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Vascular relaxation induced by NO donor in mesenteric resistance artery from 2K‐1C rats involves reactive oxygen species and potassium channels activation
Author(s) -
Andrade Fernanda Aparecida,
Silva Roberto Santana,
Bendhack Lusiane Maria
Publication year - 2013
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.27.1_supplement.877.3
Subject(s) - mesenteric arteries , apocynin , phenylephrine , chemistry , reactive oxygen species , electrical impedance myography , vasodilation , potassium channel , artery , medicine , endocrinology , anesthesia , nadph oxidase , biochemistry , blood pressure
This study aimed to evaluate the effect of the inhibition of soluble guanylyl‐cyclase (sGC) by ODQ, K + channels by TEA and ROS production by apocynin on the relaxation to the NO donor RuBPY in mesenteric resistance artery from normotensive (2K) and 2K‐1C rats. Concentration‐effect curves to RuBPY were constructed in isolated denuded mesenteric arteries from 2K and 2K‐1C rats contracted with phenylephrine, in the absence or in the presence of ODQ, TEA, or Apocynin. The maximum relaxation induced by RuBPY was similar in 2K (77.6±8.9%, n=7) and 2K‐1C (76.9±4.5%,n=13), that was inhibited by ODQ in 2K (36.5±2.9%,n=5) and 2K‐1C arteries (24.6±5.5%, n=5). The relaxation induced by RuBPY was reduced by TEA (50.5±10.6%, n =8) and apocynin (45.7±3.9%,n=4) only in 2K‐1C arteries. These results indicate that although RuBPY induces relaxation with similar efficacy in mesenteric arteries from normotensive and hypertensive rats and that the NO released from RuBPY activates sGC, the NO signaling can differ. It involves ROS production and K + channels activation only in 2K‐1C arteries. Supported by FAPESP and CNPq.