The Effect of Imidazoline Receptors and α2-adrenoceptors on the Anesthetic Requirement (MAC) for Halothane in Rats 

1997 ◽  
Vol 87 (4) ◽  
pp. 963-967 ◽  
Author(s):  
Kiyokazu Kagawa ◽  
Tadanori Mammoto ◽  
Yukio Hayashi ◽  
Takahiko Kamibayashi ◽  
Takashi Mashimo ◽  
...  
Keyword(s):  
Minimum Alveolar Concentration ◽  
Inhibitory Effect ◽  
Imidazoline Receptors ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
The Central Nervous System ◽  
Anesthetic Requirement ◽  
Alpha2 Adrenoceptor ◽  
Pharmacologic Actions

Background Recent evidences have documented that several pharmacologic actions of alpha2-adrenoceptor agonists are mediated via activation of not only alpha2-adrenoceptors, but also by imidazoline receptors, which are nonadrenergic receptors in the central nervous system. However, the effect of imidazoline receptors on the anesthesia is not well known, and it is important to clarify the effects of both receptors on anesthesia. Methods Seventy-two rats were anesthetized with halothane, and the anesthetic requirement for halothane was evaluated as minimum alveolar concentration (MAC). The MAC for halothane was determined in the presence of dexmedetomidine (0, 10, 20, and 30 microg/kg, intraperitoneally [IP]), a selective alpha2-adrenoceptor agonist with weak affinity for imidazoline receptors. Then, the authors evaluated the inhibitory effect of rauwolscine (20 mg/kg, IP), an alpha2-adrenoceptor antagonist with little affinity for imidazoline receptors, on the MAC-reducing action of dexmedetomidine (30 microg/kg). Further, the effect of rilmenidine (20, 50, 100, 1000 microg/kg, IP), a selective imidazoline receptor agonist, on the MAC for halothane was also investigated. Results Dexmedetomidine decreased the MAC for halothane dose-dependently, and this MAC-reducing action of dexmedetomidine was completely blocked by rauwolscine. Rilmenidine alone did not change the MAC for halothane. Conclusions The present data indicate that the anesthetic sparing action of dexmedetomidine is most likely mediated through alpha2- adrenoceptors, and the stimulation of imidazoline receptors exerts little effect on the anesthetic requirement for halothane.

Central catecholaminergic neurons are involved in expression of the 10-Hz rhythm in SND

1996 ◽  
Vol 270 (2) ◽  
pp. R333-R341 ◽  
Author(s):  
H. S. Orer ◽  
S. Zhong ◽  
S. M. Barman ◽  
G. L. Gebber
Keyword(s):  
Intravenous Administration ◽  
Sympathetic Nerve ◽  
Ventrolateral Medulla ◽  
Imidazoline Receptors ◽  
Catecholaminergic Neurons ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Nerve Discharge ◽  
Lower Frequencies

We studied the effects of adrenoceptor agonists and antagonists on sympathetic nerve discharge (SND) of urethan-anesthetized, baroreceptor-denervated cats. In cats in which a 10-Hz rhythm coexisted with irregular 2- to 6-Hz oscillations in SND, intravenous clonidine, an alpha 2-adrenoceptor agonist, blocked the 10-Hz rhythm without affecting power at lower frequencies. In contrast, power at frequencies < or = 6 Hz was depressed by clonidine in cats in which the 10-Hz rhythm was absent. These effects were reversed by intravenous administration of alpha 2-adrenoceptor antagonists, idazoxan and rauwolscine. Rauwolscine is devoid of affinity for imidazoline receptors. Furthermore, in cats untreated with clonidine, idazoxan and rauwolscine enhanced or induced the 10-Hz rhythm without affecting power at lower frequencies. Prazosin, an alpha 1-adrenoceptor antagonist, selectively blocked the 10-Hz rhythm in SND. Finally, the 10-Hz rhythm in SND was blocked by microinjection of clonidine into the rostral or caudal ventrolateral medulla. The results support the view that central catecholaminergic neurons play a role in expression of the 10-Hz rhythm in SND.

