Adrenoreceptors of the guinea-pig urinary bladder. (1/1083)

1 Adrenaline, noradrenaline and isoprenaline (5 mug/ml) did not affect the resting tone of the isolated urinary bladder of the guinea-pig. 2 The catecholamines (1-2 mug/ml) inhibited neuronally evoked contractions at various stimulation frequencies; the inhibition was maximum at 2 Hz and minimum at 50 Hz. Isoprenaline produced maximum inhibition. 3 Propranolol (0.5 mug/ml) completely blocked the catecholamine-induced inhibition at all the frequencies employed. The concentration-response curves of isoprenaline at 2, 10 and 50 Hz were characteristically shifted by propranolol (50 ng/ml). Phenoxybenzamine (0.2 mug/ml) was totally ineffective. 4 In some experiments adrenaline significantly raised the tone of the bladder exposed to propranolol; this effect could be blocked by phenoxybenzamine. 5 Acetylcholine-induced bladder contractions were inhibited by adrenaline (2 mug/ml); the inhibition was completely blocked by propranolol (0.5 mug/ml). 6 The results indicate the presence of an inhibitory beta-adrenoceptor and suggest the possibility of an excitatory alpha-adrenoceptor in guinea-pig urinary bladder.  (+info)

Neuroregulation by vasoactive intestinal peptide (VIP) of mucus secretion in ferret trachea: activation of BK(Ca) channels and inhibition of neurotransmitter release. (2/1083)

1. The aims of this study were to determine: (1) whether vasoactive intestinal peptide (VIP) regulates cholinergic and 'sensory-efferent' (tachykininergic) 35SO4 labelled mucus output in ferret trachea in vitro, using a VIP antibody, (2) the class of potassium (K+) channel involved in VIP-regulation of cholinergic neural secretion using glibenclamide (an ATP-sensitive K+ (K(ATP)) channel inhibitor), iberiotoxin (a large conductance calcium activated K+ (BK(ca)) channel blocker), and apamin (a small conductance K(ca) (SK(ca)) channel blocker), and (3) the effect of VIP on cholinergic neurotransmission using [3H]-choline overflow as a marker for acetylcholine (ACh) release. 2. Exogenous VIP (1 and 10 microM) alone increased 35SO4 output by up to 53% above baseline, but suppressed (by up to 80% at 1 microM) cholinergic and tachykininergic neural secretion without altering secretion induced by ACh or substance P (1 microM each). Endogenous VIP accounted for the minor increase in non-adrenergic, non-cholinergic (NANC), non-tachykininergic neural secretion, which was compatible with the secretory response of exogenous VIP. 3. Iberiotoxin (3 microM), but not apamin (1 microM) or glibenclamide (0.1 microM), reversed the inhibition by VIP (10 nM) of cholinergic neural secretion. 4. Both endogenous VIP (by use of the VIP antibody; 1:500 dilution) and exogenous VIP (0.1 microM), the latter by 34%, inhibited ACh release from cholinergic nerve terminals and this suppression was completely reversed by iberiotoxin (0.1 microM). 5. We conclude that, in ferret trachea in vitro, endogenous VIP has dual activity whereby its small direct stimulatory action on mucus secretion is secondary to its marked regulation of cholinergic and tachykininergic neurogenic mucus secretion. Regulation is via inhibition of neurotransmitter release, consequent upon opening of BK(Ca) channels. In the context of neurogenic mucus secretion, we propose that VIP joins NO as a neurotransmitter of i-NANC nerves in ferret trachea.  (+info)

Effects of vasopressin on the sympathetic contraction of rabbit ear artery during cooling. (3/1083)

