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AT1 receptor mediated augmentation of intrarenal angiotensinogen in angiotensin II-dependent hypertension.
Hypertension. 2004 May; 43(5):1126-32.H

Abstract

Angiotensin (Ang) II-infused hypertensive rats exhibit increases in renal angiotensinogen mRNA and protein, as well as urinary angiotensinogen excretion in association with increased intrarenal Ang II content. The present study was performed to determine if the augmentation of intrarenal angiotensinogen requires activation of Ang II type 1 (AT1) receptors. Male Sprague-Dawley rats (200 to 220 g) were divided into 3 groups: sham surgery (n=10), subcutaneous infusion of Ang II (80 ng/min, n=11), and Ang II infusion plus AT1 blocker (ARB), olmesartan (5 mg/d, n=12). Ang II infusion progressively increased systolic blood pressure (SBP) compared with sham (178+/-8 mm Hg versus 119+/-4 at day 11). ARB treatment prevented hypertension (113+/-6 at day 11). Twenty-four-hour urine collections were taken at day 12, and plasma and tissue samples were harvested at day 13. The Ang II+ARB group had a significant increase in plasma Ang II compared with Ang II and sham groups (365+/-46 fmol/mL versus 76+/-9 and 45+/-14, respectively). Nevertheless, ARB treatment markedly limited the enhancement of kidney Ang II by Ang II infusion (65+/-17 fmol/g in sham, 606+/-147 in Ang II group, and 288+/-28 in Ang II+ARB group). Ang II infusion significantly increased kidney angiotensinogen compared with sham (1.69+/-0.21 densitometric units versus 1.00+/-0.17). This change was reflected by increased angiotensinogen immunostaining in proximal tubules. ARB treatment prevented this increase (1.14+/-0.12). Urinary angiotensinogen excretion rates were enhanced 4.7x in Ang II group (4.67+/-0.41 densitometric units versus 1.00+/-0.21) but ARB treatment prevented the augmentation of urinary angiotensinogen (0.96+/-0.23). These data demonstrate that augmentation of intrarenal angiotensinogen in Ang II-infused rats is AT1-dependent and provide further evidence that urinary angiotensinogen is closely linked to intrarenal Ang II in Ang II-dependent hypertension.

Authors+Show Affiliations

Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, 1430 Tulane Avenue, #SL39, New Orleans, LA 70112-2699, USA. hkobori@tulane.eduNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

15037565

Citation

Kobori, Hiroyuki, et al. "AT1 Receptor Mediated Augmentation of Intrarenal Angiotensinogen in Angiotensin II-dependent Hypertension." Hypertension (Dallas, Tex. : 1979), vol. 43, no. 5, 2004, pp. 1126-32.
Kobori H, Prieto-Carrasquero MC, Ozawa Y, et al. AT1 receptor mediated augmentation of intrarenal angiotensinogen in angiotensin II-dependent hypertension. Hypertension. 2004;43(5):1126-32.
Kobori, H., Prieto-Carrasquero, M. C., Ozawa, Y., & Navar, L. G. (2004). AT1 receptor mediated augmentation of intrarenal angiotensinogen in angiotensin II-dependent hypertension. Hypertension (Dallas, Tex. : 1979), 43(5), 1126-32.
Kobori H, et al. AT1 Receptor Mediated Augmentation of Intrarenal Angiotensinogen in Angiotensin II-dependent Hypertension. Hypertension. 2004;43(5):1126-32. PubMed PMID: 15037565.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - AT1 receptor mediated augmentation of intrarenal angiotensinogen in angiotensin II-dependent hypertension. AU - Kobori,Hiroyuki, AU - Prieto-Carrasquero,Minolfa C, AU - Ozawa,Yuri, AU - Navar,L Gabriel, Y1 - 2004/03/22/ PY - 2004/3/24/pubmed PY - 2004/10/9/medline PY - 2004/3/24/entrez SP - 1126 EP - 32 JF - Hypertension (Dallas, Tex. : 1979) JO - Hypertension VL - 43 IS - 5 N2 - Angiotensin (Ang) II-infused hypertensive rats exhibit increases in renal angiotensinogen mRNA and protein, as well as urinary angiotensinogen excretion in association with increased intrarenal Ang II content. The present study was performed to determine if the augmentation of intrarenal angiotensinogen requires activation of Ang II type 1 (AT1) receptors. Male Sprague-Dawley rats (200 to 220 g) were divided into 3 groups: sham surgery (n=10), subcutaneous infusion of Ang II (80 ng/min, n=11), and Ang II infusion plus AT1 blocker (ARB), olmesartan (5 mg/d, n=12). Ang II infusion progressively increased systolic blood pressure (SBP) compared with sham (178+/-8 mm Hg versus 119+/-4 at day 11). ARB treatment prevented hypertension (113+/-6 at day 11). Twenty-four-hour urine collections were taken at day 12, and plasma and tissue samples were harvested at day 13. The Ang II+ARB group had a significant increase in plasma Ang II compared with Ang II and sham groups (365+/-46 fmol/mL versus 76+/-9 and 45+/-14, respectively). Nevertheless, ARB treatment markedly limited the enhancement of kidney Ang II by Ang II infusion (65+/-17 fmol/g in sham, 606+/-147 in Ang II group, and 288+/-28 in Ang II+ARB group). Ang II infusion significantly increased kidney angiotensinogen compared with sham (1.69+/-0.21 densitometric units versus 1.00+/-0.17). This change was reflected by increased angiotensinogen immunostaining in proximal tubules. ARB treatment prevented this increase (1.14+/-0.12). Urinary angiotensinogen excretion rates were enhanced 4.7x in Ang II group (4.67+/-0.41 densitometric units versus 1.00+/-0.21) but ARB treatment prevented the augmentation of urinary angiotensinogen (0.96+/-0.23). These data demonstrate that augmentation of intrarenal angiotensinogen in Ang II-infused rats is AT1-dependent and provide further evidence that urinary angiotensinogen is closely linked to intrarenal Ang II in Ang II-dependent hypertension. SN - 1524-4563 UR - https://www.unboundmedicine.com/medline/citation/15037565/AT1_receptor_mediated_augmentation_of_intrarenal_angiotensinogen_in_angiotensin_II_dependent_hypertension_ L2 - http://www.ahajournals.org/doi/full/10.1161/01.HYP.0000122875.91100.28?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -