Drugs online research references
Pharmacology. 1993 Nov;47(5):295-9.
Lipophilic beta-blockers inhibit rat skeletal muscle mitochondrial respiration.
Dreisbach AW, Greif RL, Lorenzo BJ, Reidenberg MM.
Department of Pharmacology and Medicine, Cornell University Medical College, New York, NY 10021.
Propranolol, metoprolol, acebutolol, nadolol and atenolol were incubated with isolated rat skeletal muscle mitochondria at 30 degrees C, and the rate of oxygen consumption was measured with an oxygen microelectrode. The potency of these drugs to inhibit state III respiration was correlated with lipid solubility as measured by the octanol/water partition coefficient. The most lipid-soluble beta-blocker, propranolol, had an ED50 of 0.6 mmol/l. The most water-soluble one, atenolol, showed no inhibition at concentrations up to 16 mmol/l. Inhibition of respiratory control ratio, state IV respiration and ADP/O ratio occurred at 2 mmol/l for propranolol, 16 mmol/l for metoprolol and was not consistently observed for the other beta-blockers at the concentrations tested. The inhibition of state III respiration of skeletal muscle mitochondria by lipid-soluble beta-blockers may be one of the causes of the fatigue observed in some patients receiving these drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7903463&dopt=Abstract
Med Sci Sports Exerc. 1994 Apr;26(4):459-62.
Vagal afferents reflexly inhibit exercise in conscious rats.
DiCarlo SE, Collins HL, Chen CY.
Department of Physiology, Northeastern Ohio Universities, College of Medicine, Rootstown 44272.
Activation of vagal afferents reflexly inhibited locomotion induced by stimulation of the mesencephalic locomotor region in decerebrate cats. However, this reflex has not been tested in intact mammals. Therefore, the purpose of this study was to test the hypothesis that vagal afferent stimulation would inhibit somatomotor activity in the intact conscious rat. Six Sprague-Dawley rats were chronically instrumented with carotid arterial and femoral venous catheters and electromyogram (EMG) electrodes inserted into the biceps femoris muscle. Cardiac autonomic efferent blockade [atropine methyl bromide (14 mg.kg-1, i.v.) and metoprolol (14 mg.kg-1, i.v.)] and alpha-adrenergic receptor blockade [phenoxybenzamine (5 mg.kg-1, i.v.)] was achieved to prevent bradycardia and hypotension. Vagal afferents were stimulated (phenyl-biguanide 2.5 and 5.0 micrograms.kg-1 i.v.) during steady state exercise (9.0 m.min-1, 10% grade). Phenyl-biguanide decreased exercise EMG activity 30 +/- 6% and 54 +/- 10% in a dose dependent manner without significantly altering mean arterial pressure or heart rate. We speculate that this reflex may serve as a negative feedback mechanism to indirectly reduce myocardial oxygen demands during exercise.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8201902&dopt=Abstract
Biochem Pharmacol. 1988 Oct 15;37(20):3829-35.
Xenobiotic and endobiotic inhibitors of cytochrome P-450dbl function, the target of the debrisoquine/sparteine type polymorphism.
Fonne-Pfister R, Meyer UA.
Department of Pharmacology, University of Basel, Switzerland.
Five to 10% of Caucasians are poor metabolizers (PM) of debrisoquine, sparteine, bufuralol and numerous other drugs. A deficiency in cytochrome P-450dbl (P-450dbl) function is the cause of this polymorphism of drug oxidation with autosomal recessive inheritance. In the present study, inhibition of bufuralol-1'-hydroxylase in human liver microsomes by drugs and chemicals was performed in a search for potential new substrates for this polymorphic enzyme. Among the 80 alkaloids and drugs tested, 25 were competitive inhibitors. In vitro competitive inhibition of bufuralol oxidation by a substance indicates that this compound is able to bind to the same enzymatic site as bufuralol. This may mean that the competing drug also is metabolized by P-450dbl and that its metabolism is subject to the same genetic variation as the oxidation of bufuralol. However, some of these competitive inhibitors are not oxidized by P-450dbl. In this case, however, they may interfere with the in vivo phenotyping procedure by inhibiting the formation of metabolites of test drugs such as debrisoquine, sparteine, metoprolol or dextrometorphan.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2903741&dopt=Abstract
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