In order to analyse the effects of arginine-vasopressin on the vascular contraction to sympathetic nerve stimulation during cooling, the isometric response of isolated, 2-mm segments of the rabbit central ear (cutaneous) artery to electrical field stimulation (1-8 Hz) was recorded at 37 and 30 degrees C. Electrical stimulation (37 degrees C) produced frequency-dependent arterial contraction, which was reduced at 30 degrees C and potentiated by vasopressin (10 pM, 100 pM and 1 nM). This potentiation was greater at 30 than at 37 degrees C and was abolished at both temperatures by the antagonist of vasopressin V1 receptors d(CH2)5 Tyr(Me)AVP (100 nM). Desmopressin (1 microM) did not affect the response to electrical stimulation. At 37 degrees C, the vasopressin-induced potentiation was abolished by the purinoceptor antagonist PPADS (30 microM), increased by phentolamine (1 microM) or prazosin (1 microM) and not modified by yohimbine (1 microM), whilst at 30 degrees C, the potentiation was reduced by phentolamine, yohimbine or PPADS, and was not modified by prazosin. The Ca2+-channel blockers, verapamil (10 microM) and NiCl2 (1 mM), abolished the potentiating effects of vasopressin at 37 degrees C whilst verapamil reduced and NiCl2 abolished this potentiation at 30 degrees C. The inhibitor of nitric oxide synthesis, L-NOARG (100 microM), or endothelium removal did not modify the potentiation by vasopressin at 37 and 30 degrees C. Vasopressin also increased the arterial contraction to the alpha2-adrenoceptor agonist BHT-920 (10 microM) and to ATP (2 mM) at 30 and 37 degrees C, but it did not modify the contraction to noradrenaline (1 microM) at either temperature. These results suggest that in cutaneous (ear) arteries, vasopressin potentiaties sympathetic vasoconstriction to a greater extent at 30 than at 37 degrees C by activating vasopressin V1 receptors and Ca2+ channels at both temperatures. At 37 degrees C, the potentiation appears related to activation of the purinoceptor component and, at 30 degrees C, to activation of both purinoceptor and alpha2-adrenoceptor components of the sympathetic response.  (+info)

Abnormal norepinephrine clearance and adrenergic receptor sensitivity in idiopathic orthostatic intolerance. (4/1083)

BACKGROUND: Chronic orthostatic intolerance (OI) is characterized by symptoms of inadequate cerebral perfusion with standing, in the absence of significant orthostatic hypotension. A heart rate increase of >/=30 bpm is typical. Possible underlying pathophysiologies include hypovolemia, partial dysautonomia, or a primary hyperadrenergic state. We tested the hypothesis that patients with OI have functional abnormalities in autonomic neurons regulating cardiovascular responses. METHODS AND RESULTS: Thirteen patients with chronic OI and 10 control subjects underwent a battery of autonomic tests. Systemic norepinephrine (NE) kinetics were determined with the patients supine and standing before and after tyramine administration. In addition, baroreflex sensitivity, hemodynamic responses to bolus injections of adrenergic agonists, and intrinsic heart rate were determined. Resting supine NE spillover and clearance were similar in both groups. With standing, patients had a greater decrease in NE clearance than control subjects (55+/-5% versus 30+/-7%, P<0.02). After tyramine, NE spillover did not change significantly in patients but increased 50+/-10% in control subjects (P<0.001). The dose of isoproterenol required to increase heart rate 25 bpm was lower in patients than in control subjects (0.5+/-0.05 versus 1.0+/-0.1 microg, P<0.005), and the dose of phenylephrine required to increase systolic blood pressure 25 mm Hg was lower in patients than control subjects (105+/-11 versus 210+/-12 microg, P<0.001). Baroreflex sensitivity was lower in patients (12+/-1 versus 18+/-2 ms/mm Hg, P<0.02), but the intrinsic heart rate was similar in both groups. CONCLUSIONS: The decreased NE clearance with standing, resistance to the NE-releasing effect of tyramine, and increased sensitivity to adrenergic agonists demonstrate dramatically disordered sympathetic cardiovascular regulation in patients with chronic OI.  (+info)

