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Benz, Kerstin; Orth, Stephan R.; Simonaviciene, Aurelia; Linz, Wolfgang; Schindler, Ursula; Rütten, Hartmut; Amann, Kerstin

Blood Pressure-Independent Effect of Long-Term Treatment with the Soluble Heme-Independent Guanylyl Cyclase Activator HMR1766 on Progression in a Model of Noninflammatory Chronic Renal Damage

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  • Medientyp: E-Artikel
  • Titel: Blood Pressure-Independent Effect of Long-Term Treatment with the Soluble Heme-Independent Guanylyl Cyclase Activator HMR1766 on Progression in a Model of Noninflammatory Chronic Renal Damage
  • Beteiligte: Benz, Kerstin; Orth, Stephan R.; Simonaviciene, Aurelia; Linz, Wolfgang; Schindler, Ursula; Rütten, Hartmut; Amann, Kerstin
  • Erschienen: S. Karger AG, 2007
  • Erschienen in: Kidney and Blood Pressure Research
  • Sprache: Englisch
  • DOI: 10.1159/000104091
  • ISSN: 1420-4096; 1423-0143
  • Schlagwörter: Cardiology and Cardiovascular Medicine ; Nephrology ; Cardiology and Cardiovascular Medicine ; Nephrology
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: <jats:p>Nitric oxide formation is impaired in chronic renal failure. The renoprotective effects of a nonhypotensive dose of HMR1766, a direct activator of the heme enzyme soluble guanylyl cyclase was studied in comparison to an ACE-i in the remnant kidney model. Male Sprague-Dawley rats were subtotally nephrectomized (SNX) or sham operated (sham) and left untreated or started on treatment with HMR1766 or ACE-i in non-hypotensive doses. BP, albumin excretion and parameters of renal damage were analyzed. After a 12-week study, urinary albumin excretion was significantly higher in untreated SNX than in sham; this increase was prevented by ACE-i and ameliorated by HMR1766. Relative kidney and left ventricular weight were significantly higher in untreated SNX compared to sham; these changes were completely prevented by HMR1766. In untreated SNX, glomerulosclerosis (1.02 ± 0.13) was significantly higher than in sham (0.12 ± 0.04), SNX+HMR1766 (0.27 ± 0.04) and SNX+ACE-i (0.46 ± 0.06). Tubulointerstitial changes went in parallel. Increased glomerular cell number after SNX (71.5 ± 14 vs. 60 ± 7.3 in sham) was prevented by HMR1766 (55.7 ± 7.3), but not by ACE-i (66.6 ± 9). The results document beneficial BP-independent HMR1766 effects on kidney structure and urinary albumin excretion in a noninflammatory model of renal failure and may argue for a novel therapeutic principle.</jats:p>