Drugs online research references
Res Commun Chem Pathol Pharmacol. 1975 Nov;12(3):533-40.
Bioenergetics in clinical medicine. III. Inhibition of coenzyme Q10-enzymes by clinically used anti-hypertensive drugs.
Kishi H, Kishi T, Folkers K.
Background data revealed that some American and Japanese patients with essential hypertension, including many who were not being treated with any anti-hypertensive drug, had a deficiency of coenzyme Q10. Eight clinically used anti-hypertensive drugs have now been tested for inhibition of two mitochondrial coenzyme Q10-enzymes of heart tissue, succinoxidase and NADH-oxidase. Diazoxide and propranolol significantly inhibited the CoQ10-succinoxidase and CoQ10-NADH-oxidase, respectively. Metoprolol did not inhibit succinoxidase, and was one-fourth as active as propranolol for inhibition of NADH-oxidase. Hydrochlorothiazide, hydralazine, ans clonidine also inhibited CoQ10-NADH-oxidase. Reserpine did not inhibit either CoQ10-enzyme, and methyldopa was a very eak inhibitor of succinoxidase. The internationally recognized clinical side-effects of propranolol may be due, in part, to inhibition of CoQ10-enzymes which are indispensable in the bioenergetics of cardiac function. A pre-existing deficiency of coenzyme Q10 in the myocardium of hypertensive patients could be augmented by subsequent treatment with propranolol, possibly to the "life-threatening" state described by others.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1197930&dopt=Abstract
Res Commun Chem Pathol Pharmacol. 1977 May;17(1):157-64.
Bioenergetics in clinical medicine XV. Inhibition of coenzyme Q10-enzymes by clinically used adrenergic blockers of beta-receptors.
Kishi T, Watanabe T, Folkers K.
Adrenergic blockers for beta-receptors were studied for inhibition of mitochrondrial CoQ10-enzymes. These enzymes are indispensable for the bioenegetics of the myocardium. Propranolol is frequently used to treat hypertension; in some patients, it depresses myocardial function as an adverse reaction. This side effect may be related to the inhibition by propranolol of CoQ10-enzymes of the myocardium. Timolol showed negligible inhibition of the CoQ10-enzyme, NADH-oxidase. Metoprolol was less inhibitory than propranolol. Five alprenolols showed inhibition which approached that of propranolol. The 1-isomer of alprenolol showed weak inhibition of another CoQ10-enzyme, succinoxidase, but the other beta-blockers were essentially non-inhibitory to this enzyme. The drug of choice is timolol, based on negligible inhibition of these bioenergetic enzymes of the heart, which correlates with its pharmacologically low cardiac depressant effects.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17892&dopt=Abstract
J Pharmacol Exp Ther. 1981 Sep;218(3):608-12.
Adrenergic beta receptors mediating submandibular salivary gland hypertrophy in the rat.
Brenner GM, Wulf RG.
Multiple injections of dobutamine, a selective adrenergic beta-1 receptor agonist, or isoproterenol, a nonselective beta receptor agonist, produced significant dose-dependent enlargement of the submandibular glands of male rats. The glandular enlargement induced by dobutamine or isoproterenol was characterized by significant increases in glandular protein and nucleic acid content and a marked increase in the RNA/DNA ratio. Metoprolol, a selective beta-1 receptor antagonist, significantly inhibited the glandular enlargement induced by dobutamine or isoproterenol and produced a parallel shift in the isoproterenol dose-response curve. Metoprolol also inhibited the increased protein and nucleic acid content induced by dobutamine or isoproterenol. Multiple injections of selective adrenergic beta-2 receptor agonists, terbutaline, fenoterol or salmefamole, failed to produce submandibular gland enlargement. These results indicate that adrenergic beta-1 receptors mediate submandibular gland hypertrophy in the rat.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6115050&dopt=Abstract
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