scholarly journals Relationship between intrinsic activity of .BETA.-adrenoceptor agonist and amount of spare receptors in guinea pig taenia caecum.

1983 ◽  
Vol 33 (2) ◽  
pp. 327-333 ◽  
Author(s):  
Katsuo KOIKE ◽  
Issei TAKAYANAGI
Keyword(s):  
Guinea Pig ◽  
Intrinsic Activity ◽  
Spare Receptors ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonist

scholarly journals Cyclic AMP-evoked oscillations of intracellular [Ca2+] in guinea-pig hepatocytes

1991 ◽  
Vol 275 (1) ◽  
pp. 277-280 ◽  
Author(s):  
T Capiod ◽  
J Noel ◽  
L Combettes ◽  
M Claret
Keyword(s):  
Angiotensin Ii ◽  
Cyclic Amp ◽  
Guinea Pig ◽  
Intracellular Perfusion ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Patch Pipette

The effects of the beta-adrenoceptor agonist isoprenaline and cyclic AMP (cAMP) on cytosolic free Ca2+ ([Ca2+]i) were studied in the single guinea-pig hepatocyte. In common with InsP3-dependent agonists such as noradrenaline or angiotensin II, isoprenaline (0.5-10 microM) and cAMP (50-100 mM, perfused into the cell via the patch-pipette), were able to generate fast and slow fluctuations of [Ca2+]i. Responses to isoprenaline and cAMP also were observed in the absence of external Ca2+. Isoprenaline-evoked [Ca2+]i rises were not blocked by the intracellular perfusion of heparin, suggesting that these fluctuations are independent of the binding of InsP3 to its receptor.

Inhibitory potency of isoprenaline on guinea-pig and gravid human myometrium following extraneuronal uptake blockade

1995 ◽  
Vol 7 (1) ◽  
pp. 59
Author(s):  
M Kousides ◽  
ME Story ◽  
JN Pennefather ◽  
SP Ziccone ◽  
AW Ross
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Human Myometrium ◽  
Inhibitory Effects ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Myometrial Contractility ◽  
Beta Adrenoceptor Agonists ◽  
Evoked Contractions

The hypothesis that inhibitory effects of isoprenaline on myometrial contractility may be constrained by activation of putative intracellular beta-adrenoceptors negatively-coupled to adenylate cyclase was examined. Field-stimulated preparations of guinea-pig and human myometrium were used to examine the influence of the catecholamine extraneuronal uptake2 inhibitors, corticosterone and beta-oestradiol, on the inhibitory effects of the beta-adrenoceptor agonist, isoprenaline, on uterine contraction. Longitudinal and circular myometrial layers were obtained from guinea-pigs in dioestrus, primed with oestrogen before progesterone, or pregnant (Days 62-65). In the guinea-pig myometrium, corticosterone (30 microM) did not affect responses to isoprenaline. beta-oestradiol (10 microM) induced a small potentiation of the effects of isoprenaline on longitudinal myometrium from dioestrus guinea-pigs. Myometrial preparations were obtained from pregnant women (36-40 weeks gestation) undergoing caesarean section. Isoprenaline inhibited stimulation-evoked contractions in 7 of 10 preparations of the inner myometrial layer and in 5 of 8 preparations of outer myometrial layer. Corticosterone (30 microM) reduced the effects of isoprenaline on the inner layer and did not affect the outer layer. These results do not support the existence of mechanism involving isoprenaline-sensitive intracellular receptors which constrain responses to beta-adrenoceptor agonists.

Actions of norepinephrine on rat hypoglossal motoneurons

1995 ◽  
Vol 74 (5) ◽  
pp. 1911-1919 ◽  
Author(s):  
M. A. Parkis ◽  
D. A. Bayliss ◽  
A. J. Berger
Keyword(s):  
Choline Chloride ◽  
Reversal Potential ◽  
Repetitive Firing ◽  
Inward Current ◽  
Hypoglossal Motoneurons ◽  
Beta Adrenoceptor ◽  
Adrenoceptor Antagonist ◽  
Perfusion Solution ◽  
Adrenoceptor Agonist ◽  
Firing Properties

1. We used conventional intracellular recording techniques in 400-microns-thick slices from the brain stems of juvenile rats to investigate the action of norepinephrine (NE) on subthreshold and firing properties of hypoglossal motoneurons (HMs). 2. In recordings in current-clamp mode, 50 or 100 microM NE elicited a reversible depolarization accompanied by an increase in input resistance (RN) in all HMs tested (n = 74). In recordings in single-electrode voltage-clamp mode, NE induced a reversible inward current (INE) accompanied by a reduction in input conductance. The average reversal potential for INE was -104 mV. The NE responses could be elicited in a Ca(2+)-free solution containing tetrodotoxin, indicating that they were postsynaptic. 3. The NE response could be blocked by the alpha-adrenoceptor antagonist prazosin, but not by the beta-adrenoceptor antagonist propranolol, and could be mimicked by the alpha 1-adrenoceptor agonist phenylephrine but not by the alpha 2-adrenoceptor agonist UK 14,304 or by the beta-adrenoceptor agonist isoproterenol when alpha-adrenoceptors were blocked. 4. Substitution of barium for calcium in the perfusion solution blocked the increase in RN in response to NE without completely blocking the depolarization. Replacement of sodium chloride with choline chloride in the barium-substituted perfusion solution blocked the remaining depolarization. 5. The neuropeptide thyrotropin-releasing hormone (TRH), which also depolarizes and increases the RN of HMs, occluded the response of HMs to NE. 6. NE altered HM firing properties in three ways: it always lowered the minimum amount of injected current needed to elicit repetitive firing, it increased the slope of the firing frequency versus injected current relation in 8 of 14 cells tested, and it increased the delay from the onset of the depolarizing current pulse to the first evoked spike in all cells tested. 7. We conclude that NE acts directly on alpha 1-adrenoceptors to increase the excitability of HMs. It does this by reducing a barium-sensitive resting potassium current and activating a barium-insensitive inward current carried primarily by sodium ions. A portion of the intracellular pathway for these actions is shared by TRH. In addition, there is evidence that NE alters HM firing patterns by affecting currents that are activated following depolarization.

Downregulation of beta-adrenergic receptors and signal transduction response in salivary glands of NOD mice

1994 ◽  
Vol 266 (3) ◽  
pp. G433-G443
Author(s):  
Y. Hu ◽  
K. R. Purushotham ◽  
P. Wang ◽  
R. Dawson ◽  
M. G. Humphreys-Beher
Keyword(s):  
Salivary Glands ◽  
Adrenergic Receptor ◽  
Radioligand Binding ◽  
Nod Mice ◽  
Exocrine Function ◽  
Beta Adrenergic ◽  
Beta Adrenoceptor ◽  
Stimulus Response ◽  
Adrenoceptor Agonist ◽  
Second Messenger Signaling

The nonobese diabetic (NOD) mouse is subject to autoimmune disease-associated lymphocytic attack on the salivary glands with a corresponding loss of exocrine function. Downregulation of stimulus response to the beta-adrenoceptor agonist, isoproterenol, appears to be related to a decline in beta-adrenergic receptor density, changes in the level of intracellular second messenger signaling component adenosine 3',5'-cyclic monophosphate, and protein kinase A activity. An autoantibody to the beta 1-adrenergic receptor present in the sera of diabetic NOD mice may be involved in the reduced agonist response by virtue of its ability to retard dihydroalprenolol radioligand binding to receptors in the membranes of salivary glands from control mice and recognition of purified beta 1-adrenergic receptor by immunoblotting techniques.

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