From the Department of Physiology, Monash University, Clayton, Victoria,
Australia.
AbstractWe have previously shown
that chronic treatment with angiotensin-converting enzyme
inhibition (ACEI) did not reverse hypertrophy of the renal
arterial wall in spontaneously hypertensive rats (SHR). In
this study we determined the effects of perindopril on the functional
properties of the renal vasculature in vivo and on its resistance to
flow at maximal dilatation in vitro, a measure of vessel lumen
diameter. Two groups of SHR were studied: untreated or treated with
perindopril (3 mg/kg per day) in their drinking water from 4 weeks of
age. At 10 weeks, (1) vessel lumen characteristics were assessed using
a maximally dilated in vitro isolated kidney perfusion and (2) the
renal vasoconstrictor responses to bolus doses of vasoactive agents
(angiotensin II and phenylephrine) administered
into the renal artery were measured in vivo (anesthetized
rats). Mean arterial pressure was significantly lower in
conscious SHR treated with perindopril (132±2 versus 97±2
mm Hg, P<.001). In vitro, the pressure-flow
relationship and the pressureglomerular filtration rate
relationship were both shifted significantly to the left
(P<.001). The perindopril-treated kidneys began
filtering at a significantly lower threshold perfusion pressure than
nontreated controls (P<.001). In vivo, renal
vasoconstrictor responses to increasing doses of both vasoconstrictor
agents were significantly less marked in the perindopril-treated SHR
than in untreated SHR (P<.05). Thus, chronic ACEI
increased average renal vessel lumen diameter in SHR, predominantly in
preglomerular vessels, and reduced renal vasoconstrictor
responsiveness in vivo, findings compatible with remodeling of the
preglomerular vasculature around a greater lumen.
© 1998 American Heart Association, Inc.
Scientific Contributions
Perindopril Treatment Affects Both Preglomerular Renal Vascular Lumen Dimensions and In Vivo Responsiveness to Vasoconstrictors in Spontaneously Hypertensive Rats
Key Words: : angiotensin-converting enzyme inhibitors kidney perfusion rats, inbred SHR vascular resistance
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