Mutations in the zebrafish unmask shared regulatory pathways controlling the development of catecholaminergic neurons. (5/1083)

The mechanism by which pluripotent progenitors give rise to distinct classes of mature neurons in vertebrates is not well understood. To address this issue we undertook a genetic screen for mutations which affect the commitment and differentiation of catecholaminergic (CA) [dopaminergic (DA), noradrenergic (NA), and adrenergic] neurons in the zebrafish, Danio rerio. The identified mutations constitute five complementation groups. motionless and foggy affect the number and differentiation state of hypothalamic DA, telencephalic DA, retinal DA, locus coeruleus (LC) NA, and sympathetic NA neurons. The too few mutation leads to a specific reduction in the number of hypothalamic DA neurons. no soul lacks arch-associated NA cells and has defects in pharyngeal arches, and soulless lacks both arch-associated and LC cell groups. Our analyses suggest that the genes defined by these mutations regulate different steps in the differentiation of multipotent CA progenitors. They further reveal an underlying universal mechanism for the control of CA cell fates, which involve combinatorial usage of regulatory genes.  (+info)

IL-1beta and IL-6 excite neurons and suppress nicotinic and noradrenergic neurotransmission in guinea pig enteric nervous system. (6/1083)

Conventional intracellular microelectrodes and injection of biocytin were used to study the actions of IL-1beta and IL-6 on electrical and synaptic behavior in morphologically identified guinea pig small intestinal submucous neurons. Exposure to nanomolar concentrations of either IL-1beta or IL-6 stimulated neuronal excitability. The excitatory action consisted of depolarization of the membrane potential, decreased membrane conductance, and increased discharge of action potentials. Excitatory action of IL-1beta was suppressed by the natural IL-1beta human receptor antagonist. Electrical stimulation of sympathetic postganglionic axons evoked inhibitory postsynaptic potentials (IPSPs), and stimulation of cholinergic axons evoked nicotinic fast excitatory postsynaptic potentials (EPSPs). Both kinds of synaptic potentials occurred in neurons with uniaxonal morphology believed to be secretomotor neurons. Either IL-1beta or IL-6 suppressed the noradrenergic IPSPs and the fast EPSPs, and the two acted synergistically when applied in combination. Suppression of the IPSP resulted from presynaptic inhibition of the release of norepinephrine from sympathetic nerves. The results suggest that the presence of either or both inflammatory cytokines will release the sympathetic brake from secretomotor neurons to the intestinal crypts and from nicotinic synapses in the integrative microcircuits, where norepinephrine is known to have a presynaptic inhibitory action. This, in concert with excitation of secretomotor neurons, may lead to neurogenic secretory diarrhea.  (+info)

Involvement of cGMP-dependent protein kinase in adrenergic potentiation of transmitter release from the calyx-type presynaptic terminal. (7/1083)

I have previously reported that norepinephrine (NE) induces a sustained potentiation of transmitter release in the chick ciliary ganglion through a mechanism pharmacologically distinct from any known adrenergic receptors. Here I report that the adrenergic potentiation of transmitter release was enhanced by a phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine (IBMX) and by zaprinast, an inhibitor of cGMP-selective phosphodiesterase. Exogenous application of the membrane-permeable cGMP, 8-bromo-cGMP (8Br-cGMP), potentiated the quantal transmitter release, and after potentiation, the addition of NE was no longer effective. On the other hand, 8Br-cAMP neither potentiated the transmitter release nor occluded the NE-induced potentiation. The NE-induced potentiation was blocked by neither nitric oxide (NO) synthase inhibitor nor NO scavenger. The quantal transmitter release was not potentiated by NO donors, e.g., sodium nitroprusside. The NE-induced potentiation and its enhancement by IBMX was antagonized by two inhibitors of protein kinase G (PKG), Rp isomer of 8-(4-chlorophenylthio) guanosine-3', 5'-cyclic monophosphorothioate and KT5823. As with NE-induced potentiation, the effects of 8Br-cGMP on both the resting intraterminal [Ca2+] ([Ca2+]i) and the action potential-dependent increment of [Ca2+]i (DeltaCa) in the presynaptic terminal were negligible. The reduction of the paired pulse ratio of EPSC is consistent with the notion that the NE- and cGMP-dependent potentiation of transmitter release was attributable mainly to an increase of the exocytotic fusion probability. These results indicate that NE binds to a novel adrenergic receptor that activates guanylyl cyclase and that accumulation of cGMP activates PKG, which may phosphorylate a target protein involved in the exocytosis of synaptic vesicles.  (+info)

