Abstract
We investigated the effects of 5-hydroxytryptamine (5-HT), adenosine, and adenine nucleotides on the canine isolated cerebral resistance arteries ranging from 300 to 500 μm in diameter. Addition of 5-HT and 5-carboxami-dotryptamine (5-CT) produced concentration-dependent contractions in the resistance arteries. Methiothepin (10−8 M-10−6 M) caused a parallel shift to the right of the dose-response curves for 5-HT and 5-CT. Neither ketanserin (10−7 M, 10−6 M) nor [(1αH, 5αH)-8-methyl-8 azabicyclo [3,2,1] oct-3α-y1]1H-indole-3-carboxylate hydrochloride (ICS 205–930 10−7M, 10−6M) caused any significant shift of the dose-response curve for 5-HT. Adenosine, ATP, ADP, and AMP caused concentration-dependent relaxations in the resistance arteries following contraction with PGF2α. The adenosine analogs also caused a dose-dependent relaxation of the arterial segments contracted by PGF2α. The decreasing order of potency of the agonists was 5′-N-ethylcarboxamido adenosine (NECA)>adenosine ≥L-diasteroisomers of phenylisopropyl adenosine (L-PIA). The relaxant response to NECA was competitively antagonized by 8-phenyltheophylline. The pretreatment with 3×10−5 M NG-monomethyl-L-arginine (L-NMMA) or 5×10−5 M aspirin caused no significant effect on the adenosine-induced relaxation in the resistance arteries. These results suggest that 5-HT produces contraction of the canine isolated cerebral resistance arteries, which is mainly mediated via 5-HT1-like receptors. Adenosine causes an endothelium-independent relaxation of the resistance arteries through the activation of adenosine A2-receptors.
