Premium
Metabolic alkalosis vasodilation: role of endothelium and nitric oxide
Author(s) -
Celotto Andrea Carla,
Baldo Caroline Floreoto,
Capellini Verena Kise,
Evora Paulo Roberto
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.952.11
Subject(s) - phenylephrine , chemistry , nitric oxide , vasodilation , thoracic aorta , endothelium , endocrinology , medicine , aorta , vascular smooth muscle , vasoconstriction , nitric oxide synthase , endothelium derived relaxing factor , blood vessel , pharmacology , smooth muscle , blood pressure
For long it has been known that changes in vascular smooth muscle tone plays an important role in blood flow distribution and blood pressure control. pH changes features as one of the factors influencing vascular smooth muscle tone. The aim of the present study was to investigate the effects of mild and severe alkalosis on endothelium‐dependent vasodilatatory responses and the role of nitric oxide (NO) on isolated rat thoracic aorta. We assessed the in vitro (¡̈organ chambers¡̈) effects of increasing pH in vascular function of thoracic aorta rings. pH‐response curves (7.4 to 8.5) were generated using NaOH in phenylephrine pre‐contracted rings. Experiments were conducted in the presence and absence of indomethacin, NG‐nitro‐L‐arginina metil ester (L‐NAME), N5‐(1‐iminoethyl)‐L‐ornithine hydrochloride (L‐NIO), N‐(6‐Aminohexyl)‐5‐chloro‐1‐naphthalenesulfonamide (W‐7), 2,5‐dimethylbenzimidazole (DMB) and methyl‐ƒÒ‐cyclodextrin (CD). Our investigation demonstrated that alkalosis vasodilatory effect on rat thoracic aorta: 1) is endothelium‐dependent and induced by NO; 2) is prostacyclin‐independent; 3) is dependent of the constitutive endothelium NO synthase isoform and of the complex Ca+2/calmodulin; 4) has Na+/Ca+2 exchanger and caveolae as important components in relaxing mechanism. Support: FAPESP; FAEPA‐HC/FMRP.