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Sodium-phosphate cotransport and vascular reactivity.
G E Plante1, J Dubé, L Bouffard
1Department of Pharmacology, University of Sherbrooke, Québec.
Summary
Phosphonoformate (PFA) impacts vascular smooth muscle (VSM) reactivity by inhibiting inorganic phosphate (PO4) transport. This study reveals PFA significantly reduces VSM contractions, especially under high PO4 conditions.
Area of Science:
- Cardiovascular Physiology
- Renal Physiology
- Vascular Biology
Background:
- Inorganic phosphate (PO4) significantly influences vascular reactivity, with low PO4 reducing and high PO4 augmenting it.
- Phosphonoformate (PFA) is a known phosphaturic compound that inhibits the renal sodium-phosphate co-transporter.
Purpose of the Study:
- To investigate the presence and function of a PO4 transport mechanism in vascular smooth muscle (VSM).
- To assess the effect of PFA on VSM reactivity in aorta, mesenteric artery, and vein under varying PO4 concentrations.
Main Methods:
- Rabbit aorta, mesenteric artery, and vein strips were superfused in Ringer's solutions with normal, low, or high PO4 concentrations.
- The contractile response to angiotensin II (AII) was measured in the presence and absence of PFA.
- Contraction values were compared between control and PFA-treated tissues across different PO4 conditions.
Main Results:
- PFA significantly reduced VSM contractions in aorta and mesenteric artery at higher AII doses under normal PO4 conditions.
- Vein contractions were markedly reduced by PFA across all AII doses under normal PO4.
- Under high PO4 conditions, PFA-induced reductions in contractions were approximately double those observed under normal PO4.
Conclusions:
- A PO4 transport mechanism likely exists in VSM, as evidenced by PFA's inhibitory effect on vascular reactivity.
- PFA's impact on VSM contraction is potentiated under conditions of high extracellular PO4.
- These findings suggest a role for PO4 transport in regulating vascular tone and reactivity.