Related Experiment Videos
Effects of digoxin on islated human mesenteric vessels
Acta Pharmacologica Et Toxicologica
|July 1, 1979
Summary
Digoxin causes contractions in human mesenteric vessels by acting directly on muscle cells, potentiating noradrenaline effects. These actions require extracellular calcium and influence potassium-induced vascular responses.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Vascular Biology
Background:
- Digoxin is a cardiac glycoside with known effects on heart muscle.
- Its direct effects on human mesenteric vasculature are not fully understood.
Purpose of the Study:
- To investigate the contractant effects of digoxin on isolated human mesenteric arteries and veins.
- To determine the role of extracellular calcium and noradrenaline in digoxin-mediated vascular responses.
Main Methods:
- Isolated human mesenteric arteries and veins were exposed to digoxin.
- Contractile responses were measured in the presence and absence of nifedipine, phentolamine, and varying calcium and potassium concentrations.
- Responses to noradrenaline were assessed.
Main Results:
- Digoxin induced concentration-dependent contractions in mesenteric arteries and veins, with veins being more sensitive.
- These contractions were calcium-dependent, abolished by nifedipine and calcium-free solutions.
- Digoxin potentiated the contractile effects of noradrenaline on mesenteric vessels.
- Digoxin influenced potassium-induced changes in venous tension.
Conclusions:
- Digoxin directly contracts human mesenteric vessels via a calcium-dependent mechanism.
- Digoxin enhances the vascular response to noradrenaline.
- Digoxin modulates mesenteric vascular reactivity to potassium.