Renal renin-angiotensin system activity in naturally reared and cross-fostered spontaneously hypertensive rats
Young (4 week) spontaneously hypertensive rats (SHR) exhibit greater renal responses to angiotensin II (Ang II) than normotensive Wistar Kyoto (WKY) rats. SHR pups cross-fostering to a WKY dam at birth (SHRX) are less sensitive to Ang II and have lower adult blood pressure. The aim of this study was...
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Published in | American journal of hypertension Vol. 16; no. 10; pp. 864 - 869 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Elsevier Inc
01.10.2003
Oxford University Press Elsevier Science |
Subjects | |
Online Access | Get full text |
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Summary: | Young (4 week) spontaneously hypertensive rats (SHR) exhibit greater renal responses to angiotensin II (Ang II) than normotensive Wistar Kyoto (WKY) rats. SHR pups cross-fostering to a WKY dam at birth (SHRX) are less sensitive to Ang II and have lower adult blood pressure. The aim of this study was to compare renal renin-angiotensin system activity in young naturally reared and cross-fostered SHR pups.
SHR and WKY rats were reared either by their natural mothers or by a foster mother of the opposite strain. At 5, 10, and 15 days of age, renal tissue renin activity and Ang II concentration were measured by radioimmunoassay. Renin-secreting cells were identified by in situ hybridization and AT1 receptor expression was compared using Western blots. Ang II-mediated cAMP generation was measured in isolated proximal tubules.
Tissue renin activity and numbers of renin-secreting cells did not differ, but Ang II was higher in SHRX. The AT1 receptor expression was significantly lower in SHRX compared with SHR. Basal and Ang II-stimulated cAMP was lower in SHR tubules compared with WKY and SHRX tubules.
Cross-fostering reversed the increased renal sensitivity of the SHR to Ang II. These data suggest that renal AT1 receptor expression can be manipulated during the postnatal period and that this may affect adult blood pressure. |
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Bibliography: | href:16_10_864.pdf istex:F9C9D4B1CB68958F13300102154F1DC1A54684B6 ark:/67375/HXZ-Q8VS67KC-M This study was funded by the British Heart Foundation (PG/97185). ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0895-7061 1879-1905 1941-7225 |
DOI: | 10.1016/S0895-7061(03)00999-3 |