Drugs online research references
Am J Physiol. 1994 May;266(5 Pt 2):R1664-9.
Angiotensin II overflow from canine skeletal muscle in vivo: importance of plasma angiotensin I.
Schwieler JH, Nussberger J, Kahan T, Hjemdahl P.
Department of Pharmacology, Karolinska Institutet, Stockholm, Sweden.
The overflows (i.e., veno-arterial concentration differences multiplied by plasma flow) of angiotensin-(1-10) decapeptide (ANG I) and angiotensin-(1-8) octapeptide (ANG II) from blood-perfused canine gracilis muscle in situ were studied. Special precautions were taken to minimized ex vivo generation and/or degradation of angiotensins in the sampled blood. ANG I was found to be generated in the catheter system supplying the gracilis muscle with arterial blood, but plasma renin activity and ANG II levels were uninfluenced by the catheter system. A positive venoarterial concentration difference over the muscle itself was found for ANG II but not for ANG I under basal conditions. Isoprenaline elicited vasodilatation, reduced ANG I overflow, and tended to increase ANG II overflow, whereas beta-adrenoceptor blockade by propranolol had no effect on these variables. In conclusion, we found no evidence for a local de novo synthesis of ANG II from the gracilis muscle vasculature in vivo. The net overflow of ANG II was most likely caused by local conversion in the tissue of ANG I artifactually generated in the arterial catheter system. beta-Adrenoceptor stimulation enhanced the local conversion of ANG I to ANG II, probably by exposing a greater endothelial surface containing angiotensin-converting enzyme activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8203648&dopt=Abstract
Behav Neural Biol. 1994 Mar;61(2):150-5.
Interaction of GABAergic and beta-noradrenergic drugs in the regulation of memory storage.
Introini-Collison IB, Castellano C, McGaugh JL.
Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717-3800.
These experiments examined the interaction of drugs affecting noradrenergic and GABAergic systems, administered post-training, in influencing retention of an inhibitory avoidance response. Male CD1 mice (23-28 g) were trained in an inhibitory avoidance task, given immediate post-training ip injections of saline or GABAergic and adrenergic drugs administered either alone or concurrently. Retention was tested 48 h later. In agreement with extensive previous evidence, the GABAergic antagonist bicuculline (0.3, 1.0, or 3.0 mg/kg) produced dose-dependent (inverted-U) enhancement of retention and the GABAergic agonist muscimol (1.0 mg/kg) impaired retention. The retention-enhancing effects of bicuculline were blocked by concurrent administration of the beta-nor-adrenoceptor antagonist propranolol (2.0 mg/kg). Also in agreement with previous evidence, the beta-adrenoceptor agonist clenbuterol (0.030, 0.100, or 0.300 mg/kg, ip) produced dose-dependent (inverted-U) enhancement of retention. Clenbuterol also blocked the retention-impairing effects of muscimol (1.0 mg/kg). In addition, propranolol (2.0 mg/kg) potentiated the retention impairing effects of muscimol (1.0 or 3.0 mg/kg, ip). These findings support the view that GABAergic systems modulate memory through an interaction with beta-noradrenergic mechanisms.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8204080&dopt=Abstract
Eksp Klin Farmakol. 1993 May-Jun;56(3):27-30.
[The antiarrhythmic activity of the polymeric forms of quinidine, trimecaine, etatsizin, propranolol and verapamil]
[Article in Russian]
Sidorenko GI, Gurin AV, Koliadko MG, Iurkshtovich TL, Nedorezov VL.
The antiarrhythmic activity and acute toxicity of polymeric formulations of quinidine, trimecaine, ethacizine, propranolol, verapamil which had been immobilized on a cellulose carrier (monocarboxylcellulose) and low molecular analogues were studied in various experimental animals (rats, mice, dogs). The polymeric formulations of trimecaine and verapamil were found to have a higher antiarrhythmic activity in different arrhythmia models than trimecaine and verapamil. The toxicity of all new compounds was no more than the values of conventional antiarrhythmic drugs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8219985&dopt=Abstract
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