A receptor known beta 1 adrenergic nor as ADRB1 (β1 adrenergic receptor), and β-adrenergic receptor, but, human gene is coding. This is G protein-coupled receptors coupled to trimeric G-protein heterotrimer Gs that is predominantly expressed in cardiac tissue.

Action of the receptor β1 is as follows.

• Stimulation of a viscous, full amylase secreted by the salivary glands
• I increase the cardiac output
• Increase in heart rate sinoatrial node (SA node) and (chronotropic effect)
• Increase of atrial myocardial contractility. (Inotropic effect)
• I will improve automaticity and contractility of the ventricular myocardium.
• Conductivity is high automatic atrioventricular (AV node)
• Renin release from juxtaglomerular cells.
• The lipolysis in adipose tissue.
• Receptors are also present in the cerebral cortex.

To interact with the beta 1 adrenergic receptor has been shown, DLG4 GIPC1.Interaction between 1β-AR and testosterone are shown in anxiety in the basolateral amygdala.

It is the prototype of the guanine nucleotide-binding regulatory protein-coupled receptor family that mediates physiological action of the neurotransmitter norepinephrine (α1 subtype, α2, β1, β2) and hormone epinephrine adrenergic receptor. Can affect the resting heart rate and also are shown, specific polymorphisms of this gene may be involved in heart failure.

The β1 adrenergic receptor human displays constitutive activity, β-adrenergic antagonists tested the hypothesis that is distinguished by its ability to modulate the constitutive activity we. Transfection of cDN A of the β2-adrenergic receptor and human β1 in COS-7 cells, basal to suggest constitutive activity for both subtypes, increased in proportion to the level of the receptor I caused the cAMP. It is about five times higher than for the β2-β1-subtype receptors increase cAMP of the base at a level comparable. As a model for enhanced organ in the overall level of β-adrenergic signaling, we have used transgenic mice with heart-specific overexpression of β1-adrenergic receptor of human. In this model, β1-adrenergic receptor exhibits constitutive activity, as evidenced by the high percentage of spontaneous beating right atria isolated of β1-transgenic mice and wild-type. This difference is eliminated by the addition of CGP20712A showing inverse agonist properties of the compound. Then, the various β-adrenergic antagonists, the ability to modulate the constitutive activity of the cardiac β1-adrenergic receptors was tested whether it is being used clinically now for the treatment of heart failure are different it. bisoprolol and metoprolol β1 selective antagonists showed significant inverse agonist activity at the β1-adrenergic receptor. Carvedilol acted as showed partial agonist activity which xamoterol and neutral antagonists have been marked. Β1 adrenergic receptor of human conclude that it is displayed, the constitutive activity significantly lower than that of the β2 subtype we. The β-adrenergic antagonists, the ability to exhibit inverse agonist activity at different β1 adrenergic receptor, the human is likely to contribute to its therapeutic effects are currently in clinical.

Activation of the heart of the β-adrenergic receptor plays a central role in the regulation of physiological action of the heart to the increase in demand. Chronic activation of the heart of the β-adrenergic receptor occurs in heart failure due to an increase in circulating levels of catecholamines and sympathetic nerve activity. The adaptive response, in order to meet the requirements of evaluation hemodynamic as positive inotropic support traditionally is to compensate for the inability of the heart, but the recognition of the phenomenon has been changed to 10 years. Currently, sympathetic activity chronic observed in heart failure is harmful and some evidence indicates that plays an important role in the pathogenesis of this disease in practice. It flows through the exhaust myocardial catecholamine, it has been demonstrated in both animal and human experiments. Recently, activation of chronic heart failure-specific β1-adrenergic receptor in transgenic animal models, the myocyte hypertrophy, myocardial fibrosis, and to induce heart failure eventually is shown. In large-scale clinical trials of several β-adrenergic receptor antagonists, and shows a significant advantage of the principles of this treatment. Thus, over the past 10 years, paradigm shift is occurring in the inotropic support to pharmacological inhibition of sympathetic activation.

However, agents that provide the maximum benefit in determining the failure of available β-adrenergic receptor antagonists is unknown. A common feature of the one that contributes to the therapeutic effect of the drug receptor antagonist, is the ability to modulate the activation state of the receptor. G protein-coupled receptors, shows different levels of constitutive activity. It has significant constitutive activity on adrenergic receptors between the β2-adrenergic receptor has been found and is used as one of the receptors for the prototype development of the concept of inverse agonism. The β2-adrenergic receptor human 200-fold overexpression animals.Transgenic, was performed using an in vitro system that shows a significant increase in beating frequency and basal tension, these experiments transfection of receptors in cell culture Isolated atrial be reconstructed later, was extended to transgenic mice Rather, compared to wild type animals. This increase was inhibited 70% by the addition of ICI-118, 551 that act as inverse agonists at that receptor.

In this study, it is to evaluate the intrinsic activity of both the β2-adrenergic receptor and β1. Then, to determine the effect of activation level of xamoterol of β1-adrenergic receptor in the atrium of the heart and β1-adrenergic receptor human propranolol, metoprolol, bisoprolol, CGP 20712A, transgenic mice overexpressing and carvedilol.

By binding to receptors on the cell surface, (TGF-β1) causes renal fibrosis transforming growth factor-β1 in fibrotic cytokines, but the receptors correlated TGF-β superfamily and renal fibrosis It is not known either. To solve this, to quantify the expression of the receptor TGF-β superfamily in the kidney of unilateral ureteral obstruction rats using real-time PCR, gene sequences. I fell in rat kidney interfere significantly ALK6 mRNA expression expression of mRNA TGF-β receptor II (ALK) -5, and ALK7 activin-like kinase receptor (TGF-βRII) has increased significantly. Fucosylation is essential for both ALK5 and TGF-βRII in epithelial cells proximal tubule human kidney were cultured in vitro to function properly. Therefore, from adenovirus-mediated knockdown of FUT8 mRNA in in vivo, and the purpose of regulatory post-translational fucosylated by fucosyltransferase α-1, 6 (FUT8), we, ALK5 expression of renal fibrosis and TGF-βRII I measure the progress. Inhibition of relaxation Koafukoshiru prevention of long-term injury, the progression of renal fibrosis and TGF-βRIIALK5, in spite of the effect independent of expression and TGF-βRIIALK5. Therefore, it is to regulate the core fucosylation TGF-β1 receptor can be used to provide a novel therapeutic strategy potential for the treatment of renal fibrosis.