiens) were investigated in intact fibers with the three-microelectrode voltage-clamp technique and isometric tension measurements. Application of epinephrine (10(-6) to 10(-5) M) to the bath increased the amplitude of IBa. This increase was blocked by the beta-antagonist propranolol (3 microM), and a similar increase was observed with the beta-specific agonist isoproterenol (1 microM). Thus the epinephrine effect was mediated mainly by beta-adrenergic receptors. External application of permeable 8-bromoadenosine 3',5'-cyclic monophosphate (0.5 mM) increased the amplitude of both IBa and K+ contractures. The present results suggest that beta-adrenergic modulation of IBa in slow skeletal muscle fibers could reflect a modulation of Ca2+ channels via adenosine 3',5'-cyclic monophosphate (cAMP). cAMP (0.5 mM) also potentiated the K(+)-evoked tension in these slow fibers. The physiological contribution made by the modulation of slow skeletal muscle Ca2+ channels to the increase in tension is still not completely understood.

The α1- and β1-Adrenergic Modulation of Lacrimal Gland Function in the Mouse

2007 ◽  
Vol 48 (4) ◽  
pp. 1504 ◽  
Author(s):  
Chuanqing Ding ◽  
Benjamin Walcott ◽  
Kent T. Keyser
Keyword(s):  
Lacrimal Gland ◽  
Adrenergic Modulation ◽  
Gland Function
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