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Alpha Adrenergic Receptor

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W. Keith Mcelroy – One of the best experts on this subject based on the ideXlab platform.

  • Influence of chlordimeform on AlphaAdrenergic Receptor-associated mechanisms of hormonal regulation in the rat: pituitary and adrenocortical secretion.
    Toxicology, 1991
    Co-Authors: Tammy E. Stoker, Jerome M. Goldman, Ralph L. Cooper, W. Keith Mcelroy

    The acaricide chlordimeform (CDF) has been reported to have effects on the central nervous system that appear to involve an interaction with AlphaAdrenergic Receptor-mediated mechanisms of neurotransmission. The present study examined the effects of CDF on adrenocortical and pituitary prolactin secretion, which are known to involve central Adrenergic Receptors. Male Long-Evans rats were injected i.p. with 20 or 50 mg/kg CDF and killed after 1, 4, 8 or 24 h. Both noninjected and saline-injected controls were included. Dosing was structured so that trunk blood could be collected during the morning nadir of circulating corticosterone (CORT). Assays for plasma adrenocorticotropic hormone (ACTH), CORT and prolactin (PRL) showed that with 50 mg/kg, all three hormones rose sharply by 1 h. CORT increased in a dose-dependent fashion and declined over the ensuing 8 h. Other rats were treated with the AlphaAdrenergic antagonist phenoxybenzamine (PBZ, 20 mg/kg) or the Alpha-agonist clonidine (CLON, 0.6 mg/kg) 40 min before and killed 1 h after CDF (25 mg/kg) injection. CLON was found to completely suppress the CDF-induced rise in CORT, while PBZ enhanced the CORT/ACTH response to CDF. CLON also significantly elevated PRL, an alteration not seen in the CLON-pretreated CDF rats. Dexamethasone was able to block the CDF-induced rise in CORT and significantly suppressed PRL levels in both saline- and CDF-treated groups. These effects indicate that CDF is interfering with a regulatory signal mediated by AlphaAdrenergic Receptor-associated activity.

Martin C. Michel – One of the best experts on this subject based on the ideXlab platform.

  • the Alpha 1a Adrenergic Receptor subtype mediates biochemical molecular and morphologic features of cultured myocardial cell hypertrophy
    Journal of Biological Chemistry, 1993
    Co-Authors: Kirk U Knowlton, Martin C. Michel, M Itani, H E Shubeita, K Ishihara, Joan Heller Brown, Kenneth R Chien

    Alpha 1-Adrenergic agonists induce a hypertrophic phenotype in cultured neonatal rat ventricular myocytes. Quantifiable markers of this phenotype include stimulation of phosphoinositide hydrolysis, transcriptional induction of atrial natriuretic factor (ANF) gene expression, and an increase in myocardial cell size. The aim of the present work was to determine which Alpha 1-Adrenergic Receptor subtype mediates the acquisition of these parameters of myocardial cell hypertrophy. Phosphoinositide hydrolysis is inhibited by low concentrations of 5-methylurapidil (log Ki = -8.7) and (+)-niguldipine (log Ki = -10.6). The AlphaAdrenergic Receptor-induced increase in transcriptional activation of an ANF luciferase reporter gene is inhibited over the same range of concentrations of 5-methylurapidil (log Ki = -8.2) and (+)-niguldipine (log Ki = -11.2) that inhibit phosphoinositide hydrolysis. In addition, the increase in cell size that accompanies AlphaAdrenergic Receptor stimulation of cultured ventricular myocytes is blocked by similar concentrations of 5-methylurapidil (log Ki = -8.0) and (+)-niguldipine (log Ki = -10.6). In contrast, treatment with the Alpha 1B selective antagonist chlorethylclonidine at a concentration of 10 microM had no effect on the Adrenergically mediated induction of ANF luciferase reporter gene expression or the Adrenergically induced increase in myocardial cell size. These findings demonstrate that pharmacologically identifiable Alpha 1A-Adrenergic Receptors mediate not only the early effects of Alpha 1-Adrenergic stimulation such as phosphoinositide hydrolysis, but that they activate the signaling pathways that control transcriptional induction of the ANF luciferase reporter gene and an increase in myocardial cell size. Studies using Alpha 1-Adrenergic Receptor cDNAs to delineate and alter the direct interaction of this Receptor subtype with proximal signaling molecules, e.g. GTP binding proteins, should provide a powerful means of assessing their role in the induction of the molecular and morphologic parameters of myocardial cell hypertrophy.

  • On the role of renal AlphaAdrenergic Receptors in spontaneously hypertensive rats.
    Hypertension (Dallas Tex. : 1979), 1992
    Co-Authors: Martin C. Michel, S Jäger, R. Casto, Rainer Rettig, C Graf, Morton P. Printz, Paul A. Insel, T Philipp, Otto-erich Brodde

    We tested the hypothesis that a genetically determined increase in renal AlphaAdrenergic Receptor density might be a pathophysiologically important factor in the spontaneously hypertensive rat model of genetic hypertension. In a first study, we compared renal Alpha 1 and Alpha 2-Adrenergic Receptor density with systolic blood pressure in 45 rats of an F2 generation of Wistar-Kyoto x spontaneously hypertensive rat hybrids but were unable to detect significant cosegregation between either Receptor density or blood pressure. In a second study, we determined renal Alpha 1- and Alpha 2-Adrenergic Receptor density in Wistar-Kyoto and spontaneously hypertensive rat kidneys that were transplanted into an F1 generation of Wistar-Kyoto x spontaneously hypertensive rat hybrids. Although Wistar-Kyoto kidneys lowered blood pressure in these animals and spontaneously hypertensive rat kidneys increased blood pressure, renal AlphaAdrenergic Receptor densities were similar in membranes from both types of kidneys. Since rat kidney coexpresses Alpha 1A- and Alpha 1B-Adrenergic Receptors, we also investigated whether differential regulation of these two subtypes might conceal ongoing alterations. The Alpha 1A/Alpha 1B-Adrenergic Receptor ratio, however, was similar in Wistar-Kyoto rats, spontaneously hypertensive rats, and F1 rats transplanted with a kidney from either strain. Taken together these data do not support the hypothesis that genetically determined alterations of renal AlphaAdrenergic Receptor numbers play an important role in the development of elevated blood pressure in the spontaneously hypertensive rat.

Claus G. Roehrborn – One of the best experts on this subject based on the ideXlab platform.

  • Efficacy of AlphaAdrenergic Receptor Blockers in the Treatment of Male Lower Urinary Tract Symptoms.
    Reviews in urology, 2009
    Co-Authors: Claus G. Roehrborn

    Male lower urinary tract symptoms (LUTS) are one of the most common causes for a consultation with a health care provider, and one of the most common causes of male LUTS is benign prostatic hyperplasia (BPH). In recent decades, medical therapy has established itself as viable and cost effective for the majority of men. For the treatment of male LUTS in the United States, the 5 currently available AlphaAdrenergic Receptor blockers are alfuzosin, doxazosin, silodosin, terazosin, and tamsulosin. Alpha-Blockers remain one of the mainstays in the treatment of male LUTS and clinical BPH. They exhibit an early onset of efficacy (within less than 1 week) with regard to both symptoms and flow rate improvement, maintain such improvements in open-label and controlled trials for up to 5 years, and have been shown to prevent symptomatic progression.