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Contractile activity of ATP and diadenosine tetraphosphate on urinary bladder in the rat: role of A1- and P2X-purinoceptors and nitric oxide

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Summary

1 Both adenosine-5′-triphosphate (ATP) and diadenosine tetraphosphate (AP4A) produced a dose-dependent contraction of the isolated rat urinary bladder rings. AP4A dose–response curve was to the left of that of ATP, and maximum response was greater than that produced by ATP.

2 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), the A1-purinergic receptor blocker (0.01 mm) significantly inhibited the ATP- and AP4A-induced contractions at the whole dose range. The inhibition was between 31–41%, and 15–25% for ATP and AP4A respectively.

3 Pyridoxal phosphate 6-azophenyl-2′,4′-disulphonic acid (PPADS), the P2X-purinoceptor antagonist (0.01 mm) potently inhibited the bladder contractions in response to ATP and AP4A by around 75–80%.

4 The nitric oxide (NO) precursorl-arginine reduced the bladder contractile response to ATP by about 22–41% and that of AP4A to a lesser extent by around 20–32%.

5 The nitric oxide synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME, 0.1 mm), did not produce any significant effect on ATP except for a weak inhibition of about 14% at the lowest dose of ATP. The contractions in response to AP4A were only slightly reduced byl-NAME by about 20%.

6 In conclusion, the contractile response of the bladder to ATP and to the dinucleotide AP4A is mediated mainly through P2X-purinoceptors and A1-purinergic receptors. In the detrusor muscle, NO donation possesses an inhibitory effect on ATP-mediated contractility more than that produced by the dinucleotide AP4A.
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Keywords: A1-purinoceptors; adenosine-5′-triphosphate; contractility; diadenosine tetraphosphate; nitric oxide; urinary bladder

Document Type: Research Article

Publication date: January 1, 2007

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