Title : Renal intramedullary infusion of tempol normalizes the blood pressure response to intrarenal blockade of heme oxygenase-1 in angiotensin II-dependent hypertension.

Pub. Date : 2016 Apr

PMID : 26922123






5 Functional Relationships(s)
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1 Previous studies have demonstrated that intramedullary inhibition of heme oxygenase-1 (HO-1) increases the blood pressure and superoxide production response to angiotensin II (Ang II) infusion. Superoxides angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus
2 Previous studies have demonstrated that intramedullary inhibition of heme oxygenase-1 (HO-1) increases the blood pressure and superoxide production response to angiotensin II (Ang II) infusion. Superoxides angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus
3 The present study was designed to test the hypothesis that increased renal medullary superoxide production contributes to the increase in blood pressure in response to blockade of renal medullary HO-1 in Ang II-induced hypertension. Superoxides angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus
4 Renal medullary superoxide production in Ang II-treated mice was significantly increased by infusion of QC-13 alone. Superoxides angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus
5 These results demonstrate that renal medullary interstitial blockade of HO-1 exacerbates Ang II-induced hypertension via a mechanism that is dependent on enhanced superoxide generation and highlight the important antioxidant function of HO-1 in the renal medulla. Superoxides angiotensinogen (serpin peptidase inhibitor, clade A, member 8) Mus musculus