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Renal growth and development in mice lacking AT(1A) receptors for angiotensin II

Publication ,  Journal Article
Oliverio, MI; Madsen, K; Best, CF; Ito, M; Maeda, N; Smithies, O; Coffman, TM
Published in: American Journal of Physiology - Renal Physiology
January 1, 1998

To examine the role of the type 1A (AT(1A)) angiotensin receptor in renal growth and development, we analyzed F2 progeny from a series of crosses between F1 mice that were heterozygous for a targeted disruption of the AT(1A) receptor gene [Agtr1A-(+/-)]. Among 21-day-old weanling F2 mice, we found that 194 (32%) were homozygous for the wild-type allele Agtr1A-(+/+), 299 (49%) were Agtr1A-(+/-), and 119 (19%) were Agtr1A-(-/-). This differed significantly from the proportions predicted by Mendelian genetics (P = 0.01), suggesting that the complete absence of AT(1A) receptors is associated with a mild survival disadvantage. Agtr1A-(-/-) mice grew normally, and we found no significant differences in body weight or heart and kidney weights in Agtr1A-(+/+) and Agtr1A-(-/-) mice examined at 21, 60, and 100 days. Protein and DNA content of kidneys and hearts were also similar in weanling or adult Agtr1A-(+/+) and Agtr1A-(-/-) mice. By light microscopy with immunohistochemistry, kidneys from Agtr1A-(-/-) were essentially normal, with two exceptions: 1) there was marked hypertrophy of the juxtaglomerular apparatus (JGA) and proximal expansion of renin-producing cells along the afferent arterioles, and 2) some glomeruli showed evidence of mesangial expansion. We did not find the severe renal vascular lesions or papillary atrophy that have been observed in angiotensinogen- or angiotensin converting enzyme-deficient animals. We conclude that the AT(1A) receptor is not essential for the normal organogenesis of the kidney; however, its absence is associated with mild mesangial expansion and JGA hypertrophy.

Duke Scholars

Published In

American Journal of Physiology - Renal Physiology

EISSN

1522-1466

ISSN

1931-857X

Publication Date

January 1, 1998

Volume

274

Issue

1 43-1

Related Subject Headings

  • Urology & Nephrology
  • 3208 Medical physiology
  • 3202 Clinical sciences
  • 1116 Medical Physiology
  • 1103 Clinical Sciences
  • 0606 Physiology
 

Citation

APA
Chicago
ICMJE
MLA
NLM
Oliverio, M. I., Madsen, K., Best, C. F., Ito, M., Maeda, N., Smithies, O., & Coffman, T. M. (1998). Renal growth and development in mice lacking AT(1A) receptors for angiotensin II. American Journal of Physiology - Renal Physiology, 274(1 43-1).
Oliverio, M. I., K. Madsen, C. F. Best, M. Ito, N. Maeda, O. Smithies, and T. M. Coffman. “Renal growth and development in mice lacking AT(1A) receptors for angiotensin II.” American Journal of Physiology - Renal Physiology 274, no. 1 43-1 (January 1, 1998).
Oliverio MI, Madsen K, Best CF, Ito M, Maeda N, Smithies O, et al. Renal growth and development in mice lacking AT(1A) receptors for angiotensin II. American Journal of Physiology - Renal Physiology. 1998 Jan 1;274(1 43-1).
Oliverio, M. I., et al. “Renal growth and development in mice lacking AT(1A) receptors for angiotensin II.” American Journal of Physiology - Renal Physiology, vol. 274, no. 1 43-1, Jan. 1998.
Oliverio MI, Madsen K, Best CF, Ito M, Maeda N, Smithies O, Coffman TM. Renal growth and development in mice lacking AT(1A) receptors for angiotensin II. American Journal of Physiology - Renal Physiology. 1998 Jan 1;274(1 43-1).

Published In

American Journal of Physiology - Renal Physiology

EISSN

1522-1466

ISSN

1931-857X

Publication Date

January 1, 1998

Volume

274

Issue

1 43-1

Related Subject Headings

  • Urology & Nephrology
  • 3208 Medical physiology
  • 3202 Clinical sciences
  • 1116 Medical Physiology
  • 1103 Clinical Sciences
  • 0606 Physiology