Similar renoprotection after renin-angiotensin-dependent and -independent antihypertensive therapy in 5/6-nephrectomized Ren-2 transgenic rats: are there blood pressure-independent effects?
Language English Country Australia Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Aldosterone urine MeSH
- Angiotensin II blood metabolism MeSH
- Antihypertensive Agents pharmacology MeSH
- Angiotensin II Type 1 Receptor Blockers pharmacology MeSH
- Kidney Failure, Chronic drug therapy metabolism prevention & control MeSH
- Diabetic Nephropathies drug therapy prevention & control MeSH
- Diuretics pharmacology MeSH
- Furosemide pharmacology MeSH
- Hydrochlorothiazide pharmacology MeSH
- Hypertension drug therapy metabolism MeSH
- Indoles pharmacology MeSH
- Angiotensin-Converting Enzyme Inhibitors pharmacology MeSH
- Cardiomegaly drug therapy prevention & control MeSH
- Drug Therapy, Combination MeSH
- Creatinine blood metabolism urine MeSH
- Blood Pressure drug effects MeSH
- Rats MeSH
- Labetalol pharmacology MeSH
- Losartan pharmacology MeSH
- Rats, Sprague-Dawley MeSH
- Rats, Transgenic MeSH
- Proteinuria blood metabolism urine MeSH
- Renin-Angiotensin System drug effects MeSH
- Renin metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Aldosterone MeSH
- Angiotensin II MeSH
- Antihypertensive Agents MeSH
- Angiotensin II Type 1 Receptor Blockers MeSH
- Diuretics MeSH
- Furosemide MeSH
- Hydrochlorothiazide MeSH
- Indoles MeSH
- Angiotensin-Converting Enzyme Inhibitors MeSH
- Creatinine MeSH
- Labetalol MeSH
- Losartan MeSH
- Renin MeSH
- trandolapril MeSH Browser
1. Hypertension plays a critical role in the progression of chronic kidney disease (CKD) to end-stage renal disease (ESRD), but it has also been postulated that antihypertensive drugs that block the renin-angiotensin system (RAS) show class-specific renoprotective actions beyond their blood pressure (BP)-lowering effects. 2. Because this notion has recently been questioned, in the present study we compared the effects of a RAS-dependent antihypertensive therapy (a combination of trandolapril, an angiotensin-converting enzyme inhibitor (ACEI) and losartan, an angiotensin-II (AngII) receptor subtype 1A receptor antagonist) with a 'RAS-independent' antihypertensive therapy (a combination of labetalol, an alfa- and beta-adrenoreceptor antagonist with the diuretics, hydrochlorothiazide and furosemide) on the progression of CKD after 5/6 renal ablation (5/6 NX) in Ren-2 renin transgenic rats (TGR), a model of AngII-dependent hypertension. Normotensive transgene-negative Hannover Sprague-Dawley (HanSD) rats after 5/6 NX served as controls. 3. RAS-dependent and -independent antihypertensive therapies normalized BP and survival rate, and prevented the development of cardiac hypertrophy and glomerulosclerosis to the same degree in 5/6 NX HanSD rats and in 5/6 NX TGR. The present findings show that renoprotection, at least in rats after 5/6 NX, is predominantly BP-dependent. When equal lowering of BP was achieved, leading to normotension, cardio- and renoprotective effects were equivalent irrespective of the type of antihypertensive therapy. 4. These findings should be taken into consideration in attempts to develop new therapeutic approaches and strategies aimed to prevent the progression of CKD and to lower the incidence of ESRD.
References provided by Crossref.org
Empagliflozin Is Not Renoprotective in Non-Diabetic Rat Models of Chronic Kidney Disease