Brain noradrenergic receptors in major depression and schizophrenia. (8/1083)

The binding of [125I]p-iodoclonidine to alpha-2, and/or [125I]iodopindolol to beta-1 and beta-2 adrenoceptors was measured in right prefrontal cortex (Brodmann's area 10) and right hippocampus from subjects with DSM-III-R diagnoses of major depression (n = 15) or schizophrenia (n = 8) as well as from control subjects (n = 20). No significant differences between study groups were observed in binding to alpha-2 adrenoceptors in any of the six layers of prefrontal cortex or in any of the hippocampal fields. Likewise, there were no significant differences in beta-1 or beta-2 adrenoceptor binding in any of the hippocampal fields between control and major depressive subjects. In contrast, binding to beta-1 adrenoceptors, but not beta-2 adrenoceptors, was significantly lower (-13 to -27%) in most hippocampal fields of schizophrenic subjects as compared to control subjects or to major depressives. Alterations in beta-1 adrenoceptor binding in the hippocampus of schizophrenics provide further evidence for a role of central noradrenergic neurons in the neurochemical pathology of schizophrenia.  (+info)

Beta adrenergic receptor kinase Beta adrenergic receptor kinase-2 There is no α1C receptor. There was a subtype known as C, but ... and β-Adrenergic Receptors Theory of receptor activation Desensitization of β1 receptors (Webarchive template wayback links, ... The adrenergic receptors or adrenoceptors are a class of G protein-coupled receptors that are targets of many catecholamines ... There are also α2 receptors on the nerve terminal membrane of the post-synaptic adrenergic neuron. Actions of the α2 receptor ...
Citation Information: J Clin Invest. 1994;93(3):1349-1349. https://doi.org/10.1172/JCI116867C1 ...
Rapid desensitization of neonatal rat liver beta-adrenergic receptors. A role for beta-adrenergic receptor kinase.. ... Rapid desensitization of neonatal rat liver beta-adrenergic receptors. A role for beta-adrenergic receptor kinase.. ... Exposure of beta-adrenergic receptors (BAR) to agonists often leads to a rapid loss of receptor responsiveness. The proposed ... Furthermore, our data indicate that in addition to its suggested role as a rapid modulator of adrenergic receptor function at ...
Beta-2 Adrenergic Receptors (B2ARs) are a type of G Protein-Coupled Receptor (GPCR). GPCRs are the largest family of integral ... An activated G protein-coupled receptor (human β-2 adrenergic receptor in blue ) in a complex with a heterotrimeric G protein ( ... Adrenergic receptor Nobel Prize Related to the Structures. Robert J. Lefkowitz and Brian K. Kobilka share the 2012 Nobel Prize ... The April 2008 RCSB PDB Molecule of the Month feature on Adrenergic Receptors by David S. Goodsell is 10.2210/rcsb_pdb/mom_2008 ...
Antibodies for proteins involved in adrenergic receptor signaling pathway pathways, according to their Panther/Gene Ontology ... Antibodies for proteins involved in adrenergic receptor signaling pathway pathways; according to their Panther/Gene Ontology ...
Rabbit recombinant monoclonal beta 2 Adrenergic Receptor antibody [EPR707(N)] conjugated to Alexa Fluor® 488. Validated in IHC ... Anti-beta 2 Adrenergic Receptor antibody [EPR707(N)] (ab182136) *Anti-beta 2 Adrenergic Receptor antibody [EPR707(N)] - BSA and ... Alexa Fluor® 488 Anti-beta 2 Adrenergic Receptor antibody [EPR707(N)]. See all beta 2 Adrenergic Receptor primary antibodies. ... Belongs to the G-protein coupled receptor 1 family. Adrenergic receptor subfamily. ADRB2 sub-subfamily. ...
