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1 Ped, Pharm, Patho., University of Montreal, Montreal, Canada
2 Pharmacology, University of Sherbrooke, Montreal, Canada
3 Microbiology/Immunology, University of Montreal, Montreal, Canada
* To whom correspondence should be addressed. E-mail: anne-monique.nuyt{at}recherche-ste-justine.qc.ca.
The renin angiotensin system plays a key role in the initiation and maintenance of elevated blood pressure associated with altered intra uterine milieu. The current studies were undertaken to verify whether vascular response to AngII is increased in adult offspring of low protein fed dams (LP) compared to control (CTRL) and if so, to examine underlying mechanism(s). AngII-induced contraction of carotid rings was increased in LP (Emax relative to maximal response to KCl 80 mM: 230 ± 3% LP vs. 201 ± 2% CTRL, p<0.05). In both groups, contraction to AngII was mediated solely by AT1R. Responses to thromboxane A2 analogue U46619 and to KCl 80 mM under step increases in tension were similar between groups. Endothelium depletion enhanced contraction to AngII in both groups, more so in LP. Blockade of endothelin formation had no effect on response to AngII, and angiotensin 1-7 did not elicit vasomotor response in either group. Superoxide dismutase (SOD) analogue Tempol normalized LP without modifying CTRL response to AngII. Basal levels of superoxide (aortic segments, lucigenin-enhanced chemiluminescence and fluorescent dye hydroethidine) were higher in LP. AngII further increased superoxide production in LP only and this was inhibited by co-incubation with diphenylene iodonium or apocynin (inhibitor of NADPH oxidase complex). AT1R expression in carotid arteries was increased in LP whereas SOD expression was unchanged. In conclusion, vasoconstriction to AngII is exaggerated in this model of developmental programming of hypertension, secondary to enhanced vascular production of superoxide anion by NADPH oxidase with concomitant increase of AT1R expression.
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