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

Why is nisoldipine a specific agent in ischemic left ventricular dysfunction?

A M Knorr1

  • 1Bayer AG, Wuppertal, Germany.

The American Journal of Cardiology
|April 27, 1995
PubMed
Summary
This summary is machine-generated.

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

Chronic imipramine administration alters the activity and phosphorylation state of tyrosine hydroxylase in dopaminergic regions of rat brain.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology·1995
Same author

Basal ganglia research and Tourette's syndromes.

Trends in neurosciences·1991
Same author

Influence of nifedipine on experimental arteriosclerosis.

Cardiovascular drugs and therapy·1990
Same author

The anxiogenic beta-carboline FG-7142 increases in vivo and in vitro tyrosine hydroxylation in the prefrontal cortex.

Brain research·1989
Same author

Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension.

Journal of hypertension·1988
Same author

K+-dependent stimulation of tyrosine hydroxylation in striatal slices: role of Ca2+/calmodulin and Ca2+/phospholipid-dependent mechanisms.

Biochemical pharmacology·1986

Nisoldipine, a calcium channel blocker, selectively inhibits vascular smooth muscle contraction, especially in coronary arteries. Its potency is linked to membrane depolarization, suggesting potential benefits for ischemic heart tissue.

Area of Science:

  • Pharmacology
  • Cardiovascular Physiology

Background:

  • Nisoldipine is a dihydropyridine calcium entry blocker.
  • It exhibits greater potency in inhibiting vascular smooth muscle contraction compared to myocardial contractility.

Purpose of the Study:

  • To review the hypothesis relating nisoldipine's vascular smooth muscle selectivity to membrane potential sensitivity.
  • To explore the potential for ischemia selectivity of nisoldipine.

Main Methods:

  • Review of existing literature and experimental evidence.
  • Comparison of nisoldipine's effects with nifedipine, verapamil, and diltiazem on isolated human coronary and internal mammary arteries, and electrically driven myocardium.

Main Results:

  • Nisoldipine potently inhibited tonic contractions in isolated human coronary arteries, with significantly higher potency than in internal mammary arteries or myocardium.

Related Experiment Videos

  • Nisoldipine's effect is enhanced by cell membrane depolarization, unlike verapamil and diltiazem.
  • Vascular smooth muscle cells and human coronary arteries exhibit greater depolarization than myocardial cells.

    • Conclusions:

    • Nisoldipine's potency in vascular smooth muscle, particularly coronary arteries, is related to membrane potential sensitivity.
    • This selectivity suggests a potential for targeted vasodilation in ischemic myocardium, sparing normoxic tissue.