The β-Adrenergic Receptor Antagonist Metipranolol Blunts Zinc-Induced Photoreceptor and RPE Apoptosis

2006 ◽  
Vol 47 (7) ◽  
pp. 3178 ◽  
Author(s):  
Neville N. Osborne ◽  
John P. M. Wood
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor

Inhibition of Glutamatergic Synaptic Input to Spinal Lamina IIo Neurons by Presynaptic α2-Adrenergic Receptors

2002 ◽  
Vol 87 (4) ◽  
pp. 1938-1947 ◽  
Author(s):  
Yu-Zhen Pan ◽  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Receptor Antagonist ◽  
Synaptic Input ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Dorsal Root ◽  
Primary Afferents ◽  
Noradrenergic System ◽  
Analgesic Action ◽  
Adrenergic Agonists ◽  
Excitatory Synaptic Input

Activation of spinal α2-adrenergic receptors by the descending noradrenergic system and α2-adrenergic agonists produces analgesia. However, the sites and mechanisms of the analgesic action of spinally administered α2-adrenergic receptor agonists such as clonidine are not fully known. The dorsal horn neurons in the outer zone of lamina II (lamina IIo) are important for processing nociceptive information from C-fiber primary afferents. In the present study, we tested a hypothesis that activation of presynaptic α2-adrenergic receptors by clonidine inhibits the excitatory synaptic input to lamina IIo neurons. Whole cell voltage-clamp recordings were performed on visualized lamina IIo neurons in the spinal cord slice of rats. The miniature excitatory postsynaptic currents (mEPSCs) were recorded in the presence of tetrodotoxin, bicuculline, and strychnine. The evoked EPSCs were obtained by electrical stimulation of the dorsal root entry zone or the attached dorsal root. Both mEPSCs and evoked EPSCs were abolished by application of 6-cyano-7-nitroquinoxaline-2,3-dione. Clonidine (10 μM) significantly decreased the frequency of mEPSCs from 5.8 ± 0.9 to 2.7 ± 0.6 Hz (means ± SE) without altering the amplitude and the decay time constant of mEPSCs in 25 of 27 lamina IIo neurons. Yohimbine (2 μM, an α2-adrenergic receptor antagonist), but not prazosin (2 μM, an α1-adrenergic receptor antagonist), blocked the inhibitory effect of clonidine on the mEPSCs. Clonidine (1–20 μM, n = 8) also significantly attenuated the peak amplitude of evoked EPSCs in a concentration-dependent manner. The effect of clonidine on evoked EPSCs was abolished in the presence of yohimbine ( n = 5). These data suggest that clonidine inhibits the excitatory synaptic input to lamina IIo neurons through activation of α2-adrenergic receptors located on the glutamatergic afferent terminals. Presynaptic inhibition of glutamate release from primary afferents onto lamina IIoneurons likely plays an important role in the analgesic action produced by activation of the descending noradrenergic system and α2-adrenergic agonists.

Assessment of MK-467, a peripheral α2-adrenergic receptor antagonist, with intravenous clonidine

1991 ◽  
Vol 50 (1) ◽  
pp. 71-77 ◽  
Author(s):  
John B Warren ◽  
Colin T Dollery ◽  
David Sciberras ◽  
Michael R Goldberg
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor

Presynaptic modulation of acetylcholine release from cardiac parasympathetic neurons

1985 ◽  
Vol 248 (1) ◽  
pp. H33-H39 ◽  
Author(s):  
G. T. Wetzel ◽  
J. H. Brown
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Acetylcholine Release ◽  
Electrical Field Stimulation ◽  
Inhibitory Effect ◽  
Muscarinic Agonist ◽  
Parasympathetic Nerve ◽  
Presynaptic Modulation ◽  
Rat Atria ◽  
Alpha Adrenergic Receptors

Acetylcholine can be released from parasympathetic nerve endings in rat atria by 57 mM K+ depolarization or by electrical field stimulation. We have studied the presynaptic modulation of [3H]acetylcholine release from superfused rat atria prelabeled with [3H]choline. Exogenous acetylcholine and the specific muscarinic agonist oxotremorine inhibit the stimulation-induced overflow of [3H]acetylcholine into the superfusion medium. The half-maximal inhibitory concentration (IC50) of oxotremorine is 0.3 microM. The cholinesterase inhibitor neostigmine also decreases K+-stimulated [3H]acetylcholine overflow, whereas the muscarinic antagonist atropine enhances the overflow of [3H]acetylcholine. These data suggest that acetylcholine release in atria is modulated through negative feedback by the endogenous transmitter. The sympathetic adrenergic neurotransmitter norepinephrine and the neurohormone epinephrine also inhibit the overflow of [3H]acetylcholine by approximately 60%. The IC50 values for the inhibitory effects of these catecholamines are 6.3 and 2.2 microM, respectively. The inhibitory effect of norepinephrine is blocked by the alpha-adrenergic receptor antagonist yohimbine but not by the beta-adrenergic receptor antagonist propranolol. We suggest that presynaptic muscarinic and alpha-adrenergic receptors participate in the physiological and pharmacological control of cardiac parasympathetic activity.