scholarly journals Various Systemic Effects of MK-467, A Peripherally Acting α2-adrenoceptor Antagonist in Different Animal Species: An Overview

2020 ◽  
Author(s):  
Akash . ◽  
M. Hoque ◽  
Amarpal .
Keyword(s):  
Animal Species ◽  
Minimum Alveolar Concentration ◽  
Cardiovascular Effects ◽  
Concomitant Administration ◽  
Plasma Drug ◽  
Adrenoceptor Antagonist ◽  
Α2 Adrenoceptor ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Cardiopulmonary System

Most commonly used α2-adrenoceptor agonist shows adverse cardiovascular effects during anaesthesia. They mainly depress the cardiovascular system by provoking vasoconstriction followed by bradycardia. Although α2-adrenoceptor antagonist like atipamezole can reverse these effects along with that they also reverse the sedation and nociception. Concomitant administration of peripherally acting α2-adrenoceptor antagonist MK-467 can reverse the adverse cardiovascular effect of α2-adrenoceptor agonists without affecting the sedation and nociception. MK-467 has been successfully used in different animals like dogs, cats, sheep, horses along with different α2-adrenoceptor agonist drugs. This review aims to summarize the effects of MK-467 on sedation, cardiopulmonary system, the minimum alveolar concentration of different inhalant anaesthetics, plasma drug concentration, plasma glucose and insulin in different animals.

α2AAdrenoceptors Contribute to Feedback Inhibition of Capsaicin-induced Hyperalgesia

2004 ◽  
Vol 101 (1) ◽  
pp. 185-190 ◽  
Author(s):  
Heikki Mansikka ◽  
Janne Lähdesmäki ◽  
Mika Scheinin ◽  
Antti Pertovaara
Keyword(s):  
Knockout Mice ◽  
Feedback Inhibition ◽  
Pain Behavior ◽  
Spontaneous Pain ◽  
Wild Type ◽  
Pain Hypersensitivity ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Alpha2 Adrenoceptor

Background Studies on receptor knockout mice have so far shown that of the three alpha2-adrenoceptor subtypes, the alpha(2A) adrenoceptor has a major role in mediating the powerful central analgesia induced by synthetic alpha2-adrenoceptor agonists. However, because a knockout of the gene for the alpha(2A) adrenoceptor has produced only little if any change in the pain sensitivity of control, nerve-injured, or inflamed animals, it has not been clear whether activation of alpha(2A)-adrenoceptors by endogenous ligands has a significant pain regulatory role. Methods The authors assessed spontaneous pain behavior and mechanical hypersensitivity induced by administration of capsaicin in the colon or paw of alpha(2A)-adrenoceptor knockout mice versus their wild-type controls. Results Enhanced pain hypersensitivity was observed in alpha(2A)-adrenoceptor knockout mice 20 min or more after administration of capsaicin, but before, hypersensitivity and spontaneous pain were of equal magnitude in alpha(2A)-adrenoceptor knockout and wild-type mice. When wild-type mice were pretreated with an alpha2-adrenoceptor antagonist, capsaicin-induced pain hypersensitivity increased to a level equal to that in alpha(2A)-adrenoceptor knockout mice. Capsaicin-induced hypersensitivity was suppressed in wild-type but not alpha(2A)-adrenoceptor knockout mice by a centrally acting alpha2-adrenoceptor agonist, whereas a peripherally acting alpha2-adrenoceptor agonist was without effect on hypersensitivity, although it attenuated capsaicin-induced spontaneous pain behavior in wild-type mice. Conclusions This study shows that central alpha(2A)-adrenoceptors contribute to feedback inhibition of pain hypersensitivity. Also, alpha(2A)-adrenoceptors are critical for not only somatic but also visceral antinociceptive effects induced by synthetic alpha2-adrenoceptor agonists.