To understand better the cellular mechanisms of NE and its adrenergic receptors in the LA, we used antibodies directed against ... or against two different isoforms of the beta-adrenergic receptors (βARs), one that predominately recognizes neurons (βAR 248) ... or against two different isoforms of the beta-adrenergic receptors (βARs), one that predominately recognizes neurons (βAR 248) ... To understand better the cellular mechanisms of NE and its adrenergic receptors in the LA, we used antibodies directed against ...
3-adrenergic receptor gene on weight gain in morbid obesity," International Journal of Obesity and Related Metabolic Disorders ... 3-adrenergic-receptor gene with features of the insulin resistance syndrome in finns," The New England Journal of Medicine, vol ... 3-Adrenergic receptor (. 3-AR) and uncoupling protein 1 (UCP1) are involved in energy expenditure of the adipocytes, and the ... 3-adrenergic receptor gene and obesity in Japanese men: a longitudinal analysis," The Journal of Clinical Endocrinology & ...
Functional desensitization of the isolated beta-adrenergic receptor by the beta-adrenergic receptor kinase: potential role of ... Overexpression of the cardiac beta(2)-adrenergic receptor and expression of a beta-adrenergic receptor kinase-1 (betaARK1) ... receptor substrates, such as the beta-adrenergic receptor, triggering events leading to receptor desensitization. beta ARK ... The beta-adrenergic receptor kinase 1 (beta ARK1) is a member of the G protein-coupled receptor kinase (GRK) family that ...
A signaling molecule activates a GPCR by binding to it and causing the receptor to change its shape. This triggers a cascade of ... Proteins known as G protein-coupled receptors, or GPCRs for short, detect and respond to hormones and other signaling molecules ... Here we show in atomistic detail how the human β2-adrenergic receptor (β2AR) - a prototypical G protein-coupled receptor - is ... A signaling molecule activates a GPCR by binding to it and causing the receptor to change its shape. This triggers a cascade of ...
Alpha-1 Adrenergic Receptor Antagonists for Preventing Acute Respiratory Distress Syndrome and Death from Cytokine Storm ... Faculty & Research Working Papers Alpha-1 Adrenergic Receptor Antagonists for Preventing Acute Respiratory Distress Syndrome ... We previously demonstrated that alpha-1 adrenergic receptor (α1-AR) antagonists can prevent cytokine storm syndrome in mice. ...
β-Adrenergic receptor stimulation with norepinephrine (1 μmol/L) attenuated alternans by 60 [52-65]% [interquartile range] and ... β-adrenergic receptor stimulation with norepinephrine (1 µmol/L) attenuated alternans by 60 [52-65] % [interquartile range] and ... We hypothesize that the border zone is most vulnerable to alternans, that β-adrenergic receptor stimulation can suppresses this ... Simulations also demonstrated that β-adrenergic receptor stimulation in this specific region reduced the formation of ...
Multiple agonists of G-protein coupled receptors (GPCRs), beta-adrenergic receptors (β-ARs) in particular, scored in this ... Beta-adrenergic receptor signaling regulates ER-mitochondria contacts. View ORCID ProfileYoungshin Lim, Il-Taeg Cho, Helmut G. ... Beta-adrenergic receptor signaling regulates ER-mitochondria contacts Message Subject (Your Name) has forwarded a page to you ... Significance Statement Here we identify β-adrenergic receptor (β-AR) signaling as an essential pathway controlling ER-Mito ...
