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10.1161/HYPERTENSIONAHA.115.05320

http://scihub22266oqcxt.onion/10.1161/HYPERTENSIONAHA.115.05320
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C4825680!4825680!26150439
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suck abstract from ncbi


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pmid26150439      Hypertension 2015 ; 66 (3): 534-42
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  • SALT SENSITIVITY IN RESPONSE TO RENAL INJURY REQUIRES RENAL ANGIOTENSIN-CONVERTING ENZYME #MMPMID26150439
  • Giani JF; Bernstein KE; Janjulia T; Han J; Toblli JE; Shen XZ; Rodriguez-Iturbe B; McDonough AA; Gonzalez-Villalobos RA
  • Hypertension 2015[Sep]; 66 (3): 534-42 PMID26150439show ga
  • Recent evidence indicates that salt-sensitive hypertension can result from a subclinical injury that impairs the kidneys? capacity to properly respond to a high salt diet. However, how this occurs is not well understood. Here, we showed that while previously salt resistant wild-type mice became salt-sensitive after the induction of renal injury with the nitric oxide synthase inhibitor N?-Nitro-L-arginine methyl ester hydrochloride (L-NAME); mice lacking renal angiotensin-converting enzyme, exposed to the same insult, did not become hypertensive when faced with a sodium load. This is because the activity of renal angiotensin-converting enzyme plays a critical role in: 1) augmenting the local pool of angiotensin II and, 2) the establishment of the anti-natriuretic state via modulation of glomerular filtration rate and sodium tubular transport. Thus, this study demonstrates that the presence of renal angiotensin-converting enzyme plays a pivotal role in the development of salt sensitivity in response to renal injury.
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