PMID: 13584729Sep 1, 1958Paper

The mode of action of quinidine on isolated rabbit atria interpreted from intracellular potential records

British Journal of Pharmacology and Chemotherapy
E M VAUGHAN WILLIAMS

Abstract

An attempt has been made to show why quinidine, which has long been known not to lengthen the duration of the cardiac action potential, measured with external electrodes, and also not to lengthen, and sometimes to shorten, the absolute refractory period, nevertheless reduces the maximum frequency at which atria can respond to a stimulus. Simultaneous measurements have been made in electrically driven isolated rabbit atria of contractions, conduction velocity and intracellular potentials before and during exposure to a wide range of concentrations of quinidine sulphate. The resting potential remained undiminished, in contrast to the effect of quinidine on Purkinje fibres. In the therapeutic range of doses, up to 10 mg./l., the half-time for repolarization was either shortened or unchanged, thus providing an explanation for the failure of quinidine to prolong the absolute refractory period. In contrast, even at low concentrations of quinidine, conduction velocity and the rate of rise of the action potential were greatly slowed, and the height of the overshoot was reduced. The terminal phase of the action potential was prolonged. It is known that the rate of rise of the action potential is a function of the level of repolarization...Continue Reading

References

Aug 1, 1952·The American Journal of Medicine·M PRINTZMETAL
Feb 27, 1953·The Journal of Physiology·A S V BURGEN, K G TERROUX
Apr 28, 1953·The Journal of Physiology·P FATT, B KATZ
Jan 1, 1953·Pflügers Archiv : European journal of physiology·W TRAUTWEINK FEDERSCHMIDT
Mar 1, 1954·British Journal of Pharmacology and Chemotherapy·S BRISCOE, J H BURN
Oct 1, 1954·The American Journal of Physiology·B F HOFFMAN, E E SUCKLING
Jan 27, 1956·The Journal of Physiology·J M MARSHALL, E M VAUGHAN WILLIAMS
May 1, 1956·Circulation Research·J H BURNJ M WALKER
Jun 28, 1956·The Journal of Physiology·G S DAWES, J R VANE
Jan 1, 1957·Circulation Research·A K ARMITAGEA J GUNNING
Sep 1, 1957·The American Journal of Physiology·B F HOFFMANE E SUCKLING
Sep 1, 1957·The American Journal of Physiology·W C HOLLAND
Mar 1, 1958·British Journal of Pharmacology and Chemotherapy·M J RAND, J M WALKER
Sep 30, 1957·The Journal of Physiology·A L HODGKIN, R D KEYNES
Sep 1, 1951·The Journal of Physiology·M H DRAPER, S WEIDMANN
Jan 1, 1950·The American Journal of Medicine·H GOLD
May 1, 1950·Medicine·J R DIPALMA, J E SCHULTZ
Aug 1, 1950·American Practitioner and Digest of Treatment·R FRANCE
Aug 3, 1921·The Journal of Physiology·E D Adrian

