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Acta Ophthalmol (Copenh). 1979 Apr;57(2):236-42.
The effect of metoprolol on intra-ocular pressure in glaucoma. A pilot study.

Alm A, Wickstrom CP, Eckstrom C, Ohman L.

Eleven patients with previously untreated glaucoma of one eye were given metoprolol, 50 mg x 3 for one day. Intraocular pressure (IOP) and heart rate were significantly reduced during treatment, and increased after withdrawal of the drug. In the eyes with glaucoma, the mean IOP was reduced from 30.1 to 20.6 mmHg during treatment. Systolic and diastolic blood pressures were also reduced during treatment, but stayed at the same level after withdrawal of the drug. It is concluded that at least part of the reductions observed for IOP and heart rate are drug-induced, while the effect on blood preassure is mainly induced by factors other than the drug. The effect on IOP is considered large enough to be of clinical interest.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=452883&dopt=Abstract




J Pharmacol. 1983;14 Suppl 2:49-60.
Beta-adrenoceptor blocking agents induce different counter-regulatory responses to insulin.

Schluter KJ, Kerp L.

Simultaneous treatment with antidiabetic drugs and beta-adrenoceptor blocking agents is frequent on account of the high incidence of diabetes and cardiovascular disease. The effects of oral doses of pindolol, metoprolol, and propranolol on the response to insulin-induced hypoglycemia and an oral glucose load were investigated. During hypoglycemia metoprolol and propranolol inhibited the clearance of insulin (2 p less than 0.01) and caused a delay of glucose nadirs. This was not observed after pindolol. Epinephrine secretion and the counterregulatory response of growth hormone, ACTH and cortisol during hypoglycemia was significantly increased following metoprolol and propranolol but not after pindolol. The hypoglycemic symptoms and signs showed a prevalence of sweating and prolonged changes in skin conductivity while palpitations were not observed during beta-blockade. Asymptomatic hypoglycemia did not occur.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6138471&dopt=Abstract




Biochim Biophys Acta. 1984 Oct 4;795(3):481-6.
Regulation of liver lipase. II. Involvement of the alpha 1-receptor.

Schoonderwoerd K, Hulsmann WC, Jansen H.

The effects of different adrenergic agents on high density lipoprotein (HDL) cholesterol concentration and on the neutral NaCl-resistant triacylglycerol hydrolase (liver lipase) activity of the liver were studied in rats. Treatment of rats with the beta-blockers metoprolol, atenolol or propranolol led to a lowering of the HDL-cholesterol (esterified and non-esterified) content. The alpha 1-antagonist prazosin had no effect. Administration of norepinephrine for 10 days resulted in an increase of HDL non-esterified cholesterol. This effect of norepinephrine was largely abolished by prazosin, but not by propranolol. In normal rats the liver lipase activity was not influenced by alpha- or beta-blockade. Adrenergic stimulation, either short-term (by diethyl ether stress) or long-term (by norepinephrine treatment), led to a lowered liver lipase activity. The lipase activity was restored by prazosin but not by propranolol. The apparent involvement of the alpha 1-receptor in the regulation of liver lipase activity was further studied in vitro. Blockade of alpha- or beta-receptors with prazosin or propranolol did not affect the secretion of the liver lipase activity by isolated parenchymal liver cells. Stimulation of alpha- or beta-receptors by epinephrine led to a lower secreted lipase activity. Selective stimulation by isoprenaline had no effect. The effect of epinephrine could be abolished by prazosin but not by propranolol. Vasopressin and the calcium ionophore A23187 also lowered the secretion of liver lipase activity in vitro. Glucagon and/or the phosphodiesterase inhibitor Ro 20-1724 had no effect. These results indicate an involvement of the alpha 1-receptor in the regulation of liver lipase activity at the level of synthesis or secretion of the lipase. The effect of the alpha 1-receptor is presumably mediated through changes in the intracellular free calcium concentration. The effect of adrenergic modulation on HDL-cholesterol concentrations can partly be explained through modification of the liver lipase activity.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6148107&dopt=Abstract













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