Drugs online research references
Endocrinol Jpn. 1989 Oct;36(5):687-94.
Effects of beta-adrenergic blockers with different ancillary properties on lipid peroxidation in hyperthyroid rat cardiac muscle.
Asayama K, Dobashi K, Hayashibe H, Kato K.
Department of Pediatrics, Yamanashi Medical College, Japan.
To determine whether beta-blockade protects rat heart against thyroxine (T4)-induced accelelation of lipid peroxidation, in vivo effects of 3 beta-blockers with different ancillary properties on the mitochondrial oxidative enzyme, antioxidant enzymes and lipid peroxide were investigated. The rats were rendered hyperthyroid by adding T4 to their drinking water for 3 weeks and were treated simultaneously with either carteolol (a blocker with partial agonist activity; 30 mg/kg/day), atenolol (50 mg/kg/day) or arotinolol (a blocker with weak alpha-blocking action; 50 mg/kg/day). The T4-induced tachycardia was alleviated completely by either atenolol or arotinolol, but only partially by carteolol. Cytochrome c oxidase activity in the heart muscle was increased by T4 with a parallel increase in manganese (mitochondrial) superoxide dismutase. Atenolol, but neither carteolol nor arotinolol, suppressed this increase. Similarly, the T4-induced acceleration of lipid peroxidation was suppressed by atenolol alone. Glutathione peroxidase was markedly decreased, and both copper zinc (cytosolic) superoxide dismutase and catalase were also decreased or tended to be decreased by T4. The levels of these 3 enzymes were only minimally affected by the beta-blocker treatments. These results suggest that beta-blockade suppresses mitochondrial hypermetabolism and protects heart muscle against oxidative stress in hyperthyroidism, and that the ancillary properties of beta-blockers such as partial agonist activity and alpha-blocking action negate the protection.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2575990&dopt=Abstract
Am J Med Sci. 1985 Jul;290(1):15-8.
Differences in response of black hypertensives to alpha vs. beta adrenergic antagonists: preliminary findings.
Anderson S, Graham RM, Brater DC.
We tested our clinical impression that black hypertensives in our clinic population responded better to alpha-adrenergic blocking agents (clonidine and prazosin) than to beta-adrenergic blockers (atenolol, nadolol and propranolol). Compared to no effect from eight weeks of therapy with beta-blockers, clonidine significantly decreased erect mean arterial pressure (MAP) when assessed weekly for four weeks (p = 0.027 to 0.046). However, the decrease in supine MAP was not significant. The effects of prazosin were more modest. Supine MAP was significantly less than with beta-blockade (p = 0.032) at two weeks but not at four weeks and decrements in erect MAP were not significant. In this preliminary study, black hypertensives appeared to be more responsive to alpha-adrenergic antagonists than to beta-blockers, with clonidine more effective than prazosin. Elucidation of possible mechanisms of the difference and of its clinical importance warrant further study.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2863982&dopt=Abstract
J Clin Pharmacol. 1987 Jul;27(7):475-80.
Short-term effects of beta blockers atenolol, nadolol, pindolol, and propranolol on lipoprotein metabolism in normolipemic subjects.
Harvengt C, Heller FR, Martiat P, Van Nieuwenhuyze Y.
Laboratoire de Pharmacotherapie, Universite Catholique de Louvain, Brussels, Belgium.
The short-term effect of the blockade of the beta-adrenergic receptors on serum lipoproteins and the plasma activities of the enzymes involved in the metabolism of the serum lipoproteins: lipoprotein lipase (LPL), hepatic lipase (HL) and lecithin: cholesterol acyltransferase (LCAT) was evaluated in ten healthy normolipemic and normotensive subjects. In the first part of the study, the first three-day period of placebo was followed by another three-day period during which propranolol (120 mg/d) was given. In the second, third, and fourth part of the study, the same schedule was used but pindolol (15 mg/d), nadolol (160 mg/d), atenolol (100 mg/d) were given respectively instead of propranolol. The four drugs induced a significant blockade of the beta-adrenergic receptors as evaluated by the measurement of the double two-step test of Master (-45%). Despite similar blockade, the effect on serum lipid concentrations depended on the type of drug: propranolol induced an increase in triglycerides and apoprotein B-concentrations and a decrease in serum high density lipoprotein cholesterol (HDL-C) and apoprotein AI-concentrations. Pindolol provoked only a slight decrease of serum HDL-C concentration. Nadolol and atenolol elicited a lowering of the same magnitude in HDL-C. Except for a possible slight increase in plasma LCAT activity on propranolol, there was no significant change in the plasma activities of LPL, HL, and LCAT during the blockade of the beta-adrenergic receptors with the drugs used.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2888790&dopt=Abstract
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