Drugs online research references
Cardiovasc Res. 1990 May;24(5):404-10.
Attenuation of the rise in extracellular potassium concentration during myocardial ischaemia by d.l-sotalol and d-sotalol.
Hicks MN, Cobbe SM.
Department of Medical Cardiology, Royal Infirmary, Glasgow, United Kingdom.
STUDY OBJECTIVE--The aim was to study the effects of d.l-sotalol, d-sotalol or atenolol on the rate of rise of extracellular potassium concentration [( K+]o) and the electrophysiological changes that occur during myocardial ischaemia. DESIGN--The study was performed in isolated, arterially perfused interventricular septa from rabbit. Six septa were treated with d.l-sotalol 10(-4) mol.litre-1, six with d-sotalol 10(-4) mol.litre-1, six with atenolol 10(-5) mol.litre-1, and there were seven untreated controls. At these concentrations d.l and d-sotalol are equipotent in their class III effect, though d-sotalol has only 7% of the beta blocking activity of the racemic form, and atenolol is equipotent in its beta blocking activity to d.l-sotalol. [K+]o and electrophysiological variables were compared before and during a 30 min period of global zero flow ischaemia. MEASUREMENTS AND MAIN RESULTS--Prior to ischaemia [K+]o, measured using potassium sensitive valinomycin electrodes, was similar in all the groups. [K+]o rose during ischaemia in all the groups, and at 30 min was 13.0 (SEM 0.7) mmol.litre-1 in the control group which was not different from 12.7(0.5) mmol.litre-1 in the atenolol group. In the d.l and d-sotalol groups the increases were markedly attenuated, reaching 9.2(1.0) and 8.8(0.7) mmol.litre-1 respectively. During ischaemia the class III effect of d.l and d-sotalol was lost within 6 min though the fall in maximum upstroke velocity of the action potentials (dV/dtmax) and the extent of resting membrane potential (Em) depolarisation were less in comparison to the control and atenolol groups. CONCLUSIONS--The results indicate an attenuation by sotalol of the ischaemic rise in [K+]o, with preservation of dV/dtmax and Em, despite the loss of an effect on action potential duration. This potentially antiarrhythmic effect of sotalol in ischaemic myocardium is attributable to a direct membrane effect rather than beta adrenoceptor antagonism.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2372795&dopt=Abstract
Circ Res. 1995 Apr;76(4):664-74.
Contribution of Na(+)-Ca2+ exchange to stimulation of transient inward current by isoproterenol in rabbit cardiac Purkinje fibers.
Han X, Ferrier GR.
Department of Pharmacology, Dalhousie University, Halifax, Nova Scotia, Canada.
Cellular mechanisms underlying beta-adrenergic stimulation of the arrhythmogenic transient inward current (TI) were investigated by using a two-microelectrode voltage-clamp technique in rabbit cardiac Purkinje fibers. TI induced by elevating [Ca2+]o to 30 mmol/L and substituting [Na+]o with N-methyl-D-glucamine (NMG) chloride had a distinct reversal potential (EREV) of -25 mV, suggesting that Na(+)-Ca2+ exchange was not the charge carrier for TI. In the absence of [Na+]o, isoproterenol (ISO, 0.01 to 5.0 mumol/L) had no effect on either inward or outward TI or on the current-voltage relation of TI. However, ISO (0.1 mumol/L) significantly increased both inward and outward TIs without affecting the EREV of TI, if [Na+]o was present. Pretreatment with propranolol (0.2 mumol/L) or atenolol (0.2 mumol/L) abolished the stimulatory effects of ISO. Addition of propranolol (0.2 to 0.5 mumol/L) after the effects of ISO had developed caused only partial reversal of TI stimulation. This indicates persistence of stimulatory effects downstream from the initial agonist-receptor interaction. Forskolin (1 mumol/L), a direct adenylate cyclase activator, also strongly increased both inward and outward TI in the presence of [Na+]o. These effects also were abolished when [Na+]o was substituted by NMG. Inward and outward TIs enhanced by either ISO or forskolin were reversed by two putative Na(+)-Ca2+ exchange blockers, dodecylamine (20 mumol/L) and quinacrine (20 mumol/L). These results suggest that beta-adrenergic stimulation of TI is mediated by the Na(+)-Ca2+ exchange; stimulation likely involves phosphorylation of the exchanger or some factor that modulates exchanger activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7895340&dopt=Abstract
Am J Physiol. 1994 Feb;266(2 Pt 1):E230-41.
Effect of renal nerves on expression of renin and angiotensinogen genes in rat kidneys.
Nakamura A, Johns EJ.
Department of Physiology, Medical School, Birmingham, West Midlands, United Kingdom.
In this study, we try to determine the influence of renal nerve activity on renal function, plasma renin activity (PRA), and the corresponding expression of renin and angiotensinogen genes in the kidney. In pentobarbitone-anesthetized rats, the left renal nerves were stimulated (15 V, 0.2 ms) at frequencies to reduce left renal blood flow by 15, 30, and 45%. There were corresponding reductions in glomerular filtration rate from 12 to 52% and absolute and fractional sodium excretions from 20 to 75%. PRA levels in control rats were 10.8 +/- 1.5 and were increased to 65.9 +/- 9.1, 144.2 +/- 19.7, and 277.2 +/- 22.0 ng angiotensin I.h-1.ml-1 after 1 h at each of the three levels of nerve stimulation. Renal renin mRNA was similar in innervated and denervated kidneys and was not affected by the lowest level of nerve stimulation; however, neurally induced decreases in blood flow to 30 and 45% increased renin mRNA levels by 3.0- and 3.4-fold (both P < 0.05), respectively. Angiotensinogen mRNA levels were higher (P < 0.05) in kidneys subjected to the lowest level of nerve stimulation, but when renal blood flow was reduced by 30 and 45%, expression of this gene was unchanged. Stimulation of the renal nerves in the presence of the beta 1-adrenoceptor antagonist atenolol only doubled PRA at the highest rates of stimulation. Neither renal renin nor angiotensinogen mRNA were changed during neurally mediated reductions in renal blood flow of 15 or 30% after administration of atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8141281&dopt=Abstract
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