Drugs online research references
Lancet. 1995 Mar 11;345(8950):623-4.
Is neurally mediated hypotension an unrecognised cause of chronic fatigue?
Rowe PC, Bou-Holaigah I, Kan JS, Calkins H.
Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21287.
Neurally mediated hypotension is now recognised as a common cause of otherwise unexplained recurrent syncope, but has not been reported in association with chronic fatigue. We describe seven consecutive non-syncopal adolescents with chronic post-exertional fatigue, four of whom satisfied strict criteria for chronic fatigue syndrome. Upright tilt-table testing induced significant hypotension in all seven (median systolic blood pressure 65 mm Hg, range 37-75), consistent with the physiology of neurally mediated hypotension. Four had prompt improvement in their chronic fatigue when treated with atenolol or disopyramide. These observations suggest an overlap in the symptoms of chronic fatigue syndrome and neurally mediated hypotension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7898182&dopt=Abstract
Am J Physiol. 1996 Oct;271(4 Pt 2):R982-9.
Norepinephrine-mediated hypoxic stimulation of embryonic red cell carbonic anhydrase and 2,3-DPG synthesis.
Dragon S, Glombitza S, Gotz R, Baumann R.
Physiologisches Institut, Universitat Regensburg, Germany.
Hypoxia is the stimulus for activation of red cell carbonic anhydrase II (CAII) and 2,3-diphosphoglycerate (2,3-DPG) synthesis of chick red blood cells during late embryonic development. We have tested whether plasma catecholamines are involved as hormonal mediators, because hypoxia is a well-known stimulus for catecholamine release in mammalian fetuses. Plasma catecholamines were measured in 8- to 16-day-old chick embryos. Plasma levels of norepinephrine (NE) were initially low, but its concentration increased rapidly from 2.7 nM (day 12) to 13.4 nM at day 13 and 25.5 nM at day 16. Epinephrine (E) was not detectable before day 13. Short-term hypoxic exposure of day 11 embryos (1-h incubation at 13.5% O2) increased plasma NE concentration fivefold compared with the controls but had no effect on E. During 15-h in vitro incubation of red blood cells from day 11, addition of 1 microM NE to the incubation medium increased the red cell 2,3-DPG concentration nearly threefold and CAII activity sixfold compared with the control. The CAII activity and 2,3-DPG concentration were also increased when cells were incubated with plasma from late chick embryos. The activation was induced by beta-adrenergic stimulation of adenylyl cyclase. Atenolol and propranolol blocked the effects of NE and embryonic chick plasma. Analysis of de novo protein synthesis ([35S]methionine incorporation) demonstrated that catecholamines stimulate the synthesis of several proteins besides CAII. The results indicate that developmental changes of plasma NE concentration are instrumental in the adenosine 3',5'-cyclic monophosphate-dependent activation of CAII and 2,3-DPG synthesis of red blood cells from late chick embryos.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8897991&dopt=Abstract
J Pharmacol Exp Ther. 1989 Sep;250(3):759-63.
A stereoselective central hypotensive action of atenolol.
Pearson AA, Gaffney TE, Walle T, Privitera PJ.
Department of Cellular and Molecular Pharmacology, Medical University of South Carolina, Charleston.
Previous studies have demonstrated that propranolol can lower arterial pressure through an action within the central nervous system. The purpose of this study was to determine 1) whether the hydrophilic beta blocking drug atenolol which is devoid of membrane stabilizing activity can reduce arterial pressure through a central action and 2) whether this action is stereoselective for the (-)-, or beta receptor blocking enantiomer. Studies were conducted in the anesthetized spontaneously hypertensive (SH) rats in which the cardiovascular effects of (-)- and (+)- atenolol were compared after i.v. or intracisternal administration. Intravenous injection of 100 micrograms/kg of (-)-atenolol reduced mean arterial pressure 25 +/- 5 mm Hg (P less than .02) and lowered heart rate 58 +/- 7 bpm (P less than .02). The same dose of (+)-atenolol i.v. produced no significant changes in either mean arterial pressure or heart rate. Similarly, intracisternal (-)-atenolol, 66 micrograms/kg, significantly (P less than .05) reduced mean arterial pressure and heart rate whereas the same dose of the (+)-isomer was without effect. When the i.v. dose of (-)-atenolol was lowered to 33 micrograms/kg, heart rate was decreased markedly but mean arterial pressure was not reduced. In contrast, 33 micrograms/kg of intracisternal (-)- atenolol significantly reduced mean arterial pressure 17 +/- 6 mm Hg and reduced heart rate. These results suggest that atenolol possesses a central hypotensive action that is selective for the (-)-, beta receptor blocking enantiomer.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2778713&dopt=Abstract
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