PMID- 8298797
OWN - NLM
STAT- MEDLINE
DCOM- 19940304
LR  - 20190512
IS  - 0007-1188 (Print)
IS  - 0007-1188 (Linking)
VI  - 110
IP  - 3
DP  - 1993 Nov
TI  - Effects of pyrimidines on the guinea-pig coronary vasculature.
PG  - 1091-7
AB  - 1. The effects of the pyrimidines, uridine 5'-triphosphate (UTP), thymidine 
      5'-triphosphate (TTP) and cytidine 5'-triphosphate (CTP), were examined in the 
      guinea-pig coronary bed, by use of a Langendorff technique. Comparisons were made 
      with the actions of the purines adenosine 5'-triphosphate (ATP), inosine 
      5'-triphosphate (ITP) and guanosine 5'-triphosphate (GTP). The effect of, the 
      nitric oxide synthase inhibitor, L-NG-nitroarginine methyl ester (L-NAME) and, 
      the prostaglandin synthesis inhibitor, indomethacin on the vasodilator response 
      to these purines and pyrimidines was examined. The effects of these inhibitors 
      were assessed on their ability to inhibit both the amplitude and the area of the 
      vasodilator response. 2. The relative order of potency of the purines and 
      pyrimidines studied was ATP > UTP > ITP >> GTP, TTP, CTP. 3. The maximum 
      amplitude and area of the vasodilator response to the pyrimidines, UTP (5 x 
      10(-10)-5 x 10(-7) mol), TTP (5 x 10(-8)-5 x 10(-7) mol) and CTP (5 x 10(-7) 
      mol), and purines, ITP (5 x 10(-9)-5 x 10(-7) mol) and GTP (5 x 10(-8)-5 x 10(-7) 
      mol), were significantly reduced by L-NAME (3 x 10(-5) and 10(-4) M). 4. The 
      inhibition of the response to ATP (5 x 10-8 mol), UTP (5 x 10-8 mol), ITP (5 x 
      10-8 mol), TTP(5 x 10-7 mol), CTP (5 x 10- mol) and GTP (5 x 10- mol) by L-NAME 
      (3 x 10-5 M) was significantly reversed by L-arginine (1.5 x 10-3 M).5. L-NAME (3 
      x 10-5 and 10-4 M) only inhibited the amplitude of the vasodilator response to a 
      low dose of ATP (5 x 10-mol), although the area of vasodilator response to ATP(5 
      x 10-11-5 x 10-7 mol) was significantly reduced by L-NAME (3 x 10-5 and 10-4 
      M).6. The maximum amplitude of the vasodilator response to ATP (5 x 10-10-5 x 
      10-7 mol) was significantly reduced by indomethacin (10-6 M), although the area 
      of the vasodilator response to ATP was only significantly reduced at one 
      intermediate dose (5 x 10-9 mol). Indomethacin (10-6 M) did not affect the 
      maximum amplitude or area of the vasodilator responses to UTP (5 x 10-11-5 x 10-7 
      mol),ITP (5 x 10-10-5 x 10-7 mol), CTP (5 x 10-7 mol), TTP (5 x 10-8-5 x 10-7 
      mol) and GTP(5 x 10-8-5 x 10-7 mol).7. It is concluded that in the guinea-pig 
      coronary vasculature, the vasodilatation evoked by the pyrimidines, UTP, TTP and 
      CTP, was mediated in large part via nitric oxide, as were the vasodilatations 
      evoked by the purines ITP and GTP. The vasodilatations evoked by ATP, however, 
      appear to involve prostanoids in addition to the release of nitric oxide.
FAU - Vials, A J
AU  - Vials AJ
AD  - Department of Anatomy and Developmental Biology, University College London.
FAU - Burnstock, G
AU  - Burnstock G
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Br J Pharmacol
JT  - British journal of pharmacology
JID - 7502536
RN  - 0 (Purine Nucleotides)
RN  - 0 (Pyrimidine Nucleotides)
RN  - 0 (Vasodilator Agents)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 94ZLA3W45F (Arginine)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
RN  - XXE1CET956 (Indomethacin)
SB  - IM
MH  - Animals
MH  - Arginine/analogs & derivatives/pharmacology
MH  - Coronary Vessels/*drug effects
MH  - Dose-Response Relationship, Drug
MH  - Female
MH  - Guinea Pigs
MH  - In Vitro Techniques
MH  - Indomethacin/pharmacology
MH  - Male
MH  - Muscle Relaxation/drug effects
MH  - Muscle, Smooth, Vascular/drug effects/physiology
MH  - NG-Nitroarginine Methyl Ester
MH  - Nitric Oxide/biosynthesis
MH  - Purine Nucleotides/pharmacology
MH  - Pyrimidine Nucleotides/*pharmacology
MH  - Vasodilator Agents/pharmacology
PMC - PMC2175825
EDAT- 1993/11/01 00:00
MHDA- 1993/11/01 00:01
PMCR- 1994/11/01
CRDT- 1993/11/01 00:00
PHST- 1993/11/01 00:00 [pubmed]
PHST- 1993/11/01 00:01 [medline]
PHST- 1993/11/01 00:00 [entrez]
PHST- 1994/11/01 00:00 [pmc-release]
AID - 10.1111/j.1476-5381.1993.tb13926.x [doi]
PST - ppublish
SO  - Br J Pharmacol. 1993 Nov;110(3):1091-7. doi: 10.1111/j.1476-5381.1993.tb13926.x.