The Effect of α1-Adrenergic Receptor Antagonist Tamsulosin (Flomax) on Iris Dilator Smooth Muscle Anatomy

Ophthalmology ◽  
2010 ◽  
Vol 117 (9) ◽  
pp. 1743-1749 ◽  
Author(s):  
Ricardo M. Santaella ◽  
John J. Destafeno ◽  
Sandra S. Stinnett ◽  
Alan D. Proia ◽  
David F. Chang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Receptor Antagonist ◽  
Adrenergic Receptor

scholarly journals Role of α1-adrenergic receptor subtypes in contractility of the rabbit abdominal aorta in vitro

2013 ◽  
Vol 82 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Jan Gnus ◽  
Albert Czerski ◽  
Stanisław Ferenc ◽  
Wojciech Zawadzki ◽  
Wojciech Witkiewicz ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Receptor Antagonist ◽  
Abdominal Aorta ◽  
Adrenergic Receptor ◽  
Receptor Subtypes ◽  
Organ Bath ◽  
Dependent Manner ◽  
Receptor Antagonists ◽  
Selective Antagonists

Investigation of the effect of α1-adrenergic receptor subtypes on the contraction of the abdominal aorta will allow for more effective treatment of hypertension by use of selective antagonists. The aim of the study was to evaluate the participation of α1-adrenergic receptor subtypes in the contractility of the aortic smooth muscle cells in rabbits. The in vitro experiments were performed in isolated tissue preparations from 30 adult female New Zealand rabbits. The abdominal aortic sections were placed in organ bath chambers and contracted with increasing doses of non-selective α1-adrenergic receptor agonist phenylephrine without pre-incubation or after incubation in α1-adrenergic receptor subtype-selective or non-selective antagonists. Separate sections were incubated with increasing concentrations of antagonists. Phenylephrine caused maximal rise in arterial smooth muscle tone to 4.75 ± 0.47 mN. The most potent in blocking phenylephrine induced contraction was 5-metylurapidil (α1A-adrenergic receptor antagonist) followed by phentolamine and prazosin (non-selective α1-adrenergic receptor antagonists); BMY 7378 (α1D-adrenergic receptor antagonist), cyclazosin and L-765.314 (α1B-adrenergic receptor antagonists) were less effective. All antagonists, except BMY 7378 elicited relaxation of non-precontracted aorta in dose dependent manner. Our results indicate that postsynaptic α1A receptors are the most potent in producing rabbit abdominal aorta contraction, while α1B and α1D subtypes are less effective.

scholarly journals Octopamine and occupancy: an aminergic mechanism for intruder–resident aggression in crickets

2010 ◽  
Vol 278 (1713) ◽  
pp. 1873-1880 ◽  
Author(s):  
Jan Rillich ◽  
Klaus Schildberger ◽  
Paul A. Stevenson
Keyword(s):  
Receptor Antagonist ◽  
Adrenergic Receptor ◽  
Receptor Blocker ◽  
Field Crickets ◽  
Behavioural Strategy ◽  
Neuronal Mechanisms ◽  
Selective Depletion ◽  
Octopamine Receptor ◽  
The Central Nervous System ◽  
Aggressive Motivation

Aggression is a behavioural strategy for securing resources (food, mates and territory) and its expression is strongly influenced by their presence and value. While it is known that resource holders are generally highly aggressive towards intruding consexuals and usually defeat them, the underlying neuronal mechanisms are not known. In a novel intruder–resident paradigm for field crickets ( Gryllus bimaculatus ), we show that otherwise submissive losers of a preceding aggressive encounter readily fight and often defeat aggressive winners after occupying an artificial shelter. This aggression enhancing effect first became evident after 2 min residency, and was maximal after 15 min, but absent 15 min after shelter removal. The residency effect was abolished following non-selective depletion of biogenic amines from the central nervous system using reserpine, or semi-selective depletion of octopamine and dopamine using α-methyl-tyrosine, but not following serotonin depletion using α-methyl-tryptophan. The residency effect was also abolished by the treatment with phentolamine, an α-adrenergic receptor antagonist, or epinastine, a highly selective octopamine receptor blocker, but not by propranolol, a ß-adrenergic receptor antagonist, or by yohimbine, an insect tyramine receptor blocker. We conclude that crickets evaluate residency as a rewarding experience that promotes aggressive motivation via a mechanism involving octopamine, the invertebrate analogue of noradrenaline.

scholarly journals The beta adrenergic receptor antagonist propranolol alters mitogenic and apoptotic signaling in late stage breast cancer

2019 ◽  
Vol 42 (3) ◽  
pp. 155-165 ◽  
Author(s):  
Alexa Montoya ◽  
Armando Varela-Ramirez ◽  
Erin Dickerson ◽  
Eddy Pasquier ◽  
Alireza Torabi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Receptor Antagonist ◽  
Late Stage ◽  
Adrenergic Receptor ◽  
Beta Adrenergic Receptor ◽  
Beta Adrenergic ◽  
Apoptotic Signaling
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