PMID- 10028953
OWN - NLM
STAT- MEDLINE
DCOM- 19990505
LR  - 20190724
IS  - 0160-2446 (Print)
IS  - 0160-2446 (Linking)
VI  - 33 Suppl 1
DP  - 1999
TI  - Valsartan and the kidney: present and future.
PG  - S37-40; discussion S41-3
AB  - Angiotensin (Ang) II type 1 (AT1) receptor antagonists are orally active drugs 
      that specifically block the subtype 1 of Ang receptors. In contrast to AT1 
      receptor antagonists, angiotensin-converting enzyme (ACE) inhibitors block the 
      actions of Ang II incompletely. Furthermore, the bradykinin-potentiating effects 
      of ACE inhibitors may contribute to the mechanism of action of ACE inhibitors. 
      Data in experimental animals suggest that AT1 receptor antagonists decrease the 
      glomerular filtration rate (GFR) to a lesser degree than ACE inhibitors. The 
      greater effect of ACE inhibitors in decreasing glomerular pressure was attenuated 
      with a bradykinin antagonist. In rat models of renal damage with proteinuria, 
      acute reduction of proteinuria was seen with ACE inhibitors but not with AT1 
      receptor antagonists, whereas long-term reductions of proteinuria were of similar 
      magnitude with both agents. Renal histology after several months revealed that 
      AT1 receptor antagonists and ACE inhibitors were equally renoprotective in 
      various renal damage models. AT1 receptor antagonists, like ACE inhibitors, 
      exhibit a natriuretic effect equal to moderate doses of a thiazide diuretic. In 
      patients with severe volume depletion, use of AT1 receptor antagonists may lead 
      to acute renal failure. Valsartan was tested in a double-blind trial in patients 
      with moderate to severe renal failure and led to a substantial decrease in 
      diastolic and systolic blood pressure, whereas there was no difference from 
      placebo for changes in GFR. Urine protein increased with placebo and decreased 
      with valsartan. The data indicate that valsartan in renal failure patients is 
      effective in lowering blood pressure while leaving renal excretory function 
      unaltered. Whether there is a renoprotective effect can only be shown in 
      long-term trials, which are under way.
FAU - Mann, J F
AU  - Mann JF
AD  - Schwabing Hospital, University of Munich, Germany.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Cardiovasc Pharmacol
JT  - Journal of cardiovascular pharmacology
JID - 7902492
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Tetrazoles)
RN  - 11128-99-7 (Angiotensin II)
RN  - 80M03YXJ7I (Valsartan)
RN  - HG18B9YRS7 (Valine)
SB  - IM
MH  - Angiotensin II/*antagonists & inhibitors
MH  - Angiotensin-Converting Enzyme Inhibitors/therapeutic use
MH  - Animals
MH  - Antihypertensive Agents/*therapeutic use
MH  - Humans
MH  - Hypertension/*drug therapy
MH  - Kidney Diseases/*drug therapy
MH  - Renal Insufficiency/metabolism
MH  - Tetrazoles/*therapeutic use
MH  - Valine/*analogs & derivatives/therapeutic use
MH  - Valsartan
RF  - 19
EDAT- 1999/02/24 00:00
MHDA- 1999/02/24 00:01
CRDT- 1999/02/24 00:00
PHST- 1999/02/24 00:00 [pubmed]
PHST- 1999/02/24 00:01 [medline]
PHST- 1999/02/24 00:00 [entrez]
AID - 10.1097/00005344-199900001-00008 [doi]
PST - ppublish
SO  - J Cardiovasc Pharmacol. 1999;33 Suppl 1:S37-40; discussion S41-3. doi: 
      10.1097/00005344-199900001-00008.