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Differential changes in vasopressin‐induced vasoconstriction in renal vascular bed and aorta from endotoxemic rats (849.5)
Author(s) -
Guarido Karla,
SilvaSantos José Eduardo
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.849.5
Subject(s) - vasopressin , vasoconstriction , medicine , endocrinology , lipopolysaccharide , perfusion , aorta , septic shock , vascular smooth muscle , myosin light chain phosphatase , chemistry , sepsis , phosphatase , phosphorylation , biochemistry , smooth muscle
Hyporesponsiveness to vasoconstrictors is a well‐known characteristic of septic shock. We hypothesized that the degree of vascular hyporesponsiveness may vary among different vascular systems. Both aortic rings and perfused kidneys obtained from male Wistar rats treated with lipopolysaccharide (LPS; 10 mg/kg, i.p.) were evaluated for their reactivity to vasopressin (AVP), 6 and 24 h after LPS injection (LPS 6 and LPS 24 h groups, respectively). AVP‐induced contraction was reduced by 30‐80% in aortic rings from LPS 6 and 24 h groups, while perfused kidneys showed enhanced responses to AVP. For instance, AVP (10 pmol) increased the renal perfusion pressure by 27.5 ± 4.7, 95 ± 12.8, and 150.6 ± 11.4 mm Hg in control, LPS 6 and LPS 24 h groups, respectively. Western blotting analysis revealed increased levels of phosphorylated MYPT1 in kidneys, but not in aortas from LPS 6 and 24 h rats. Our results demonstrate that vascular systems may present different profiles of responses to vasoconstrictors during endotoxemia. At least for AVP, it appears to involve a differential regulation of intracellular mechanisms responsible for the control of vascular contractility, such as the myosin phosphatase. Grant Funding Source : Supported by CNPq, Brazil; and FAPESC, Brazil.