Effects of α-adrenoceptor agonists and antagonists on thyroid hormone secretion

1985 ◽  
Vol 108 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Bo Ahrén
Keyword(s):  
Thyroid Hormone ◽  
Dose Level ◽  
Hormone Secretion ◽  
High Dose ◽  
Inhibitory Effects ◽  
High Dose Level ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists

Abstract. The effects of various α-adrenoceptor agonists and antagonists on blood radioiodine levels were studied in mice pre-treated with 125I and thyroxine. The non-selective α-adrenoceptor agonist noradrenaline and the selective α1-adrenoceptor agonist phenylephrine both enhanced blood radioiodine levels. Noradrenaline was more potent than phenylephrine. Contrary, the selective α2-adrenoceptor agonist clonidine depressed basal levels of blood radioiodine. The non-selective α-adrenoceptor antagonist phentolamine and the selective α1-adrenoceptor antagonist prazosin both inhibited the noradrenaline-induced elevation of radioiodine levels, whereas the α2-adrenoceptor antagonist yohimbine had no such effect, except at a high dose level. All three α-adrenoceptor agonists, noradrenaline, phenylephrine and clonidine, inhibited the radioiodine response to TSH. In addition, TSH-induced increase in radioiodine levels was inhibited by prazosin, whereas yohimbine had no effect. Phentolamine inhibited the radioiodine response to TSH when given 2 h prior to TSH, whereas when given 15 min prior to TSH the response to TSH was potentiated by Phentolamine. It is concluded, that under in vivo conditions in the mouse, α1-adrenoceptor activation stimulates basal thyroid hormone secretion and inhibits TSH-induced thyroid hormone secretion. Further, α2-adrenoceptor activation inhibits basal thyroid hormone secretion. In addition, TSH-induced thyroid hormone secretion is inhibited by α1-adrenoceptor antagonism. Thus, α-adrenoceptors induce both stimulatory and inhibitory effects of thyroid function.

scholarly journals Catecholamines modulate podocyte function.

1998 ◽  
Vol 9 (3) ◽  
pp. 335-345 ◽  
Author(s):  
T B Huber ◽  
J Gloy ◽  
A Henger ◽  
P Schollmeyer ◽  
R Greger ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Patch Clamp Technique ◽  
Extracellular Solution ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Adrenoceptor Agonists ◽  
Beta 2 ◽  
Cl Conductance ◽  
Stimulation Of ◽  
Ion Conductances

The aim of this study was to investigate the influence of adrenoceptor agonists on the intracellular calcium activity ([Ca2+]i), membrane voltage (Vm), and ion conductances (Gm) in differentiated mouse podocytes. [Ca2+]i was measured by the Fura-2 fluorescence method in single podocytes. Noradrenaline and the alpha 1-adrenoceptor agonist phenylephrine induced a reversible and concentration-dependent biphasic increase of [Ca2+]i in podocytes (EC50 approximately 0.1 microM for peak and plateau), whereas the alpha 2-adrenoceptor agonist UK 14.304 did not influence [Ca2+]i. The [Ca2+]i response induced by noradrenaline was completely inhibited by the alpha 1-adrenoceptor antagonist prazosin (10 nM). In a solution with a high extracellular K+ (72.5 mM), [Ca2+]i was unchanged and the [Ca2+]i increase induced by noradrenaline was not inhibited by the L-type Ca2+ channel blocker nicardipine (1 microM). Vm and Gm were examined with the patch-clamp technique in the slow whole-cell configuration. Isoproterenol, phenylephrine, and noradrenaline depolarized podocytes and increased Gm. The order of potency for the adrenoceptor agonists was isoproterenol (EC50 approximately 1 nM) > noradrenaline (EC50 approximately 0.3 microM) > phenylephrine (EC50 approximately 0.5 microM). The beta 2-adrenoceptor antagonist ICI 118.551 (5 to 100 nM) inhibited the effect of isoproterenol on Vm. Stimulation of adenylate cyclase by forskolin mimicked the effect of isoproterenol on Vm and Gm (EC50 approximately 40 nM). Isoproterenol induced a time- and concentration-dependent increase of cAMP in podocytes. The effect of isoproterenol was unchanged in the absence of Na+ or in an extracellular solution with a reduced Ca2+ concentration, whereas it was significantly increased in an extracellular solution with a reduced Cl- concentration (from 145 to 32 mM). The data indicate that adrenoceptor agonists regulate podocyte function: They increase [Ca2+]i via an alpha 1-adrenoceptor and induce a depolarization via a beta 2-adrenoceptor. The depolarization is probably due to an opening of a cAMP-dependent Cl- conductance.

