The alpha-2B adrenergic receptor (α2B adrenoceptor), is a G-protein coupled receptor. It is a subtype of the adrenergic receptor family. The human gene encoding this receptor has the symbol ADRA2B. ADRA2B orthologs have been identified in several mammals. α2-adrenergic receptors include 3 highly homologous subtypes: α2A, α2B, and α2C. These receptors have a critical role in regulating neurotransmitter release from sympathetic nerves and from adrenergic neurons in the central nervous system. This gene encodes the α2B subtype, which was observed to associate with eIF-2B, a guanine nucleotide exchange protein that functions in regulation of translation. A polymorphic variant of the α2B subtype, which lacks 3 glutamic acids from a glutamic acid repeat element, was identified to have decreased G protein-coupled receptor kinase-mediated phosphorylation and desensitization; this polymorphic form is also associated with reduced basal metabolic rate in obese subjects and may therefore contribute ...
This gene encodes the α2B subtype, which was observed to associate with eIF-2B, a guanine nucleotide exchange protein that functions in regulation of translation. A polymorphic variant of the α2B subtype, which lacks 3 glutamic acids from a glutamic acid repeat element, was identified to have decreased G protein-coupled receptor kinase-mediated phosphorylation and desensitization; this polymorphic form is also associated with reduced basal metabolic rate in obese subjects and may therefore contribute to the pathogenesis of obesity. This gene contains no introns in either its coding or untranslated sequences.[5]. A deletion variant of the α2B adrenergic receptor has been shown to be related to emotional memory in Europeans and Africans.[7] This variant also predisposed people who had it to focus more on negative aspects of a situation.[8] This predisposition remained present in people with the variant gene who took a single dose of the noradrenergic antidepressant reboxetine, but was weakened ...
The aim of this perforated-patch study was to test the effect of isoproterenol on the membrane potential in mPFC (medial prefrontal cortex) pyramidal neurons. Isoproterenol depolarized the membrane potential recorded from the soma. This effect was absent in the presence of metoprolol, suggesting the involvement of β1-adrenergic receptors. The adenylate cyclase activator forskolin also depolarized the membrane potential. Moreover, the effect of isoproterenol was abolished by the adenylate cyclase inhibitor SQ 22536. This suggested that adenylate cyclase was involved in mediating the effect of the β-adrenergic receptor agonist. The isoproterenol-induced depolarization persisted after inhibition of protein kinase A with H-89. The effect of β-adrenergic receptor activation on the membrane potential was dependent on Ih channels because it was abolished in the presence of the Ih channel inhibitor ZD 7288. Dendritic recordings were also performed. In the dendritic segments between 100 μm and 150 ...
alpha(1B)-Adrenergic receptors mediate many of the actions of the natural catecholamines, adrenaline and noradrenaline. They belong to the seven transmembrane domains G protein-coupled receptor superfamily and exert their actions mainly through activation of Gq proteins and phosphoinositide turnover/calcium signaling. Many hormones and neurotransmitters are capable of inducing alpha(1B)-adrenergic receptor phosphorylation and desensitization; among them: adrenaline and noradrenaline, phorbol esters, endothelin-I, bradykinin, lysophosphatidic acid, insulin, EGF, PDGF, IGF-I, TGF-beta, and estrogens. Key protein kinases for these effects are G protein coupled receptor kinases and protein kinase C. The lipid/protein kinase, phosphoinositide-3 kinase also appears to play a key role, acting upstream of protein kinase C. In addition to the agents employed for cells stimulation, we observed that paracrine/autocrine mediators also participate; these processes include EGF transactivation and ...
Previous studies have reported that the α1-adrenergic system can activate spinal rhythm generators belonging to the central respiratory network. In order to analyse α1-adrenergic effects on both cranial and spinal motoneuronal activity, phenylephrine (1-800 μm) was applied to in vitro preparations of neonatal rat brainstem-spinal cord. High concentration of phenylephrine superfusion exerted multiple effects on spinal cervical outputs (C2-C6), consisting of a lengthening of respiratory period and an increase in inspiratory burst duration. Furthermore, in 55% of cases a slow motor rhythm recorded from the same spinal outputs was superimposed on the inspiratory activity. However, this phenylephrine-induced slow motor rhythm generated at the spinal level was observed neither in inspiratory cranial nerves (glossopharyngeal, vagal and hypoglossal outputs) nor in phrenic nerves. Whole-cell patch-clamp recordings were carried out on cervical motoneurons (C4-C5), to determine first which motoneurons ...
