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1 Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California 90089-9142; and 2 Department of Medical Physiology, Division of Renal and Cardiovascular Research, The Panum Institute, University of Copenhagen, DK-2200 Copenhagen, Denmark
Acute hypertension inhibits proximal
tubule (PT) fluid reabsorption. The resultant increase in end proximal
flow rate provides the error signal to mediate tubuloglomerular
feedback autoregulation of renal blood flow and glomerular
filtration rate and suppresses renal renin secretion. To test whether
the suppression of the renin-angiotensin system during acute
hypertension affects the magnitude of the inhibition of PT fluid and
sodium reabsorption, plasma ANG II levels were clamped by infusion of
the angiotensin-converting enzyme (ACE) inhibitor captopril (12 µg/min) and ANG II after pretreatment with the bradykinin
B2 receptor blocker HOE-140 (100 µg/kg bolus). Because
ACE also degrades bradykinin, HOE-140 was included to block effect of
accumulating vasodilatory bradykinins during captopril infusion.
HOE-140 increased the sensitivity of arterial blood pressure to ANG II:
after captopril infusion without HOE-140, 20 ng · kg
1 · min1 ANG II had
no pressor effect, whereas with HOE-140, 20 ng · kg1 · min1 ANG II
increased blood pressure from 104 ± 4 to 140 ± 6 mmHg. ANG
II infused at 2 ng · kg1 · min1 had no
pressor effect after captopril and HOE-140 infusion ("ANG II
clamp"). When blood pressure was acutely increased 50-60 mmHg by
arterial constriction without ANG II clamp, urine output and endogenous
lithium clearance increased 4.0- and 6.7-fold, respectively. With ANG
II clamp, the effects of acute hypertension were reduced 50%: urine
output and endogenous lithium clearance increased two- and threefold,
respectively. We conclude that HOE-140, an inhibitor of the
B2 receptor, potentiates the sensitivity of arterial
pressure to ANG II and that clamping systemic ANG II levels during
acute hypertension blunts the magnitude of the pressure diuretic response.
captopril; HOE-140; bradykinin receptor; endogenous lithium clearance
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