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Renal production of endothelin is enhanced in a model of fetal programmed hypertension
Author(s) -
Grigore Daniela,
Ojeda Norma,
Robertson Elliott B.,
Alexander Barbara T.
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.lb127-a
Subject(s) - offspring , endocrinology , medicine , endothelin receptor , endothelin 1 , angiotensin ii , blood pressure , fetus , intrauterine growth restriction , renin–angiotensin system , endothelins , biology , pregnancy , receptor , genetics
Our laboratory uses a model of placental insufficiency to induce intrauterine growth restriction (IUGR) in the rat to investigate the mechanisms linking birth weight and blood pressure. We have previously reported that adult male IUGR offspring exhibit marked increases in mean arterial pressure associated with elevated levels of plasma testosterone, and activation of the intra‐renal renin angiotensin system as compared to adult male control offspring. Testosterone is suggested to enhance production of endothelin. In addition, we have previously reported that endothelin plays a role in mediating hypertension induced by chronic angiotensin II infusion in the rat. Thus, we hypothesize that up‐regulation of endothelin may contribute to hypertension in this model of fetal programming. We found that pre‐pro‐endothelin message as measured by RealTime PCR was significantly increased by 4.2 fold in the renal cortex of adult male IUGR offspring as compared to adult male control offspring. Thus, this suggests that enhanced production of endothelin may contribute to hypertension in IUGR offspring. Furthermore, testosterone or angiotensin II may serve as the stimulus for increased endothelin. Future studies will confirm the importance of endothelin in IUGR hypertension. NIH HL074927.