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January 1, 1998AJP Renal PhysiologyOpen Access

Renal growth and development in mice lacking AT1Areceptors for angiotensin II

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Why the study?

Does the absence of AT1A receptors affect renal growth and development in mice?

Population

F2 progeny from crosses between F1 mice heterozygous for a targeted disruption of the AT1A receptor gene…

Comparison

Targeted disruption of the AT1A receptor gene… vs Wild-type mice (Agtr1A-(+/+))

Design

Preclinical

Follow-up

up to 100 days

Authors

MOMichael I. OliverioUniversity of North Carolina at Chapel HillKMKirsten MadsenUniversity of Southern DenmarkCBChristopher F. BestUnited States Fish and Wildlife Service

Discussion

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Implication

AT1A receptor deletion permits normal renal growth in mice; leaves open receptor redundancy in human hypertension or CKD.

Key Points

  • This research investigates the importance of AT1A angiotensin receptors in renal growth and development in mice.
  • Analyzed F2 progeny from crosses between F1 mice heterozygous for AT1A receptor gene disruption.
  • Counted genotypes and assessed kidney and heart weights at 21, 60, and 100 days post-weaning.
  • Employed light microscopy and immunohistochemistry to evaluate kidney structure.
  • 194 (32%) were homozygous wild-type, while 119 (19%) were homozygous for absence of AT1A receptors (P = 0.01).
  • Kidney weights were similar across genotypes, indicating normal growth despite receptor absence.
  • Observed mild hypertrophy in the juxtaglomerular apparatus and some mesangial expansion in AT1A-(-/-) mice.

Structured PICO

Does the absence of AT1A receptors affect renal growth and development in mice?

P
Population
F2 progeny from crosses between F1 mice heterozygous for a targeted disruption of the AT1A receptor gene [Agtr1A-(+/-)], n=612 weanling F2 mice
I
Intervention
Targeted disruption of the AT1A receptor gene (Agtr1A-(-/-))
C
Comparator
Wild-type mice (Agtr1A-(+/+))
O
Outcome
Renal growth and development (survival proportions, body weight, heart and kidney weights, protein and DNA content, histology)surrogate

The AT1A receptor is not essential for normal kidney organogenesis, but its absence causes mild mesangial expansion and juxtaglomerular apparatus hypertrophy.

Cite This Study

Oliverio et al. (1998) studied this question.

synapsesocial.com/papers/6a1f2142cf1cd4bd52914daahttps://doi.org/10.1152/ajprenal.1998.274.1.f43
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Autoradiographic characterization of angiotensin receptor subtypes in fetal and adult human kidney1992 · 97 citations
  2. 2Control of glomerular hypertension limits glomerular injury in rats with reduced renal mass.1985 · 943 citations
  3. 3Plasma and Renal Prorenin/Renin, Renin mRNA, and Blood Pressure in Dahl Salt-Sensitive and Salt-Resistant Rats1996 · 49 citations
  4. 4Regulation of blood pressure by the type 1A angiotensin II receptor gene.1995 · 613 citations
  5. 5Tissular expression and regulation of type 1 angiotensin II receptor subtypes by quantitative reverse transcriptase-polymerase chain reaction analysis.1994 · 169 citations