scholarly journals Dexmedetomidine Reduces Long-term Potentiation in Mouse Hippocampus

2008 ◽  
Vol 108 (1) ◽  
pp. 94-102 ◽  
Author(s):  
Isao Takamatsu ◽  
Ayano Iwase ◽  
Makoto Ozaki ◽  
Tomiei Kazama ◽  
Keiji Wada ◽  
...  
Keyword(s):  
Hippocampal Slices ◽  
Long Term Potentiation ◽  
Inhibitory Effect ◽  
Paired Pulse ◽  
Adrenoceptor Antagonist ◽  
Term Potentiation ◽  
Mouse Hippocampus ◽  
Alpha2 Adrenoceptor

Background Dexmedetomidine (Precedex; Abbott Laboratories, Abbott Park, IL) is a selective alpha2-adrenergic agonist that also has affinity for imidazoline receptors. In clinical studies, dexmedetomidine has sedative effects and impairs memory, but the action of dexmedetomidine on synaptic plasticity in the brain has yet to be established. In the present study, the authors investigated the effects of dexmedetomidine on two forms of synaptic plasticity-long-term potentiation (LTP) and paired-pulse facilitation-in the CA1 region of mouse hippocampal slices. Methods The authors recorded Schaffer collateral-evoked field excitatory postsynaptic potentials from mouse hippocampal slices in CA1 stratum radiatum. The slope of the rising phase of the field excitatory postsynaptic potential was used to estimate the strength of synaptic transmission. Results Application of dexmedetomidine for 20 min before "theta burst" stimulation dose-dependently attenuated LTP, and half-inhibitory concentration of dexmedetomidine was 28.6 +/- 5.7 nm. The inhibitory effect of dexmedetomidine on LTP was not abolished by an alpha2-adrenoceptor antagonist (yohimbine), an imidazoline type 1 receptor and alpha2-adrenoceptor antagonist (efaroxan), an alpha1-adrenoceptor antagonist (prazosin), or a gamma-aminobutyric acid type A receptor antagonist (picrotoxin). However, an imidazoline type 2 receptor and alpha2-adrenoceptor antagonist (idazoxan) completely blocked the dexmedetomidine-induced attenuation. Furthermore, 2-benzofuranyl-2-imidaloline, a selective imidazoline type 2 receptor ligand, reduced LTP. 2-(4,5-dihydroimidaz-2-yl)-quinoline, another imidazoline type 2 receptor ligand, abolished the 2-benzofuranyl-2-imidaloline-induced attenuation, but the inhibitory effect of dexmedetomidine on LTP was not abolished by 2-(4,5-dihydroimidaz-2-yl)-quinoline. Dexmedetomidine did not affect paired-pulse facilitation. Conclusion Dexmedetomidine impairs LTP in area CA1 of the mouse hippocampus via imidazoline type 2 receptors and alpha2-adrenoceptors.

scholarly journals The Inhibitory Effect ofHaloxylon salicornicumon Contraction of the Mouse Uterus

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Nabila H. Saleem ◽  
Valerie A. Ferro ◽  
Ann M. Simpson ◽  
John Igoli ◽  
Alexander I. Gray ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Mouse Uterus ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Detailed Evaluation ◽  
Pharmacologic Effect ◽  
Spontaneous Contractions ◽  
Crude Aqueous Extract