Citations

Jun 1, 1990·Cardiovascular Drugs and Therapy·B N Singh
Oct 1, 1990·Pflügers Archiv : European journal of physiology·L Lagnado, P A McNaughton
Jan 1, 1968·Naunyn-Schmiedebergs Archiv für experimentelle Pathologie und Pharmakologie·O Hauswirth
Jan 1, 1971·Pflügers Archiv : European journal of physiology·R KernE G Lack
Jan 1, 1971·Naunyn-Schmiedebergs Archiv Für Pharmakologie·H Antoni
Jan 1, 1971·Naunyn-Schmiedebergs Archiv Für Pharmakologie·P Heistracher
Nov 1, 1978·Basic Research in Cardiology·M VránaV Trcka
Nov 1, 1969·Agents and Actions·P B Hollander, H R Besch
May 1, 1971·European Journal of Pharmacology·A LangsletI Oye
Feb 1, 1974·European Journal of Pharmacology·E M VAUGHAN WILLIAMS, P Polster
Feb 7, 1977·European Journal of Pharmacology·J Inui, H Imamura
Jan 1, 1973·Progress in Biophysics and Molecular Biology·H Reuter
Jan 1, 1983·Pharmacology & Therapeutics·D M Roden, R L Woosley
Jan 1, 1975·Pharmacology & Therapeutics. Part B: General & Systematic Pharmacology·E M VAUGHAN WILLIAMS
Nov 14, 1997·The American Journal of Cardiology·M D Landers, M J Reiter
Dec 1, 1963·British Journal of Pharmacology and Chemotherapy·A SEKIYA, E M VAUGHANWILLIAMS
Jan 1, 1972·British Journal of Pharmacology·B N Singh, E M VAUGHAN WILLIAMS
Apr 1, 1972·British Journal of Pharmacology·A O Durotoye, L A Salako
May 1, 1979·British Journal of Pharmacology·A M French, N C Scott
Mar 1, 1977·British Heart Journal·D S HirschfeldM M Scheinman
Jan 1, 1969·Naunyn-Schmiedebergs Archiv für experimentelle Pathologie und Pharmakologie·R MendezS Sánchez-Pérez
Jan 1, 1979·The American Journal of Cardiology·L H OpieW F Lubbe
May 6, 1974·The American Journal of Cardiology·K L PaulayA N Damato
Oct 1, 1983·American Heart Journal·B N Singh
May 1, 1983·British Journal of Pharmacology·J Manzanares, J Tamargo
Apr 1, 1984·Journal of Clinical Pharmacology·E M VAUGHAN WILLIAMS
Sep 1, 1980·British Journal of Pharmacology·S Rodriguez, J Tamargo
Mar 1, 1974·American Heart Journal·B N Singh, O Hauswirth
Nov 1, 1971·The American Journal of Cardiology·L S Gettes
Feb 1, 1968·Circulation Research·J T BiggerB F HOFFMAN
Oct 1, 1966·British Journal of Pharmacology and Chemotherapy·F CiofaloJ Roberts
Feb 1, 1969·British Journal of Pharmacology·A Bennett, B Fleshler
Jun 1, 1969·British Journal of Pharmacology·A N DohadwallaE M VAUGHAN WILLIAMS

Related Concepts

Congenital Abnormality

Trending Feeds

COVID-19

Coronaviruses encompass a large family of viruses that cause the common cold as well as more serious diseases, such as the ongoing outbreak of coronavirus disease 2019 (COVID-19; formally known as 2019-nCoV). Coronaviruses can spread from animals to humans; symptoms include fever, cough, shortness of breath, and breathing difficulties; in more severe cases, infection can lead to death. This feed covers recent research on COVID-19.

Evolution of Pluripotency

Pluripotency refers to the ability of a cell to develop into three primary germ cell layers of the embryo. This feed focuses on the mechanisms that underlie the evolution of pluripotency. Here is the latest research.

Lipidomics & Rhinovirus Infection

Lipidomics can be used to examine the lipid species involved with pathogenic conditions, such as viral associated inflammation. Discovered the latest research on Lipidomics & Rhinovirus Infection.

Spatio-Temporal Regulation of DNA Repair

DNA repair is a complex process regulated by several different classes of enzymes, including ligases, endonucleases, and polymerases. This feed focuses on the spatial and temporal regulation that accompanies DNA damage signaling and repair enzymes and processes.

Chronic Fatigue Syndrome

Chronic fatigue syndrome is a disease characterized by unexplained disabling fatigue; the pathology of which is incompletely understood. Discover the latest research on chronic fatigue syndrome here.

Torsion Dystonia

Torsion dystonia is a movement disorder characterized by loss of control of voluntary movements appearing as sustained muscle contractions and/or abnormal postures. Here is the latest research.

Archaeal RNA Polymerase

Archaeal RNA polymerases are most similar to eukaryotic RNA polymerase II but require the support of only two archaeal general transcription factors, TBP (TATA-box binding protein) and TFB (archaeal homologue of the eukaryotic general transcription factor TFIIB) to initiate basal transcription. Here is the latest research on archaeal RNA polymerases.

Alzheimer's Disease: MS4A

Variants within the membrane-spanning 4-domains subfamily A (MS4A) gene cluster have recently been implicated in Alzheimer's disease in genome-wide association studies. Here is the latest research on Alzheimer's disease and MS4A.

Central Pontine Myelinolysis

Central Pontine Myelinolysis is a neurologic disorder caused most frequently by rapid correction of hyponatremia and is characterized by demyelination that affects the central portion of the base of the pons. Here is the latest research on this disease.