IGF-1 regulates cAMP levels in astrocytes through a β2-adrenergic receptor-dependant mechanism. Int J Med Sci. 5(5):240-243. ... IGF-1 regulates cAMP levels in astrocytes through a β2-adrenergic receptor-dependant mechanism Daniel Chesik, Nadine Wilczak, ... Chesik D, Wilczak N, De Keyser J. IGF-1 regulates cAMP levels in astrocytes through a β2-adrenergic receptor-dependant ... Chesik, D.; Wilczak, N.; De Keyser, J. IGF-1 regulates cAMP levels in astrocytes through a β2-adrenergic receptor-dependant ...
Alpha2 Adrenergic Receptors We confirmed the inheritance from the induced mutations up to the T3 (F\KO and X\KO) and F3 (FX\KO ... Alpha2 Adrenergic Receptors 2012B091100153); the elected leader Base of Nanfang Medical center, Southern Medical School (no. ... Alpha2 Adrenergic Receptors Only in SKOV3ip1 cells, which communicate high levels of FR, did MORAB-003 induce prominent ... Alpha2 Adrenergic Receptors This indicates which the increased beige adipogenesis effect in these scholarly studies is ...
Glucorticoids and adrenergic stimulation are both thought to control the development of beta-adrenergic receptors/responses. In ... Regulation of postnatal beta-adrenergic receptor/adenylate cyclase development by prenatal agonist stimulation and steroids: ... Regulation of postnatal beta-adrenergic receptor/adenylate cyclase development by prenatal agonist stimulation and steroids: ... 1990). Regulation of postnatal beta-adrenergic receptor/adenylate cyclase development by prenatal agonist stimulation and ...
Pharmacological characterization of alpha adrenergic receptors in the young and old female rabbit urethra.. M Yoshida, J ... Pharmacological characterization of alpha adrenergic receptors in the young and old female rabbit urethra.. M Yoshida, J ... Pharmacological characterization of alpha adrenergic receptors in the young and old female rabbit urethra.. M Yoshida, J ... The pharmacological characteristics of alpha-1 and alpha-2 adrenergic receptors in young (6 month) and old (4.5-5 year) female ...
Adrenergic receptor blocker reverses cardiac metabolic remodeling and improves right ventricular function in experimental ... Adrenergic receptor blocker reverses cardiac metabolic remodeling and improves right ventricular function in experimental ... Adrenergic receptor blocker reverses cardiac metabolic remodeling and improves right ventricular function in experimental ... Adrenergic receptor blocker reverses cardiac metabolic remodeling and improves right ventricular function in experimental ...
EP-1455799-B1 chemical patent summary.
There are reports suggesting an association between the rs4994 polymorphism in the ADRB3 gene encoding the beta-3 adrenergic ... receptor and OAB risk in females. The injection of botulinum toxin-A into the bladder wall is recommended as a possible ... Functional Polymorphism in the ADRB3 Gene, Encoding the Beta-3 Adrenergic Receptor, and Response to Intra-Detrusor Injection of ... are reports suggesting an association between the rs4994 polymorphism in the ADRB3 gene encoding the beta-3 adrenergic receptor ...
Thr164Ile polymorphism of β2-adrenergic receptor negatively modulates cardiac contractility: implications for prognosis in ... Thr164Ile polymorphism of β2-adrenergic receptor negatively modulates cardiac contractility: implications for prognosis in ... Thr164Ile polymorphism of β2-adrenergic receptor negatively modulates cardiac contractility: implications for prognosis in ...
Pharmacophore development for antagonists at alpha::1:: adrenergic receptor subtypes. John B. Bremner, Burak Coban, Renate ... Pharmacophore development for antagonists at alpha::1:: adrenergic receptor subtypes. Journal of Computer-Aided Molecular ...
