Hemodynamic basis for the limited renal injury in rats with Angiotensin II-induced hypertension Journal Article

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Authors: Polichnowski, A. J.; Griffin, K. A.; Picken, M. M.; Licea-Vargas, H; Long, J; Williamson, G. A.; Bidani, A. K.
Article Title: Hemodynamic basis for the limited renal injury in rats with Angiotensin II-induced hypertension
Abstract: ANG II is thought to increase the susceptibility to hypertension-induced renal disease (HIRD) via BP-dependent and BP-independent pathways; however, the quantitative relationships between BP and HIRD have not been examined in ANG II-infused hypertensive rats. We compared the relationship between radiotelemetrically-measured BP and HIRD in Sprague-Dawley rats (Harlan) chronically administered ANG II (300-500 ng/kg/min, n=19) for 4 weeks vs. another commonly employed pharmacologic model of hypertension induced by the chronic administration of Nomega-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day, n=23). Despite the significantly higher average systolic BP associated with ANG II (191.1+/-3.2 mmHg) vs. L-NAME (179.9+/-2.5 mmHg) administration; the level of HIRD was very modest in the ANG II vs. L-NAME model as evidenced by significantly less glomerular injury (6.6+/-1.3% vs. 11.3+/-1.5, respectively), tubulointerstitial injury (0.3+/-0.1 vs. 0.7+/-0.1 injury score, respectively), proteinuria (66.3+/-10.0 mg/day vs. 117.5+/-10.1, respectively) and serum creatinine (0.5+/-0.04 mg/dl vs. 0.9+/-0.07, respectively). Given that HIRD severity is expected to be a function of renal microvascular BP transmission, BP-RBF relationships were examined in additional conscious rats administered ANG II (n=7) or L-NAME (n=8). Greater renal vasoconstriction was observed during ANG II vs. L-NAME administration (41% vs. 23% decrease in RBF from baseline). Moreover, ANG II, but not L-NAME, infusion was associated with a unique BP-RBF pattern in which the most substantial decreases in RBF were observed during spontaneous increases in BP. We conclude that the hemodynamic effects of ANG II may mediate the strikingly low susceptibility to HIRD in the ANG II-infused model of hypertension in rats.
Journal Title: American journal of physiology.Renal physiology
Volume: 208
Issue: 3
ISSN: 1522-1466; 1522-1466
Publisher: American Journal of Physiology - Renal Physiology  
Date Published: 2014
Start Page: F252
End Page: 260
Language: ENG
DOI/URL:

10.1152/ajprenal.00596.2014
Notes: LR: 20150811; GR: DK-40426/DK/NIDDK NIH HHS/United States; GR: DK-61653/DK/NIDDK NIH HHS/United States; GR: IK2 BX001285/BX/BLRD VA/United States; JID: 100901990; 11128-99-7 (Angiotensin II); EIN: Am J Physiol Renal Physiol. 2015 Apr 1;308(7):F796. Dosage error in published abstract; MEDLINE/PubMed abstract corrected; Dosage error in article text. PMID: 25834130; OID: NLM: PMC4312963 [Available on 02/01/16]; OTO: NOTNLM; PMCR: 2016/02/01 00:00; 2014/12/04 [aheadofprint]; ppublish