The activation of beige adipocyte thermogenesis by cold temperatures and β3-adrenergic receptor agonists induce beige adipocyte formation, function and perdurance.
There are 3 alpha-1 adrenergic receptor subtypes: alpha-1A, -1B and -1D, all of which signal through the Gq/11 family of G-proteins and different subtypes show different patterns of activation. They activate mitogenic responses and regulate growth and proliferation of many cells. ...
Patane MA, Scott AL, Broten TP, Chang RS, Ransom RW, DiSalvo J, Forray C, Bock MG (1998). „4-Amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6, 7-dimethoxyquinazoline (L-765,314): a potent and selective alpha1b adrenergic receptor antagonist ". Journal of Medicinal Chemistry. 41 (8): 1205-8. PMID 9548811. doi:10.1021/jm980053f ...
Dan E. Berkowitz, David T. Price, Elizabeth A. Bello, Stella O. Page, Debra A. Schwinn; Localization of Messenger RNA for Three Distinct α2-Adrenergic Receptor Subtypes in Human Tissues: Evidence for Species Heterogeneity and Implications for Human Pharmacology. Anesthesiology 1994;81(5):1235-1244. Download citation file:. ...
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Ruuskanen JO, Xhaard H, Marjamäki A, Salaneck E, Salminen T, Yan YL, Postlethwait JH, Johnson MS, Larhammar D, Scheinin M (2004). „Identification of duplicated fourth alpha2-adrenergic receptor subtype by cloning and mapping of five receptor genes in zebrafish". Molecular Biology and Evolution. 21 (1): 14-28. PMID 12949138. doi:10.1093/molbev/msg224 ...
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SUBSTITUTED 3-AMINO-1-OXO OR THIOXO-1,2,5,6,7,8-HEXAHYDRO-2,7-NAPHTHYRIDINE-4-CARBONITRILES ARE SELECTIVE ALPHA 2B ANTAGONISTS - The present invention provides compounds which are subtype selective antagonists of the alpha 2B adrenergic receptor and have no or weak antagonist activity at the other alpha adrenergic receptors. These compounds are useful as tool compounds and, in particular, as tool compounds for developing compounds useful in treating diseases that include but are not limited to chronic pain, visceral pain, corneal pain, neuropathic pain, glaucoma, ischemic neuropathies and other neurodegenerative diseases and conditions. These compounds are also useful as compounds for treating myocardial infarction and preventing acute coronary events. The compounds of this invention are 3-amino-1-thioxo or oxo-1,2,5,6,7,8-hexahydro-2,7-naphthyridine-4-carbonitriles or substituted derivatives thereof ...
1.Impaired vasoconstriction in animals with cirrhosis is maintained in isolated vessels in vitro, indicating an intrinsic alteration in function or structure of the cells in the vascular wall. This may be due to receptor down-regulation, a defect in post-receptor signal transduction or overproduction of vasodilator compounds. This investigation examined the role of these mechanisms in modulating α-adrenoceptor-mediated contraction in hepatic arteries from patients with advanced cirrhosis.. 2.Hepatic arteries were obtained from subjects with and without cirrhosis for functional investigation in vitro. Endothelial cell function was assessed using endothelium-dependent (acetylcholine) and independent (3′-morpholinosydnonimine) vasodilators. α-Adrenoceptor-mediated contraction was assessed by constructing cumulative concentration-response curves to the α1-selective agonist phenylephrine, the non-selective adrenoceptor agonist noradrenaline and the receptor-independent vasoconstrictor potassium ...
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Upon agonist stimulation, α1B-adrenergic receptors (α1B-ARs) couple to Gq, calcium signaling and protein kinase C activation; subsequently, the receptors are phosphorylated, desensitized and internalized. Internalization seems to involve scaffolding proteins, such as α-arrestin and clathrin. However, the fine mechanisms that participate remain unsolved. The roles of protein kinase C and the small GTPase, Rab9, in α1B-AR vesicular traffic were investigated by studying α1B-adrenergic receptor-Rab protein interactions, using Forster resonance energy transfer (FRET), confocal microscopy, and intracellular calcium quantitation. In HEK293 cells overexpressing DsRed-tagged α1B-ARs and EGFP-tagged Rab proteins, pharmacological protein kinase C activation mimicked α1B-AR traffic elicited by non-related agents, such as sphingosine 1-phosphate, i.e., transient α1B-AR-Rab5 FRET signal followed by a sustained α1B-AR-Rab9 interaction, suggesting brief receptor localization in early endosomes and ...