admin December 8, 2019 Adrenergic ??3 Receptors a 50-65 kDa Fcg receptor IIIa (FcgRIII), as well as in signal transduction and ... admin September 4, 2019 Adrenergic ??3 Receptors AKT3, Anamorelin inhibitor Leiomyoma is a benign tumor of clean muscle mass ... admin August 21, 2019 Adrenergic ??3 Receptors PSI-7977 supplier, Rabbit Polyclonal to AP-2 ... admin December 15, 2019 Adrenergic ??3 Receptors ABT-737 price, Rabbit Polyclonal to AIFM1 ...
Effect Of α1A-Adrenergic Receptors Stimulation To The Isolated Rat Hearts Chronotropy ... α1-adrenergic receptors, chronotropy, heart, rat. The name of the journal. RESEARCH JOURNAL OF PHARMACEUTICAL BIOLOGICAL AND ... The results obtained may indicate that this subtype of α1-adrenergic receptors is not involved in the regulation of heart rate ... The results obtained may indicate that this subtype of α1-adrenergic receptors is not involved in the regulation of heart rate ...
Physical Activity-dependent Effects Of Beta-adrenergic Receptor Polymorphisms On Obesity-related Phenotypes In Children. 52nd ... Physical Activity-dependent Effects Of Beta-adrenergic Receptor Polymorphisms On Obesity-related Phenotypes In Children. ... Physical Activity-dependent Effects Of Beta-adrenergic Receptor Polymorphisms On Obesity-related Phenotypes In Children. 52nd ...
α1-Adrenergic Receptor Stimulates Interleukin-6 Expression and Secretion through Both mRNA Stability and Transcriptional ... α1-Adrenergic Receptor Stimulates Interleukin-6 Expression and Secretion through Both mRNA Stability and Transcriptional ... α1-Adrenergic Receptor Stimulates Interleukin-6 Expression and Secretion through Both mRNA Stability and Transcriptional ... α1-Adrenergic Receptor Stimulates Interleukin-6 Expression and Secretion through Both mRNA Stability and Transcriptional ...
Increased voltage-dependent calcium influx produced by alpha 1B-adrenergic receptor activation in rat medullary thyroid ... Increased voltage-dependent calcium influx produced by alpha 1B-adrenergic receptor activation in rat medullary thyroid ... Increased voltage-dependent calcium influx produced by alpha 1B-adrenergic receptor activation in rat medullary thyroid ... Increased voltage-dependent calcium influx produced by alpha 1B-adrenergic receptor activation in rat medullary thyroid ...
BDNF downregulates β-adrenergic receptor-mediated hypotensive mechanisms in the paraventricular nucleus of the hypothalamus. ... BDNF downregulates β-adrenergic receptor-mediated hypotensive mechanisms in the paraventricular nucleus of the hypothalamus.. ... Thorsdottir D, Cruickshank NC, Einwag Z, Hennig GW, Erdos B (2019) BDNF downregulates β-adrenergic receptor-mediated ... signaling between the NTS and the PVN by reducing the responsiveness of PVN neurons to inhibitory hypotensive β-adrenergic ...
Alpha-1 adrenergic receptors. Details. Name. Alpha-1 adrenergic receptors. Kind. protein group. Organism. Humans. Proteins. ... Alpha-1D adrenergic receptor. P25100. Details. Drug Relations. Drug Relations. DrugBank ID. Name. Drug group. Pharmacological ... Alpha-1A adrenergic receptor. P35348. Details. Alpha-1B adrenergic receptor. P35368. Details. ...
MG acts at μ-opioid and α-adrenergic receptors in vitro, but the physiological relevan ... Mechanistically, activity at µ-opioid, α1- and α2-adrenergic receptors, but not β-adrenergic receptors contributed to the ... MG acts at μ-opioid and α-adrenergic receptors in vitro, but the physiological relevance of this activity in the context of ... Inhibition of Chemotherapy-Induced Peripheral Neuropathy in Mice is Dependent on Sex and Adrenergic and Opioid Receptors ...

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