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In vivo effects of diadenosine polyphosphates on rat renal microcirculation
G Gabriëls1, K Endlich, K H Rahn
1Medizinische Poliklinik, Experimentelle Nephrologie, Westfälische Wilhelms-Universität, Münster, Germany. gabrie@uni-muenster.de
Kidney International
|June 9, 2000
Summary
Diadenosine polyphosphates (APXA) cause temporary blood vessel constriction in rat kidneys, mediated by A1 and P2 purinoceptors. Phosphate chain length influences vasoconstriction and P2 receptor effects, with afferent arterioles most affected.
Area of Science:
- Nephrology
- Pharmacology
- Physiology
Background:
- Diadenosine polyphosphates (APXA) are vasoactive nucleotides acting via purinoceptors.
- Emerging evidence suggests APXA exert differential effects on kidney vasculature.
Purpose of the Study:
- To investigate the in vivo effects of AP3A, AP5A, and adenosine on renal microvessels.
- To elucidate the role of purinoceptors in mediating these vascular responses.
Main Methods:
- Application of AP3A, AP5A, and adenosine agonists to the hydronephrotic rat kidney.
- Preincubation with selective A1, A2, and P2 purinoceptor antagonists to assess receptor involvement.
Main Results:
- APXA induced concentration-dependent transient vasoconstriction in interlobular arteries (ILOB) and afferent arterioles (AFF), with AP5A showing the most pronounced effect.
- Vasodilation occurred in ILOB and efferent arterioles (EFF), with potency comparable across agonists, but was minimal in AFF.
- Receptor antagonist studies indicated mediation by A1 and P2 purinoceptors, with varying sensitivity to different APXA compounds and vessel types.
Conclusions:
- APXA evoke transient renal vasoconstriction via A1 and P2 purinoceptors.
- The phosphate chain length of APXA influences vasoconstriction potency and P2 receptor subtype interactions.
- Renal microvessels, particularly ILOB and AFF, are differentially affected by APXA, with afferent vasodilation potentially counteracted by vasoconstriction.