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Diadenosine polyphosphates' action on calcium and vessel contraction
M Tepel1, J Jankowski, H Schlüter
1Universitätsklinik Marienhospital, Medizinische Klinik I, Ruhr-Universität-Bochum, Herne, Germany.
American Journal of Hypertension
|January 27, 1998
Summary
Diadenosine polyphosphates like AP4A, AP5A, and AP6A cause blood vessels to constrict by increasing intracellular calcium. These platelet-derived compounds significantly elevate force in rat renal resistance vessels and aortic strips.
Area of Science:
- Cardiovascular Physiology
- Molecular Pharmacology
Background:
- Platelet-derived vasoactive compounds play a role in regulating vascular tone.
- Diadenosine polyphosphates (ApnAs) are endogenous molecules with known biological activities.
Purpose of the Study:
- To investigate the vasoconstrictive effects of diadenosine tetraphosphate (AP4A), pentaphosphate (AP5A), and hexaphosphate (AP6A).
- To determine the impact of these compounds on intracellular calcium concentration in vascular smooth muscle cells.
Main Methods:
- Vessel myography was used to measure vasoconstriction in isolated rat renal resistance vessels and aortic strips.
- Fluorescent dye techniques were employed to assess cytosolic free calcium concentration ([Ca2+]i) in cultured rat vascular smooth muscle cells (VSMC).
Main Results:
- Diadenosine polyphosphates dose-dependently increased the contractile force of both renal resistance vessels and aortic strips.
- Administration of 10 µmol/L AP4A, AP5A, or AP6A significantly increased [Ca2+]i in VSMC.
- The vasoconstriction and [Ca2+]i increase were attenuated by removing extracellular calcium and using a P2 purinoceptor inhibitor.
Conclusions:
- Diadenosine polyphosphates induce vasoconstriction.
- The mechanism involves an increase in cytosolic free calcium concentration ([Ca2+]i) via P2 purinoceptor activation.