Effect of severe aortic banding above the renal arteries on nitric oxide synthase isotype expression

Citation
Ch. Barton et al., Effect of severe aortic banding above the renal arteries on nitric oxide synthase isotype expression, KIDNEY INT, 59(2), 2001, pp. 654-661
Citations number
43
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
KIDNEY INTERNATIONAL
ISSN journal
00852538 → ACNP
Volume
59
Issue
2
Year of publication
2001
Pages
654 - 661
Database
ISI
SICI code
0085-2538(200102)59:2<654:EOSABA>2.0.ZU;2-Q
Abstract
Background Severe aortic stenosis above the renal arteries leads to a reduc tion in renal perfusion, increased renin secretion, and elevation of arteri al blood pressure above the stenotic site. Nitric oxide (NO) plays an impor tant role in regulation of renal and systemic vascular resistance, renal bl ood flow, and Na+ handling. Abdominal aortic banding provides an excellent model for simultaneous testing of the effects of increased and decreased pr essure. flow, and shear stress in the same animal. Methods. We studied protein expressions of endothelial NO synthase (eNOS). inducible NOS (iNOS). and neuroneal NOS (nNOS) isotypes in the renal cortex , renal medulla. heart, brain. and aorta segments above and below the steno sis site three weeks after abdominal aortic banding above the renal arterie s. The results were compared with those obtained in the sham-operated contr ols. NOS isotype proteins were measured by Western blot. Results. Compared with the control group, the banded group showed significa nt up-regulations of eNOS, iNOS. and nNOS in renal cortex and medulla. Like wise. heart eNOS. brain nNOS, and thoracic aorta eNOS proteins were signifi cantly increased in the banded group. However. eNOS and iNOS expressions we re unchanged in the: aorta segment below the stenotic site. Likewise. iNOS expression in the heart and thoracic aorta remained unchanged in the banded animals. No significant difference was found in creatinine clearance or ur inary protein excretion between the two groups. Conclusions. These findings clearly demonstrate the up-regulatory action of increased pressure on eNOS expression in the thoracic aorta and heart and of nNOS expression in the brain. These data further show up-regulation of a ll NOS isotypes in the kidney, which must have helped to mitigate the assoc iated hypoperfusion.