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Vol. 294, Issue 3, 1175-1181, September 2000
Department of Pharmacology and Toxicology, Cardiovascular Research
Institute Maastricht, Universiteit Maastricht, The Netherlands
(H.A.J.S.B., J.G.R.D.M.); and Medizinische Poliklinik,
Westfälische Wilhelms-Universität Münster,
Germany (M.S., E.S., K.H.R.)
The effects of diadenosine polyphosphates (APnA; n = 3-6) and adenine nucleotides on contractile reactivity of isolated
rat mesenteric resistance arteries (MrA) and superior epigastric
arteries (SEA), which display a dense and sparse autonomic innervation, respectively, were evaluated. All agonists examined, except adenosine and AMP, induced contractions. The rank order of potency was similar in
both arteries: 
,
-methylene ATP (,-meATP) > AP5A > AP6A > AP4A > ATP > ADP > AP3A.
Contractions were stable during several minutes in SEA but highly
transient in MrA. They were reduced after exposure to 10 µM
,-meATP and by 10 µM of the P2X antagonist pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid. During phenylephrine (10 µM)-induced contractions, the agonists induced a
further contraction in SEA. In MrA, however, further contraction was
followed by marked relaxation. The rank order of relaxing potency was
comparable to that of the contractile potency of agonists. Also, the
relaxing effects of APnA were blunted by 10 µM
pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid and after
exposure to ,-meATP. In vitro and in vivo sympathectomy with
6-hydroxydopamine and removal of the endothelium did not modify the
effects of APnA in MrA. Thus, the contractile effects of APnA in
resistance arteries 1) are due to a P2X purinoceptor-mediated stimulation of the smooth muscle; 2) depend on the length of the phosphate chain; and 3) are followed by endothelium-independent relaxing effects in MrA but not SEA, which may involve receptors that
are similar to those mediating contraction. The regional heterogeneity
of APnA effects cannot be attributed to a direct neurogenic influence.
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