ISSN:
1432-198X
Keywords:
Key words Mean arterial pressure
;
Neonatal angiotensin-converting enzyme inhibition
;
Oxygen tension
;
Renal blood flow
;
Renal interstitial hydrostatic pressure
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Pharmacological interruption or genetic disruption of the renin-angiotensin system before completion of nephrogenesis produces papillary atrophy and an impaired urinary concentrating ability. The mechanisms involved are yet to be elucidated, but renal hypoperfusion and subsequent ischemia, particularly to the immature renal medulla, may be hypothesized. The acute intrarenal responses to angiotensin-converting enzyme (ACE) inhibition in the newborn piglet were thus investigated by means of regional blood flow distribution, renal interstitial hydrostatic pressure (RIHP), and medullary oxygen tension (PO2) in the anesthetised 4- to 5-day-old piglet. Moreover, the calcium antagonist nifedipine and the nitric oxide synthesis inhibitor L-NAME were also given in order to reduce renal blood flow by other means. The drugs were given intravenously in equipotent pressor doses, mimicking intraperitoneal injections in neonatal rats. Enalaprilat (200 µg/kg) reduced mean arterial pressure (MAP) by 14±10% (mean±SD, P=0.006) and RIHP by 18±18% (P=0.001), whereas total renal blood flow and medullary PO2 remained unchanged. In contrast, nifedipine (0.5 mg/kg) reduced MAP and RIHP by 39±8% and 38±14%, respectively, total and regional blood flows by 30%–60%, and medullary PO2 by 46±29% (P=0.001). Acute administration of L-NAME (15 mg/kg) increased MAP by 27±10% (P=0.0005), whereas RIHP and renal blood flow decreased by 20%–50%, resulting in a reduction of the medullary PO2 by 10±12% (P=0.05). We conclude that the renal abnormalities observed after neonatal ACE inhibition are not likely to be caused by renal ischemia.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004670000387
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