Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Beta 1 adrenoceptor mediated decrease in pHi in quiescent ventricular myocardium

S Shida1, H Nakaya, S Matsumoto

  • 1Department of Pharmacology, Hokkaido University School of Medicine, Sapporo, Japan.

Cardiovascular Research
|January 1, 1994
PubMed
Summary

Beta-1 adrenergic stimulation causes intracellular acidosis in heart muscle by increasing glycolysis, while the Na+-H+ exchange system plays a compensatory role. This acidosis may influence the heart's response to adrenergic stimulation.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Neuroinflammation at single cell level: What is new?

Journal of leukocyte biology·2020
Same author

Effects of Substrate Solubility in Interesterification with Triolein by Immobilized Lipase in Supercritical Carbon Dioxide.

Bioscience, biotechnology, and biochemistry·2016
Same author

Niflumic acid-sensitive ion channels play an important role in the induction of glucose-stimulated insulin secretion by cyclic AMP in mice.

Diabetologia·2009
Same author

Photoinduced melting of a stripe-type charge-order and metallic domain formation in a layered BEDT-TTF-based organic salt.

Physical review letters·2007
Same author

A key role for the subunit SUR2B in the preferential activation of vascular KATP channels by isoflurane.

British journal of pharmacology·2006
Same author

Complete response of Sister Mary Joseph Nodule from gastric adenocarcinoma treated with combination chemotherapy of low-dose S-1 and cisplatin.

Journal of experimental & clinical cancer research : CR·2003

Area of Science:

  • Cardiovascular Physiology
  • Cellular Electrophysiology
  • Adrenergic Signaling

Background:

  • Intracellular pH (pHi) regulation is crucial for myocardial function.
  • Adrenergic stimulation significantly impacts cardiac cellular processes.
  • Understanding the interplay between adrenergic receptors and pHi is vital for cardiac health.

Purpose of the Study:

  • To investigate the effect of beta-adrenergic stimulation on ventricular myocardium pHi.
  • To compare beta-adrenergic effects on pHi with alpha-adrenergic stimulation.
  • To elucidate the mechanisms underlying beta-adrenergic mediated pHi changes.

Main Methods:

  • Simultaneous measurement of membrane potential and pHi in guinea pig papillary muscles using ion-selective electrodes.

Related Experiment Videos

  • Stimulation of beta-adrenoceptors with isoprenaline and alpha-adrenoceptors with phenylephrine.
  • Assessment of the roles of Na+-H+ exchange, Cl--HCO3- exchange, Na+-HCO3- symport, and glycolysis using specific blockers.

    • Main Results:

    • Beta-1 adrenergic stimulation (isoprenaline) induced intracellular acidosis (decreased pHi) and membrane depolarization.
    • This acidosis was mediated by beta-1 adrenoceptors and enhanced glycolysis, as evidenced by blockade with atenolol and abolition by glycolysis inhibitors.
    • Alpha-adrenergic stimulation increased pHi, an effect blocked by amiloride (Na+-H+ exchange blocker), suggesting a different regulatory mechanism.

    Conclusions:

    • Beta-1 adrenoceptor activation leads to intracellular acidosis in ventricular myocardium primarily through enhanced glycolysis.
    • The Na+-H+ exchange system acts as a compensatory mechanism against this acidosis.
    • Beta-1 adrenoceptor-induced acidosis may play a role in modulating the inotropic response to adrenergic stimuli in the heart.