Contrasting effects of norepinephrine and 5-hydroxytryptamine on contractility of abdominal aorta of two kidney-two clip hypertensive rats. Effects of inhibitors of arachidonic acid metabolic enzymes.
This study intends to: 1) define reactivity in vessels of two kidney-two clip (2K2C) hypertensive rats (6-11 days after clipping); 2) determine the possible involvement of prostaglandins in modulating contractile vascular responses. Cumulative dose-response curves to norepinephrine (NE), 5-hydroxytryptamine (5-HT) and potassium chloride (KCl) were elicited on helical strips of abdominal aorta both in the absence and in the presence of prostacyclin synthetase (transylcypromine, TCP, 0.25mM) or cyclooxygenase (indomethacin, IND, 0.014 mM and acetylsalicylic acid, ASA, 0.20 mM) inhibitors Vessels of hypertensive animals developed significantly less tension to NE (n = 21) but higher tension and lower ED50 in response to 5-HT (n = 9) than sham control rat vessels. Force development to KCl (n = 9) was not statistically different between hypertensive and sham vessels. Vascular responses were decreased with the inhibitors, but the contrasting effects of NE and 5-HT on clip vessels were maintained. Threshold doses of PGE2 significantly reversed the effect of IND but not that of TCP on NE responses. Threshold doses of PGI2 had no significant effect on NE and 5-HT responses under TCP. The results would indicate: 1) different functional alterations for contractions to NE and 5-HT appear to have developed in vessels of 2K2C hypertensive rats; 2) PGE2 effectively contributes to modulation of NE responses in rat aorta strips; 3) these experiments suggest that prostaglandins do not play a significant role in the altered contractility of vessels in hypertensive rats.
Rosón
M I
MI
Instituto de Investigaciones Cardiológicas, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Maquieira
M K
MK
de la Riva
I J
IJ
D000818:Animals; D001012:Aorta, Abdominal / Q000187:drug effects; D001241:Aspirin / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D016861:Cyclooxygenase Inhibitors; D065607:Cytochrome P-450 Enzyme Inhibitors; D003577:Cytochrome P-450 Enzyme System; D015232:Dinoprostone / Q000494:pharmacology; D011464:Epoprostenol / Q000494:pharmacology; D006978:Hypertension, Renovascular / Q000201:enzymology / Q000503:physiopathology*; D007213:Indomethacin / Q000494:pharmacology; D019746:Intramolecular Oxidoreductases; D007535:Isomerases / Q000037:antagonists & inhibitors*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012701:Serotonin / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects*
D016861:Cyclooxygenase Inhibitors; D065607:Cytochrome P-450 Enzyme Inhibitors; D012701:Serotonin; D011189:Potassium Chloride; D003577:Cytochrome P-450 Enzyme System; D011464:Epoprostenol; D007535:Isomerases; D019746:Intramolecular Oxidoreductases; C022461:prostacyclin synthetase; D015232:Dinoprostone; D001241:Aspirin; D009638:Norepinephrine; D007213:Indomethacin