G Protein coupled receptors (GPCRs) constitute an abundant family of membrane proteins which play a central role in cellular signaling and are important targets for modern medicine. Despite intensive research, central questions of the molecular mechanism of GPCR mediated signal transduction remain unresolved. This thesis concerns α1b-adrenergic receptor (α1b-AR) as a prototypic GPCR. The question whether ARs form homo- or hetero-oligomers was investigated using fluorescence resonance energy transfer (FRET). An important finding was that both α1a and α1b-AR subtypes form homo-oligomers. Also hetero-oligomers have been observed between the α1b- and the α1a-AR subtypes, but not with less related receptors. Another interesting finding concerns α1-AR co-internalization which correlates with the ability of the receptor to hetero-oligomerize. Investigating particular processes in living cells is often complicated by the complex cellular environment. Here we have developed a rather simple ...
We have used a constitutively active mutant of the α2A-AR stably expressed in CHO-K1 cells to examine mechanisms of α2A-AR signaling. From these studies, at least three new conclusions can be drawn. First, the α2A-AR T373K has enhanced signaling to both Gi and Gs. Second, the inverse efficacy of a series of α2-AR antagonists is examined, and a novel difference between idazoxan and methyl-idazoxan (RX821002) has been found. This point is important for interpreting physiological studies that use these two compounds. Finally, the fraction of active α2A-AR for the T373K CAM mutant is approximately 50% for our whole cell cAMP accumulation assay, whereas the WT receptor appears to have a very low percentage of receptor active in the absence of agonist.. The effects of constitutively active receptor mutants on different G proteins are not always concordant as reported for the α1-AR by Perez et al. (1996). Ren et al. (1993)previously showed for the α2A-AR that the T373K mutation adjacent to TM6 ...
Aktivierte G-Protein gekoppelte Rezeptoren aktivieren heterotrimere GProteine, in dem sie den Austausch von GDP zu GTP am G-Protein katalysieren. Theoretische Untersuchungen mittels eines vereinfachten kinetischen Modells des Gi/o-Protein Zyklus legen nahe, dass nicht nur GDP-,sondern auch GTP-gebundene Gi/o-Proteine mit aktivierten α2A-adrenergen Rezeptoren (α2A-AR) interagieren können. Demgemäß sollten aktivierte Gi/o-Proteine mit aktivierten α2A-AR vermehrt interagieren, wenn mehr α2A-AR aktiviert werden als für eine maximale G-Protein Aktivierung nötig sind. Dies sollte zu einer paradoxen Deaktivierung von Gi/o-Proteinen und deren Effektorproteinen, z.B. dem G-Protein gekoppelten, einwärtsgleichrichtenden Kaliumkanal (GIRK-Kanal) führen. Mittels FRET lässt sich in lebenden und in permeabilisierten Zellen unter Kontrolle der intrazellulären Nukleotide die Aktivierung von α2A-AR, die Interaktion von Gi/o-Proteinen mit α2A-AR und die Aktivierung von Gi/o-Proteinen bestimmen. Die ...
article{APS10101, author = {Jun-zhou Xin and Ji-min Wu and Guo-min Hu and Hui-jun Gu and Ye-nan Feng and Shuai-xing Wang and Wen-wen Cong and Ming-zhe Li and Wen-li Xu and Yao Song and Han Xiao and You-yi Zhang and Li Wang}, title = {α 1 -AR overactivation induces cardiac inflammation through NLRP3 inflammasome activation}, journal = {Acta Pharmacologica Sinica}, volume = {41}, number = {3}, year = {2020}, keywords = {}, abstract = {Acute sympathetic stress causes excessive secretion of catecholamines and induces cardiac injuries, which are mainly mediated by β-adrenergic receptors (β-ARs). However, α1-adrenergic receptors (α1-ARs) are also expressed in the heart and are activated upon acute sympathetic stress. In the present study, we investigated whether α1-AR activation induced cardiac inflammation and the underlying mechanisms. Male C57BL/6 mice were injected with a single dose of α1-AR agonist phenylephrine (PE, 5 or 10 mg/kg, s.c.) with or without pretreatment with α-AR ...
Ruuskanen JO, Xhaard H, Marjamäki A, Salaneck E, Salminen T, Yan YL, Postlethwait JH, Johnson MS, Larhammar D, Scheinin M (January 2004). "Identification of duplicated fourth alpha2-adrenergic receptor subtype by cloning and mapping of five receptor genes in zebrafish". Molecular Biology and Evolution 21 (1): 14-28. PMID 12949138. doi:10.1093/molbev/msg224. Cite uses deprecated parameter ...
