Disease relevance of DEXPROPRANOLOL

• Suppression of ventricular arrhythmias in man by d-propranolol independent of beta-adrenergic receptor blockade [1].
• METHODS: Rats were treated either acutely or chronically over weeks and months, with one of the above migraine prophylactic drugs, vehicle, or D-propranolol, a clinically ineffective drug [2].
• METHODS: We investigated the effect of cirrhosis on p-nitrophenol sulphation and compared this with the effect of cirrhosis on p-nitrophenol glucuronidation as well as on d-propranolol oxidation simultaneously in the single-pass isolated perfused rat liver [3].
• Left ventricular hypertrophy was also prevented by D-propranolol, 40 and 80 mg/kg per day, and disopyramide, 50 mg/kg per day, whereas timolol, 30 and 60 mg/kg per day, showed no antihypertrophic effect [4].
• ESF production in rabbits given d-propranolol or practolol during hypoxia was not significantly different from that of control animals exposed to hypoxia [5].

Psychiatry related information on DEXPROPRANOLOL

• Lack of efficacy of d-propranolol in neuroleptic-induced akathisia [6].
• DL-propranolol infused 5 min, but not 6 hr, posttraining caused a deficit in 48-hr memory for the spatial water maze task, whereas similarly administered D-propranolol, which has an equipotent "local-anesthetic" activity but significantly lower beta-blocking activity, induced no amnesia [7].
• Increased motor activity and poor performance in the active avoidance test were observed in the offspring of rats treated with dl-propranolol or sotalol during pregnancy, but not with atenolol and d-propranolol [8].

High impact information on DEXPROPRANOLOL

• A fourth group of dogs showed a rise in renin secretion from 205 to 880 U/min (P less than 0.001) in response to the first RNS, while the second RNS, given after an infusion of d-propranolol, caused a rise in renin secretion from 80 to 482 (P less than 0.005) [9].
• When endothelial cells were incubated with dl- or d-propranolol, the media had two to three times the inhibitory activity of control media [10].
• Groups of littermate rabbits were treated for various periods up to 6 weeks with twice daily subcutaneous injections of saline, D-propranolol, DL-propranolol, or metoprolol, the latter two at doses equivalent to those used in clinical therapy [11].
• In addition, d-propranolol (the non beta-blocking isomer) and the antioxidant enzymes, SOD and catalase, showed significant protection [12].
• After protein binding was accounted for, the unbound oral clearance of each enantiomer was similar in both groups. l-Propranolol was more highly protein bound than d-propranolol (p less than 0.05) in both young and older subjects [13].

Chemical compound and disease context of DEXPROPRANOLOL

• To investigate the mechanisms of ventricular arrhythmia suppression by propranolol, we determined the antiarrhythmic efficacy of d-propranolol in 10 patients with frequent ventricular ectopic depolarizations (VEDs) and nonsustained ventricular tachycardia [1].
• Role of beta-adrenoreceptor antagonism in the prevention of reperfusion ventricular arrhythmias: effects of acebutolol, atenolol, and d-propranolol on isolated working rat hearts subject to myocardial ischemia and reperfusion [14].
• During ischemia: intracellular acidosis, adenosine triphosphate (ATP) degradation, and inorganic phosphate (Pi) accumulation were found to be reduced whether the perfusion fluid contained: acebutolol 2.7 x 10(-5) M, atenolol 10(-5) M, d-propranolol 10(-5) M, or dl-propranolol 10(-5) M [15].
• The effects of d-propranolol and captopril on post-ischaemic acute renal failure in rats [16].
• In this study, superoxide dismutase (SOD), an enzyme that catalyzes the dismutations of superoxide free radical (O2-) to less toxic forms, plus reduced glutathione (GSH), and d-propranolol (PROP), were evaluated for their ability to protect against acute paraquat toxicity [17].

Biological context of DEXPROPRANOLOL

• All beta-blockers have an antihypertensive effect, regardless of other characteristics (e.g. cardio-selectivity, instrinsic sympathomimetic effect, or membrane activity). d-Propranolol has no significant effect on blood pressure [18].
• 6. The changes in muscle performance and bioenergetics observed during the incremental stimulation protocol were not observed when D-propranolol was administered and could be completely circumvented by a short period of muscle stimulation of 4 Hz prior to initiation of the incremental stimulation protocol [19].
• 5. D-propranolol, the isomer with much lower beta-receptor blocking potency, required twentyfold higher concentrations to depress automaticity and this was accompanied by evidence of direct membrane depression, i.e. reduction of upstroke velocity of action potentials [20].
• These results suggest that K-7259 and d-propranolol attenuate the H2O2-induced changes in cell shape and accumulation of NEFA, probably because of their .OH-scavenging effect [21].
• Cocaine was ineffective by itself in promoting contraction, but a cumulative concentration-response curve was obtained in the presence of DL-propranolol (1.3 x 10(-6) M); D-propranolol failed to promote cocaine-induced vasoconstriction [22].

