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(Hypertension. 2009;54:1115.)
© 2009 American Heart Association, Inc.
Original Articles |
From the Departments of Medicine, Nephrology, and Rheumatology (C.P.B., G.A.M., F.S.), Clinical Chemistry (V.W.A., M.O.), and Medical Statistics (A.Z.), Georg-August-University, Göttingen, Germany; Clinical Neurobiology Laboratory (C.Schl., E.F.), German Primate Center, Göttingen, Germany; Laboratory of Behavioural Neurobiology (C.R.P., S.M., J.F.), ETH Zurich, Schwerzenbach, Switzerland; Institute for BioMedical Research (C.Schn.), Novartis Pharma AG, Basel, Switzerland; Department of Nephropathology (K.A.), University of Erlangen-Nürnberg, Erlangen, Germany; Department of Medicine II (F.E.), Nephrology and Clinical Immunology, University Hospital, RWTH Aachen, Aachen, Germany; Current address (C.R.P.): Clinic for Affective Disorders and General Psychiatry, University Hospital Zurich, Zurich, Switzerland.
Correspondence to Carsten Paul Bramlage, Department of Nephrology and Rheumatology, Georg-August-University Göttingen, Robert-Koch Strasse 40, 37075 Göttingen, Germany. E-mail c.bramlage{at}med.uni-goettingen.de
The influence of prenatal factors on the development of arterial hypertension has gained considerable interest in recent years. Prenatal dexamethasone exposure was found to induce hypertension and to alter nephron number and size in rodents and sheep. However, it is not clear whether these findings are applicable to nonhuman primates. Thus, we examined the effects of prenatal dexamethasone treatment on blood pressure (BP) and nephron number in marmoset monkeys. Fifty-two marmosets were allotted to 3 groups according to the gestational stage during which their mothers were exposed to oral 5-mg/kg dexamethasone for 7 days (gestation period: 20 weeks): (1) the early dexamethasone group at week 7; (2) the late dexamethasone group at week 13; and (3) the control group. BP was determined by telemetric (n=12) or cuff measurements (n=30), along with cystatin C, proteinuria, and body weight. All of the animals were euthanized at the age of 24 months, and glomerular number and volume were determined. Prenatal exposure to dexamethasone did not lead to a significant difference between the groups with regard to BP, kidney morphology and function, or body weight. BP correlated significantly with body weight, relative kidney weight, and mean glomerular volume and the body weight with the glomerular volume regardless of dexamethasone treatment. In conclusion, prenatal exposure to dexamethasone in marmosets does not, in contrast to other mammals studied, result in hypertension or changes in kidney morphology. Our data support the role of body weight as a predictor of elevated glomerular volume and BP development rather than prenatal dexamethasone exposure.
Key Words: hypertension dexamethasone prenatal programming marmoset monkeys glomeruli number
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