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Cellular signals regulating the release of ANF
H Ruskoaho1, P Kinnunen, P Mäntymaa
1Department of Pharmacology and Toxicology, University of Oulu, Finland.
Canadian Journal of Physiology and Pharmacology
|October 1, 1991
Summary
Protein kinase C activation stimulates atrial natriuretic factor (ANF) secretion from heart cells. This pathway is key for regulating ANF release, even in hypertrophied ventricles, and is modulated by atrial stretch.
Area of Science:
- Cardiology
- Cell Biology
- Endocrinology
Background:
- Atrial natriuretic factor (ANF) regulates blood pressure and fluid balance.
- The cellular mechanisms linking atrial myocyte stretch to ANF secretion are not fully understood.
Purpose of the Study:
- To investigate the role of protein kinase C (PKC) and intracellular calcium (Ca2+) in regulating ANF secretion.
- To determine how atrial stretch influences ANF release and the involvement of PKC.
Main Methods:
- Experiments using isolated perfused rat hearts and cultured neonatal rat atrial myocytes.
- Stimulation with phorbol esters (PKC activator), Ca2+ ionophore A23187, and endothelin.
- Assessment of ANF secretion in response to these agents and atrial stretch.
Main Results:
- Phorbol esters and Ca2+ ionophore increased basal ANF secretion.
- PKC activation stimulated ANF secretion in cultured myocytes, independent of Ca2+.
- Endothelin and phorbol esters enhanced both basal and stretch-induced ANF secretion.
- Stretch-induced ANF release showed negative coupling with intracellular Ca2+ increase.
- Phorbol ester stimulated ANF release from hypertrophied ventricles.
Conclusions:
- PKC activity is crucial for regulating basal ANF secretion from both atrial and ventricular cells.
- Atrial stretch-induced ANF secretion is positively modulated by phorbol esters.
- Intracellular Ca2+ may be negatively coupled to stretch-induced ANF release.