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Isolated aortic rings from rats surviving sepsis present enhanced responsiveness to vasopressin and angiotensin II
Author(s) -
Souza Priscila,
Marques Maria Consuelo Andrade,
Silva-Santos José Eduardo
Publication year - 2012
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.26.1_supplement.lb533
Subject(s) - angiotensin ii , vasopressin , phenylephrine , vasoconstriction , medicine , endocrinology , sepsis , chemistry , thapsigargin , calcium , blood pressure
Epidemiological studies reveal a high mortality rate among patients that are discharged after an episode of sepsis, when compared to age‐matched people. To investigate if changes in the functionality of cardiovascular system contribute to this high mortality rate, we assessed the responses of aortic rings from 3 groups: control, and sepsis induced by cecal ligation and puncture, 30 (S30), and 60 (S60) days after recovery. The effects of potassium, phenylephrine, angiotensin I, calcium chloride, caffeine, acetylcholine, and sodium nitroprusside were not changed in vessels from sepsis‐surviving rats. However, in S60 group angiotensin II (AII)‐ and vasopressin (AVP)‐induced vasoconstriction were increased by 70 and 78%, respectively, when compared to control. It was accompanied by reduced relaxation in response to Y‐27632, a Rho‐kinase inhibitor, with EC50 of 0.43 (0.33 – 0.55) and 1.03 (0.76 – 1.40) μM in control and S60 groups, respectively. AII and AVP induced augmented contractile responses in aortic rings from S60 rats kept in calcium‐free solution, an event reversed by thapsigargin (an inhibitor of SERCA). Our results suggest that aortic rings from sepsis‐surviving rats display increased reactivity to AII and AVP by mechanisms involving changes in calcium mobilization and sensitization.