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In vitro (organ chambers) effects caused by respiratory acidosis on vascular reactivity of the rat aorta (695.6)
Author(s) -
Augusto Viviane,
Nadai Tales,
Silveira Ana Paula,
Albuquerque Agnes,
Vento Daniella,
Rodrigues Alfredo,
Celotto Andrea,
Évora Paulo
Publication year - 2014
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.28.1_supplement.695.6
Subject(s) - phenylephrine , acidosis , endothelium , respiratory acidosis , vasodilation , aorta , prostacyclin , nitric oxide , enos , chemistry , endothelin 1 , respiratory system , vascular smooth muscle , medicine , nitric oxide synthase , smooth muscle , blood pressure , receptor
Resumo In vitro (“organ chambers”) effects caused by respiratory acidosis on vascular reactivity of the rat aorta Viviane S. Augusto, Tales R. Nadai, Ana Paula S. Cassiano, Agnes A. S. Albuquerque, Daniella A. Vento, Alfredo J. Rodrigues, Andrea C. Celotto, Paulo R. B. Evora Department of Surgery and Anatomy, Ribeirão Preto School of Medicine University of São Paulo, Brazil The mechanisms by which pH influences on vascular tone or their response to certain agonists are not fully understood, but there is evidence to suggest the involvement of nitric oxide (NO), prostacyclin (PGI 2 ), potassiumchannels and calcium flux. The present investigation was carried out to study in vitro (“organ chambers”) effects caused by respiratory acidosis (RA) on vascular reactivity of the aorta from Wistar rats, and the endothelium‐dependent mechanisms involved. Many assays were carried out untiladoptingorgan baths bubbling a gas mixture of CO 2 /(40%)/02 (60%), for the construction of pH‐response curves (pH 7.4 at 6:6) registering in isometric pre‐aortic rings contracted with phenylephrine (10 ‐6 M). As main results: 1) Relaxations were seen only in endothelial rings; 2) Endothelium‐dependent relaxations were inhibited by incubation for 30 min with indomethacin (10 ‐5 M), L‐NAME (10 ‐4 M) and tetraethylammonium (10 ‐3 M). These data allow concluding by the suitability of the method and the dependence of endothelial vascular response induced by extracellular RA, including the three known mechanisms of vasodilation: cAMP, cGMP and hyperpolarization. Grant Funding Source : Supported by CNPq, FAEPA, CAPES, FAPESP