نتایج جستجو برای: adrenergic receptors adrb3
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It is well known that the renal nerve plays an important role in the regulation of renal functions such as sodium and water reabsorption in the tubules as well as in the pathogenesis of essential hypertension. The renal sympathetic nerves innervate to the basement membranes of almost all nephron segments. Specific adrenergic receptors and intracellular signal transduction systems are located in...
Background—We have recently shown that genetic inactivation of phosphoinositide 3-kinase (PI3K ), the isoform linked to G-protein–coupled receptors, results in increased cardiac contractility with no effect on basal cell size. Signaling via the G-protein–coupled -adrenergic receptors has been implicated in cardiac hypertrophy and heart failure, suggesting that PI3K might play a role in the path...
Sympathetic nerves may play a role in vascular disorders of the eye. In the present study, we hypothesized that activation of beta3-adrenergic receptors on retinal endothelial cells would promote migration and proliferation of these cells, two markers of an angiogenic phenotype. We show, for the first time, expression of beta3-adrenergic receptors on cultured retinal endothelial cells. Activati...
In this study the effect of adrenergic receptor agonists and antagonists on physostigmine induced yawning was investigated. Intraperitoneal injection of different doses of physostigmine (0.03, 0.05, 0.1 and 0.2 mg/kg) caused yawning in white rats. The greatest response was seen at a dose of 0.2 mg/kg physostigmine. Phenylephrine, an α1 agonist, and clonidine, an α2 agonist, led to a decrease in...
ATP, norepinephrine and NPY are co-released by sympathetic nerves innervating arteries. ATP elicits vasoconstriction via activation of smooth muscle P2X receptors. The functional interaction between neuropeptide Y (NPY) receptors in arteries is not known. In this study we investigate the effect on P2X1-dependent mouse mesenteric Suramin or P2X1 antagonist NF449 abolished α,β-meATP evoked vasoco...
ABSTRACT In the late 1970s, we discovered that toxic bicyclic phosphates inhibit generation of miniature inhibitory junction potentials, implying their antagonism ?-aminobutyric acid (GABA) receptors (GABARs; GABA-gated chloride channels). This unique mode action provided a strong incentive for our research on GABARs in later years. Furthermore, minor structural changes conferred insect GABAR s...
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