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ATP-stimulated ANP release through P1 receptor subtype
Chunhua Cao1, Feng Lian Piao, Jeong Hee Han
1Department of Physiology, Medical School, Institute for Medical Sciences, Chonbuk National University, 2-20 Keum-Am-Dong-San, Jeonju 561-180, Korea.
Regulatory Peptides
|February 1, 2005
Summary
Extracellular ATP increases atrial natriuretic peptide (ANP) release and decreases heart contraction, primarily through P1 receptors. UTP has the opposite effect, suggesting distinct roles for these signaling molecules in cardiovascular regulation.
Area of Science:
- Cardiovascular Physiology
- Purinergic Signaling
- Endocrinology
Background:
- Extracellular ATP regulates cardiovascular functions via P1 and P2 receptors.
- The impact of ATP on atrial natriuretic peptide (ANP) secretion remains largely uncharacterized.
Purpose of the Study:
- To investigate the effects of extracellular ATP on atrial hemodynamics and ANP release.
- To elucidate the receptor-mediated mechanisms underlying ATP's actions on ANP secretion.
Main Methods:
- Infusion of ATP and its analogs into isolated perfused beating rat atria.
- Utilized various receptor antagonists (P1, P2X1, P2XY, P2Y) to identify signaling pathways.
- Measured ANP release and atrial contractility (inotropism).
Main Results:
- ATP dose-dependently increased ANP release and induced negative inotropism.
- P1 receptor antagonist completely blocked ATP's effects, while P2 receptor antagonists had varied impacts.
- UTP decreased ANP release without affecting contractility, suggesting opposing actions to ATP.
Conclusions:
- Extracellular ATP enhances ANP release and reduces contractility predominantly via P1 receptor activation.
- Extracellular UTP exhibits an inhibitory effect on ANP release.
- ATP and UTP may play contrasting roles in regulating ANP secretion and cardiovascular function.