Several pre-formulated buffers are available for Alpha assays. These have have been developed to meet the varying needs of different Alpha assays, and one of them may be a good choice for an assay that you are developing. This buffer contains SDS in order to lyse cells and solubilize proteins in cell-based assays. This buffer is required when detecting intracellular proteins.. Formulation: proprietary. ...
68. Reliance upon the morphologic wie sollte man kamagra einnehmen of lesions on arteri- ograms also carries known hazards. The genes for components in the RAS, b-AR systems, and lipoprotein metabolic pathways are better characterized; hence, more trans- genic animals have been produced for testing drugs targeted at these compo- nents. Med.
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Several common genetic variations have been associated with type 2 diabetes, but the exact disease mechanisms are still poorly elucidated. Here, using congenic strains from the diabetic GK-rat, we identified a 1.4-Mb genomic locus that was linked to impaired insulin granule docking at the plasma membrane and reduced beta cell exocytosis. In this locus, Adra2a, encoding the alpha2A-adrenergic receptor [alpha(2A)AR], was significantly overexpressed. Alpha(2A)AR mediates adrenergic suppression of insulin secretion. Pharmacological receptor antagonism, silencing of receptor expression, or blockade of downstream effectors rescued insulin secretion in congenic islets. Furthermore, we identified a single nucleotide polymorphism in the human ADRA2A gene for which risk allele carriers exhibited overexpression of alpha(2A)AR, reduced insulin secretion, and increased type 2 diabetes risk. Human pancreatic islets from risk allele carriers exhibited reduced granule docking and secreted less insulin in ...
Looking for a-adrenergic antagonist? Find out information about a-adrenergic antagonist. 1. any muscle that opposes the action of another 2. a drug that counteracts the effects of another drug A molecule that bears sufficient structural... Explanation of a-adrenergic antagonist
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Overall the differences between treatments were not statistically significant (P = 0.11). The differences between the individual variables were statistically significant for HR P = 0.017, DIA P = 0.04 and MAP P = 0.039, but not for SYS and CVP (P = 0.37 and P = 0.3 respectively). The post hoc tests indicated no statistically significant difference between treatments for any of the variables: HR, A-AM P = 0.41; A-AR P = 0.2; AM-AR P = 0.06; SYS, A-AM P = 1.0; A-AR P = 0.48; AM-AR P = 0.65; DIA, A-AM P = 1.0; A-AR P = 0.1; AM-AR P = 0.12, MAP, A-AM P = 0.99; A-AR P = 0.12; AM-AR P = 0.08, CVP, A-AM P = 0.51; A-AR P = 0.97; AM-AR P = 0.35. For within treatments, the differences between procedures (non-abdominal surgery and abdominal surgery) for the A-group were statistically significant (P , 0.05) for HR, SYS, DIA, MAP but not for CVP (P , 0.05, Table 2). For the AM-group differences were statistically significant (P , 0.05) for DIA and MAP, but not for HR, SYS, and CVP (P , 0.05, Table 2). For ...
... are cell‐surface receptors for two major catecholamine hormones and neurotransmitters that regulate key physiological responses, including cardiovascular and pulmonary functions
What is ADRA2A? ADRA2A, located on chromosome 10, encodes the α-2A adrenergic receptor, a norepinephrine receptor that is the primary site of action for α-2A agonists. The α-2A adrenergic receptor…. ...
Similar to the scenario in neonatal rat cardiomyocytes, β1-AR stimulation with isoproterenol induces a robust increase in cAMP accumulation that is associated with an increase in the amplitude and an acceleration of the kinetics of both the calcium transient and the twitch in adult rat ventricular myocytes. In contrast, only rather high concentrations of the β2-AR agonist zinterol (10-5 mol/L) modulate contractile function in adult rat ventricular myocytes (Figure 2⇑). Parenthetically, 2 laboratories have presented data to support the theoretical argument that 10-5 mol/L zinterol (in the absence of a β1-AR blocker) acts as a mixed β1-/β2-AR agonist; β2-AR selectivity is achieved only if a β1-AR blocker (such as CGP 20712A) is included in the assay.11 73 In contrast, Xiao and Lakatta74 maintain that the effects of high concentrations of zinterol (even without a β1-AR blocker) are attributable entirely to the minor population of β2-ARs in the preparation, and they present results to ...
