Regulation of Adrenergic Receptors in the Rat Kidney
Friedrich Lübbecke, David R. Schneider, G Schütterle
Abstract
Friedrich Lübbecke, David R. Schneider, G Schütterle
Abstract
Chronic daily application of (+/-)-isoprenaline induced a selective-down regulation of beta-adrenoceptors in the kidney: the concentration of [3H]dihydroalprenolol binding sites was significantly lowered by isoprenaline treatment while [3H]prazosin and [3H]rauwolscine binding, representing alpha 1- and alpha 2-adrenoceptors, respectively, was not markedly altered. Since the proportion of high- and low-affinity sites for the non-selective alpha- but relatively beta 1-selective agonist (-)-noradrenaline remained constant and since in [3H]dihydroalprenolol competition experiments the high- and low-affinity site ratio fitted well to the beta 1/beta 2 relation, determined independently by employing ICI 118551 as a beta 2-selective ligand, a parallel decrease of both beta 1- and beta 2-adrenoceptor density can be concluded.
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Chronic daily application of (+/-)-isoprenaline induced a selective-down regulation of beta-adrenoceptors in the kidney: the concentration of [3H]dihydroalprenolol binding sites was significantly lowered by isoprenaline treatment while [3H]prazosin and [3H]rauwolscine binding, representing alpha 1- and alpha 2-adrenoceptors, respectively, was not markedly altered. Since the proportion of high- and low-affinity sites for the non-selective alpha- but relatively beta 1-selective agonist (-)-noradrenaline remained constant and since in [3H]dihydroalprenolol competition experiments the high- and low-affinity site ratio fitted well to the beta 1/beta 2 relation, determined independently by employing ICI 118551 as a beta 2-selective ligand, a parallel decrease of both beta 1- and beta 2-adrenoceptor density can be concluded.
Key concepts: Dihydroalprenolol, Rauwolscine, Isoprenaline, Prazosin, Endocrinology, Adrenergic receptor, Alpha (finance), BETA (programming language)