Normal regulation of renin-angiotensin system (RAS) restores vasodilator mechanisms in middle cerebral arteries (MCA) of consomic SS.BN13 and renin-congenic rats (CROSBI ID 740314)
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Podaci o odgovornosti
Drenjančević-Perić Ines ; Lombard, JH.
engleski
Normal regulation of renin-angiotensin system (RAS) restores vasodilator mechanisms in middle cerebral arteries (MCA) of consomic SS.BN13 and renin-congenic rats
Dahl S rats exhibit impaired regulation of the RAS with chronic low levels of angiotensin II (ANG II) while consomic SS.BN13 rats and renin-congenic (RGRR) rats with a normally functioning renin gene from the Brown Norway (BN) or Dahl salt-resistant rat exhibit normal RAS regulation. Since ANG II plays a role in maintaining normal vascular relaxation mechanisms, the goal of this study was to determine whether restoring normal RAS regulation by chromosome/gene transfer affects relaxation of MCA from rats on a low salt diet. Responses to acetylcholine (ACh) and hypoxia were assessed by videomicrometry in cannulated MCA in the absence and /or presence of indomethacin [cyclooxygenase (COX) inhibitor], L-NMMA (NOS inhibitor), and MS-PPOH (CYP450 epoxygenase inhibitor). MCA from Dahl S rats exhibited paradoxical constriction in response to acetylcholine (ACh) that was eliminated by COX inhibition, while ACh-induced dilation was completely NO dependent in BN, SS.BN13 and RGRR rats. Hypoxic constriction of MCA from Dahl S rats was converted to dilation by indomethacin. The restored dilation was unaffected by L-NMMA, but abolished with MS-PPOH suggesting a role for EETs. In SS.BN13, RGRR, and BN rats, hypoxic dilation was eliminated by indomethacin, suggesting a role for some COX metabolite, e.g., prostacyclin or PGE2. These data suggest that normalization of RAS regulation causes a switch from production of COX derived vasoconstrictor metabolites (in Dahl S rats) toward NO-dependent relaxation in response to ACh and prostaglandin-dependent dilation to hypoxia.
angiotensin II; hypertension; consomic and congenic rats; vascular reactivity
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Podaci o prilogu
A248-A249-x.
2004.
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Podaci o matičnoj publikaciji
FASEB journal
0892-6638
Podaci o skupu
Nepoznat skup
ostalo
29.02.1904-29.02.2096