Drugs online research references
J Clin Invest. 1988 Jun;81(6):1979-85.
Desensitization of the insulin receptor by antireceptor antibodies in vivo is blocked by treatment of mice with beta-adrenergic agonists.
Elias D, Rapoport M, Cohen IR, Shechter Y.
Department of Hormone Research, Weizmann Institute of Science, Rehovot, Israel.
In previous studies we reported that immunization of mice with ungulate insulins induced the development of antiinsulin antibodies, which include an idiotype that appeared to recognize the part of the insulin molecule recognized by the hormone receptor. The antiinsulin antibodies of this idiotype were replaced spontaneously by antiidiotypic antibodies. The antiidiotypic antibodies, which persisted for about 14 d, mimicked insulin and functioned as antibodies to the insulin receptor. They induced down regulation, desensitization and refractoriness of the insulin receptor and disturbances in glucose homeostasis in vivo (Shechter, Y., D. Elias, R. Maron, and I.R. Cohen., 1984; Elias, D., R. Maron, I.R. Cohen, and Y. Shechter. 1984, J. Biol. Chem. 259: 6411-6419). We now report that effects of the antiidiotypic antibodies on the insulin receptor effector system can be modified pharmacologically. Administration of the beta-adrenergic agonist isoproterenol during the period of insulin resistance (days 26-40 after primary immunization), largely restored fat cell responsiveness to insulin, and eliminated the appearance of fasting hyperglycemia. This restoration appeared to be caused by inhibition of both insulin receptor desensitization and refractoriness. In contrast, down regulation of insulin receptors was not reversed by isoproterenol treatment in vivo. The effects of treatment with isoproterenol persisted for 2-4 d after termination of treatment. The beta-antagonist, propranolol and more so, the beta 1a-antagonist metoprolol, specifically blocked the effect of isoproterenol at a molar ratio of 3-10:1. Oral administration of the cAMP phosphodiesterase inhibitor, aminophylline, was also effective in inhibiting the development of desensitization in fat cells. These results indicate that treatment with beta 1-adrenergic agonists in vivo, or other agents that elevate cellular cAMP levels, can inhibit the development of the "postbinding" defects induced by insulin-mimicking, antireceptor antibodies. These observations have both basic and clinical implications.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3290258&dopt=Abstract
Diabete Metab. 1981 Dec;7(4):235-8.
Hypoglycemic symptoms in insulin-dependent diabetics. A prospective study of the influence of beta-blockade.
Blohme G, Lager I, Lonnroth P, Smith U.
Hypoglycemic attack rate, duration and symptomatology were studied in five insulin-dependent diabetics with borderline hypertension all of whom were prone to hypoglycemia. They were treated in a double-blind, cross-over fashion with the cardioselective beta 1-blocking agent metoprolol and placebo. The treatment period on each drug lasted at least three months. No treatment-associated differences in attack rate and duration of hypoglycemic attacks were recorded. Slight, but no severe masking of hypoglycemic symptoms was recorded in one patient on metoprolol. It is concluded that cardioselective beta 1-blocking agents can be used by insulin-dependent diabetics. However, until further direct experience has been gained caution should be exercised in treating patients with obvious clinical signs of autonomic neuropathy with these drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7333405&dopt=Abstract
Cor Vasa. 1983;25(5):358-66.
The use of systolic time intervals in the evaluation of antihypertensive treatment with metoprolol, labetalol and prazosin.
Buch J, Rasmussen S.
26 patients with moderate hypertension and no signs of heart failure were treated with metoprolol, labetalol or prazosin. Systolic time intervals (STI) were measured before and after several months of treatment. During treatment with metoprolol, a decrease in the preejection period index (PEPI), and preejection period/left ventricular ejection time ratio (PEP/LVET), was found. During treatment with labetalol or prazosin, a minor decrease in PEPI was observed, so that a significant decrease in PEP/LVET was not obtained. A decrease in PEPI and PEP/LVET may be due to improved cardiac performance, but in the given type of patients it is more dependent on the reduction in afterload. The STI measurement is less sensitive in discerning different mechanisms involved in lowering the blood pressure and cannot therefore be used for selecting the optimal antihypertensive drug.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6653128&dopt=Abstract
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