Alpha1-Adrenergic Receptors (α1AR) are G protein-coupled transmembrane receptors (GPCRs) that mediate actions of the sympathetic nervous system through binding of endogenous catecholamines epinephrine and norepinephrine. Three subtypes of α1ARs (α1a, α1b, α1d) are expressed within most sympathetic tissues and in the human heart and they couple predominantly to the Gq/11 family of G proteins. α1aARs play a major role in regulating vascular tone, in blood vessel repair and in cardiovascular diseases like hypertension, myocardial hypertrophy, ischemia and heart failure. Recently, we discovered a novel, unique mechanism of hypertension triggered by naturally occurring human α1aAR-G247R (247R) genetic variant, identified in the 3rd intracellular loop (3iL) of the receptor in hypertensive patient. 247R signals in Gq-independent but βarrestin1-dependent manner leading to transactivation of epidermal growth factor receptor (EGFR) via constitutive active coupling to the βarrestin1 /MMP7/EGFR ...
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1. The aim of the present study was to investigate noradrenaline (NA)-induced regulation of alpha(1) -adrenoceptor (AR) mRNA expression in human embryonic kidney (HEK) 293 cells stably expressing cloned alpha(1) -AR subtypes with similar receptor densities. Stable transfection was performed by calcium phosphate precipitation. Receptor expression was detected by radioligand binding assay. The mRNA expression was measured by RNase protection assay.. 2. alpha(1) -Adrenoceptor subtype mRNA respond in distinct ways following prolonged exposure to NA. The mRNA level of the alpha(1A) -AR subtype was unchanged, the mRNA level of the alpha(1B) -AR subtype was increased and the mRNA level of the alpha(1D) -AR subtype declined time dependently. The protein kinase C (PKC) inhibitor calphostin C or RO 31-8220 abolished the NA-induced downregulation of alpha(1D) -AR mRNA. Phorbol myristate acetate (PMA), a PKC activator, similarly repressed the effects of NA on alpha(1D) -AR. However, calphostin C, RO 31-8220 ...
Removal of endothelial cells on rings of rat aorta increased the sensitivity to the selective alpha-1 adrenoceptor agonist phenylephrine, to the nonselective alpha adrenoceptor agonist norepinephrine and to the selective alpha-2 adrenoceptor agonist clonidine. In the case of the first two, which are strong agonists for the alpha-1 adrenoceptor-mediating contraction, removal of endothelium increased sensitivity 4- and 6-fold at the EC30 level, but produced little or no increase in maximum. In the case of clonidine, a partial agonist for the alpha-1 adrenoceptor, which gave only about 15% of the maximum given by phenylephrine on endothelium-containing rings, removal of the endothelium not only shifted the curve to the left but also increased the maximum to about 50% of that given by phenylephrine. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium-derived relaxing factor (EDRF), as hemoglobin, a specific blocking ...
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Read "The sources of calcium for noradrenaline-induced contraction in the human thoracic internal artery, Pflügers Archiv European Journal of Physiologyl of Physiology" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
An alpha 2-adrenergic receptor subtype has been cloned from a human kidney cDNA library using the gene for the human platelet alpha 2-adrenergic receptor as a probe. The deduced amino acid sequence resembles the human platelet ...
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The IUPHAR/BPS Guide to Pharmacology. α2C-adrenoceptor - Adrenoceptors. Detailed annotation on the structure, function, physiology, pharmacology and clinical relevance of drug targets.
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Alpha-1-adrenergic receptors (alpha-1-ARs) are members of the G protein-coupled receptor superfamily. They activate mitogenic responses and regulate growth and proliferat
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The regulatory function of α1B-adrenoceptors in mammalian heart homeostasis is controversial. The objective of the present study was to characterize the expression/activity of key proteins implicated in cardiac calcium handling (Na+/K+-ATPase and Ca2+-ATPases) and growth (ERK1/2, JNK1/2 and p38) in mice with cardiac-selective overexpression of constitutively active mutant α1B-adrenoceptor (CAMα1B-AR), which present a mild cardiac hypertrophy phenotype. Immunoblot assays showed that myocardial plasma membrane Ca2+-ATPase (PMCA) expression was increased by 30% in CAMα1B-AR mice (N = 6, P , 0.05), although there was no change in sarco/endoplasmic reticulum Ca2+-ATPase (SERCA2) expression. Moreover, total Ca2+-ATPase activity was not modified, but a significant increase in the activity of the thapsigargin-resistant (PMCA) to thapsigargin-sensitive (SERCA) ratio was detected. Neither Na+/K+-ATPase activity nor the expression of α1 and α2 subunit isoforms was changed in CAMα1B-AR mouse hearts. ...