Anatomical context of DEXPROPRANOLOL

• The objective of the present investigation was to study the effects of propranolol (i.e., racemic d,1 mixture) and d-propranolol upon regional cerebral blood flow (rCBF) and early ischemic changes following experimental middle cerebral artery (MCA) occlusion [23].
• Intraarterial infusions of dl-propranolol, d-propranolol, AII, and dl-propranolol-plus-AII into the superior mesenteric artery increased mesenteric venous PGE2 concentrations from 216 +/- 33 to 355 +/- 33 (p less than 0.01), 328 +/- 44 (p less than 0.05), 325 +/- 27 (p less than 0.02), and 407 +/- 44 pg/ml (p less than 0.01) respectively [24].
• Contractile actions of racemic and d-propranolol on isolated canine mesenteric and coronary arteries [25].
• Canine Purkinje fibers were exposed to both dl-propranolol, 3.4 X 10(-7) M (0.1 microgram/ml) and 1.7 X 10(-6) M (0.5 micrograms/ml), and to d-propranolol, 3.4 X 10(-7) M (0.1 micrograms/ml), in Tyrode's solution for 90 to 180 min [26].
• Mechanisms related to the inhibitory actions of low concentrations of l- and d-propranolol on adrenergic transmission were investigated in isolated preparations of guinea-pig pulmonary arteries [27].

Associations of DEXPROPRANOLOL with other chemical compounds

• Control of renin release. Effects of d-propranolol and renal denervation on furosemide-induced renin release in the dog [28].
• Treatment of the hypoxic hearts with dl-propranolol, d-propranolol and atenolol was performed during 5 to 15 min of hypoxic perfusion. dl-Propranolol and d-propranolol at the concentration of 45 microM elicited a significant recovery of cardiac contractile activity and restoration of myocardial high-energy phosphates [29].
• The decrease in blood pressure after intraventricular infusion of 1 mM pindolol, 5 mM d-propranolol and 3 mM dl-propranolol was significantly greater than the decrease after intravenous infusion of the same concentrations of each agent [30].
• Effects of d-propranolol and estradiol on the cervicovaginal epithelium [31].
• We selected three drugs to attempt to block the rise in body temperature and plasma IL-6; L-propranolol, D-propranolol and nadolol [32].

Gene context of DEXPROPRANOLOL

• The method allowed study of the depletion of S-(-)- and R-(+)-propranolol in transgenic Chinese hamster CHL cell lines expressing CYP3A4, CYP2C18 and CYP2C9 [33].
• However, d-propranolol had no major effects on HMG CoA reductase activity [34].
• An enantioselective assay for S-(-)- and R-(+)-propranolol in transgenic Chinese hamster CHL cell lines, expressing human cytochrome P450 (CYP), was developed [33].
• Both D-propranolol and L-propranolol inhibited LCAT activity, the former being a little more effective [35].
• DL-Propranolol, a beta 1, beta 2-adrenergic blocking agent, and D-propranolol, a non-beta-blocking isomer with nonspecific membrane stabilizing effects, both produced a significant (P less than 0.01) inhibition of the effects of PGE2 or PGD2 on CFU-E in murine bone marrow cultures [36].

Analytical, diagnostic and therapeutic context of DEXPROPRANOLOL

• Perfusion of the sinuses with d-propranolol or procaine at the same doses also totally inhibited the response [37].
• Intravenous infusions of adrenaline, 1 microgram/kg b.wt./min for 10 minutes also produced an increase of about 70% in the plasma levels of d-propranolol [38].
• The attenuation of reperfusion-induced metabolic changes was more marked when these drugs were present during reperfusion. d-Propranolol showed a cardioprotection similar to that by dl-propranolol [39].
• Stereoselective urinary excretion of S-(-)- and R-(+)-propranolol glucuronide following oral administration of RS-propranolol in Chinese Han subjects [40].
• In anesthetized open-chest pigs, DL- or D-propranolol (1 mg/kg i.v.) was administered 15 min prior to ligation of the left anterior descending coronary artery (LAD) about halfway from its origin [41].

References