An and ati receptor expression in fetal myocardium

L. Davis, A. Hohimer, K. Thornburg, V. Brooks, R. Magness, I. Bird

Research output: Contribution to journalArticle

Abstract

During chronic fetal anemia biventricular cardiac output increases by 50% and the heart hypertrophies as the heart/body weight ratio increases from 7.3 to 9.5 g/kg fetus. Because angiotensin n (Au) is a myocyte mitogen, we measured circulating blood An levels, plasma renin activity (PRA) and ventricular ATI receptor protein concentrations in control and anemic fetal sheep made anemic by daily isovolemic hemorrhage for 5-7 days. Four anemic fetuses (hct 14±0.7%, 132.3 ±1.7 days, meant SEM) were compared to 4 age matched non-anemic controls (hct 36±0.4%). Ventricular tissue was rapidly frozen prior to homogenization in protein lysis buffer. Solubilized protein was subjected to western analysis (50μg protein/lane) and ATI-R immunoblotting achieved using a polyclonal andsera (SantaCruz,ATI-306) with ECL detection. Sheep adrenal cortex was used as a positive control. Blots were quantified by densitometry. All and PRA levels were measured by RIA. All blood levels increased from 21.1 ±4.5 to 54.7±2.7 pg/ml and PRA from 5.9±2.7 to 8.9±1.7 ng/ml/min. ATI receptor protein concentrations were not different, 6.06±0.74 od in controls and 5.59±0.58 in anemic hearts. Conclusions: All is elevated in anemia, nevertheless, ATT receptors are not down regulated. Supported by grants HL45043, HL49210, AHA(Wisc)95GB41.

Original languageEnglish (US)
Pages (from-to)A769
JournalFASEB Journal
Volume10
Issue number3
StatePublished - Dec 1 1996

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

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