Haloxylon salicornicum(H. salicornicum) is a plant that is frequently taken as a tea by Bedouin women in Egypt who are experiencing difficulties during pregnancy, as well as to provide relief from dysmenorrhoea. Despite its medical use, there has been no detailed evaluation of the effect of this plant on uterine tissue. Therefore, the initial aim of this study was to determine whetherH. salicornicumaffected the contraction of the mouse uterusin vitro. The crude aqueous extract ofH. salicornicumwas found to inhibit the spontaneous contractions of the uterus, with the effect being rapid in onset and completely reversible upon washout. Subsequent purification of the plant extract resulted in the identification of synephrine and N-methyltyramine, both of which were found to have inhibitory effects on the spontaneous contractions of the uterus. The EC50for the purified constituent identified as synephrine was 0.82 ± 0.24 μg/mL. The inhibitory activity of crudeH. salicornicum, as well as the isolated constituents, could be prevented by pretreatment of the uterus with theβ-adrenoceptor antagonist propranolol. In conclusion, the use ofH. salicornicumduring preterm labour appears to be justified, and its pharmacologic effect is consistent with it acting as aβ-adrenoceptor agonist.

Effects of salbutamol on intracellular calcium oscillations in porcine airway smooth muscle

1997 ◽  
Vol 82 (6) ◽  
pp. 1836-1843 ◽  
Author(s):  
Y. S. Prakash ◽  
H. F. M. Van Der Heijden ◽  
M. S. Kannan ◽  
G. C. Sieck
Keyword(s):  
Smooth Muscle ◽  
Intracellular Calcium ◽  
Airway Smooth Muscle ◽  
Inhibitory Effect ◽  
Calcium Oscillations ◽  
Adrenoceptor Agonist ◽  
Intracellular Ca ◽  
Adrenoceptor Agonists ◽  
A Cell ◽  
Agonist Concentration

Prakash, Y. S., H. F. M. van der Heijden, M. S. Kannan, and G. C. Sieck. Effects of salbutamol on intracellular calcium oscillations in porcine airway smooth muscle. J. Appl. Physiol. 82(6): 1836–1843, 1997.—Relaxation of airway smooth muscle (ASM) by β-adrenoceptor agonists involves reduction of intracellular Ca2+concentration ([Ca2+]i). In porcine ASM cells, acetylcholine induces [Ca2+]ioscillations that display frequency modulation by agonist concentration and basal [Ca2+]i. We used real-time confocal microscopy to examine the effect of salbutamol (1 nM to 1 μM), a β2-adrenoceptor agonist, on [Ca2+]ioscillations in freshly dissociated porcine ASM cells. Salbutamol decreased the frequency of [Ca2+]ioscillations in a concentration-dependent fashion, completely inhibiting the oscillations at 1 μM. These effects were mimicked by a cell-permeant analog of adenosine 3′,5′-cyclic monophosphate. The inhibitory effect of salbutamol was partially reversed by BAY K 8644. Salbutamol reduced [Ca2+]ieven when sarcoplasmic reticulum (SR) Ca2+ reuptake and Ca2+ influx were blocked. Lanthanum blockade of Ca2+ efflux attenuated the inhibitory effect of salbutamol on [Ca2+]i. The [Ca2+]iresponse to caffeine was unaffected by salbutamol. On the basis of these results, we conclude that β2-adrenoceptor agonists have little effect on SR Ca2+ release in ASM cells but reduce [Ca2+]iby inhibiting Ca2+ influx through voltage-gated channels and by enhancing Ca2+ efflux.

