Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat.

Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat. Research Abstract Details 

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Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat. Abstract Text:

Christopher M Coleman,Jordan J Minor,Laura E Burt,Barbara A Thornhill,Michael S Forbes,Robert L Chevalier,

The renin-angiotensin system is activated in the developing kidney and is necessary for normal renal development, but is further activated by unilateral ureteral obstruction (UUO). During nephrogenesis, there is a switch from a preponderance of angiotensin AT(2) to AT(1) receptors in the rat. We examined the renal cellular response to angiotensin II receptor inhibition in the neonatal rat subjected to partial UUO under anesthesia within 48 h of birth. Group I ("early") received saline vehicle, losartan (AT(1) inhibitor), or PD-123319 (AT(2) inhibitor) during the completion of nephrogenesis in the first 10 days of life. Group II ("late") received each of the three treatments throughout the subsequent 10 days of life. Kidneys were harvested at 21 days, and the distribution of renin, apoptosis, macrophages, alpha-smooth muscle actin, and collagen was determined. Losartan and PD-123319 each increased vascular renin distribution in both kidneys. Partial UUO reduced growth and increased apoptosis, macrophages, alpha-smooth muscle actin, and collagen in the obstructed kidney. Early losartan treatment further increased alpha-smooth muscle actin and collagen in the obstructed kidney and induced apoptosis, macrophages, and collagen in the contralateral kidney. Late losartan treatment had no effect on any of the parameters in either kidney, and PD-123319 had no effect on either kidney. We conclude that selective inhibition of AT(1) receptors during nephrogenesis (but not during subsequent renal maturation) exacerbates injury to the obstructed kidney and also injures the contralateral kidney. These results suggest that angiotensin II receptor blockers should be avoided in the developing hydronephrotic kidney.

Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat. Publishing Authors By Initials

CM Coleman,JJ Minor,LE Burt,BA Thornhill,MS Forbes,RL Chevalier,

For similar male urogenital diseases: urologic diseases: ureteral diseases: ureteral obstruction research abstracts see: male urogenital diseases: urologic diseases: ureteral diseases: ureteral obstruction research

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Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: American journal of physiology. Renal physiology

VOLUME: 293

Page Numbers: F262-8

Journal Abbreviation: Am. J. Physiol. Renal Physiol.

ISSN: 0363-6127

DAY: 18

MONTH: 04

YEAR: 2007

Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 100901990

Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat. Keywords Mesh Terms:

KEYWORDS: Ureteral Obstruction

MESH TERMS: complications

Chemical & Substance for Abstract: Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat. Information

Substance Name: Collagen

Registry Number: 9007-34-5

Grant and Affiliation Information for Angiotensin AT1-receptor inhibition exacerbates renal injury resulting from partial unilateral ureteral obstruction in the neonatal rat.

AFFILIATION: Dept. of Pediatrics, University of Virginia, Box 800386, Charlottesville VA 22908, USA.

Country: United States

AGENCY: United States NIDDK

GRANT: DK62328

ACRONYM: DK

MEDLINETA: Am J Physiol Renal Physiol

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