β2-Adrenoceptor Regulation of CGRP Release from Capsaicin-sensitive Neurons

2003 ◽  
Vol 82 (4) ◽  
pp. 308-311 ◽  
Author(s):  
W.R. Bowles ◽  
C.M. Flores ◽  
D.L. Jackson ◽  
K.M. Hargreaves
Keyword(s):  
Dental Pulp ◽  
Nociceptive Neurons ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
In Vitro Superfusion ◽  
Adrenoceptor Agonists ◽  
Adrenoceptor Regulation ◽  
Pre Treatment ◽  
Neurotransmitter Substances

Previous studies have suggested that neurotransmitter substances from the sympatho-adrenomedullary system regulate pulpal blood flow (PBF), in part, by the inhibition of vasoactive neuropeptide release from pulpal sensory neurons. However, no study has evaluated the role of β-adrenoceptors. We evaluated the hypothesis that activation of β-adrenoceptors inhibits immunoreactive calcitonin gene-related peptide (iCGRP) release from capsaicin-sensitive nociceptive neurons via in vitro superfusion of bovine dental pulp. Either norepinephrine or epinephrine inhibited capsaicin-evoked iCGRP. The norepinephrine effect was blocked by the selective β2-adrenoceptor antagonist, ICI 118,551, but not by pre-treatment with the selective β1-adrenoceptor antagonist, atenolol. In addition, application of albuterol, a selective β2-adrenoceptor agonist, significantly blocked capsaicin-evoked release of iCGRP. Collectively, these studies demonstrate that activation of β2-adrenoceptors in dental pulp significantly reduces exocytosis of neuropeptides from capsaicin-sensitive nociceptors. This effect may have physiologic significance in regulating PBF. Moreover, since capsaicin selectively activates nociceptors, β2-adrenoceptor agonists may have clinical utility as peripherally acting therapeutics for dental pain and inflammation.

Augmentation of moxonidine-induced increase in ANP release by atrial hypertrophy

2004 ◽  
Vol 287 (1) ◽  
pp. H150-H156 ◽  
Author(s):  
Chunhua Cao ◽  
Chang Won Kang ◽  
Sung Zoo Kim ◽  
Suhn Hee Kim
Keyword(s):  
Pulse Pressure ◽  
Antagonistic Effect ◽  
Imidazoline Receptors ◽  
Imidazoline Receptor ◽  
Adrenoceptor Antagonist ◽  
Adrenoceptor Agonist ◽  
Relative Change ◽  
Dose Dependent ◽  
Regulation Of Blood Pressure

Imidazoline receptors are divided into I1 and I2 subtypes. I1-imidazoline receptors are distributed in the heart and are upregulated during hypertension or heart failure. The aim of this study was to define the possible role of I1-imidazoline receptors in the regulation of atrial natriuretic peptide (ANP) release in hypertrophied atria. Experiments were performed on isolated, perfused, hypertrophied atria from remnant-kidney hypertensive rats. The relatively selective I1-imidazoline receptor agonist moxonidine caused a decrease in pulse pressure. Moxonidine (3, 10, and 30 μmol/l) also caused dose-dependent increases in ANP secretion, but clonidine (an α2-adrenoceptor agonist) did not. Pretreatment with efaroxan (a selective I1-imidazoline receptor antagonist) or rauwolscine (a selective α2-adrenoceptor antagonist) inhibited the moxonidine-induced increases in ANP secretion and interstitial ANP concentration and decrease in pulse pressure. However, the antagonistic effect of efaroxan on moxonidine-induced ANP secretion was greater than that of rauwolscine. Neither efaroxan nor rauwolscine alone has any significant effects on ANP secretion and pulse pressure. In hypertrophied atria, the moxonidine-induced increase in ANP secretion and decrease in pulse pressure were markedly augmented compared with nonhypertrophied atria, and the relative change in ANP secretion by moxonidine was positively correlated to atrial hypertrophy. The accentuation by moxonidine of ANP secretion was attenuated by efaroxan but not by rauwolscine. These results show that moxonidine increases ANP release through (preferentially) the activation of atrial I1-imidazoline receptors and also via different mechanisms from clonidine, and this effect is augmented in hypertrophied atria. Therefore, we suggest that cardiac I1-imidazoline receptors play an important role in the regulation of blood pressure.

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