AUTOREGULATION OF RENAL BLOOD-FLOW, GLOMERULAR-FILTRATION RATE AND PLASMA-RENIN ACTIVITY IN SPONTANEOUSLY HYPERTENSIVE RATS AND NORMOTENSIVE WISTARRATS
P. Wende et al., AUTOREGULATION OF RENAL BLOOD-FLOW, GLOMERULAR-FILTRATION RATE AND PLASMA-RENIN ACTIVITY IN SPONTANEOUSLY HYPERTENSIVE RATS AND NORMOTENSIVE WISTARRATS, Medizinische Klinik, 88(4), 1993, pp. 207-211
The autoregulation of renal blood flow (RBF), glomerular filtration ra
te (GFR) and the pressure dependent renin release into the circulation
were studied in conscious chronically instrumented spontaneously hype
rtensive rats (SHR) and normotensive Wistar rats. Renal perfusion pres
sure was lowered by means of a suprarenal inflatable cuff on the abdom
inal aorta and was lowered in pressure steps of 10 mm Hg. Breakoff poi
nts for RBF- and GFR-autoregulation as well as the threshold for renin
release were calculated using non-linear regression (breakpoint analy
sis). - Wistar rats autoregulated RBF and GFR in a range between 110 a
nd 90 mm Hg (breakoff points: R.BF 88 +/- 2 mm Hg; GFR 92 +/-3 mm Hg).
Plasma-renin activity (PRA) showed a threshold of activation at 89 +/
-8 mm Hg. Breakoff points and threshold of renin release did not diffe
r significantly from each other. SHR autoregulated RBF and GFR in a ra
nge between 160 and 100 mm Hg (breakoff points: RBF 104 +/- 6 mm Hg; G
FR 99 +/- 4 mm Hg). The PRA increase had a threshold at 119 +/- 6 mm H
g. Breakoff points of R.BF- and GFR-autoregulation did not differ sign
ificantly. In SHR the threshold of renin release was at a significantl
y higher pressure than the breakoff point of GFR-autoregulation. The c
omparison between Wistar rats and SHR revealed a significant shift of
the RBF-autoregulation curve and the pressure-dependent renin release
of SHR towards higher pressures (p < 0,05). - The early increase of PR
A in SHR suggests a role of the renin-angiotensin-system (RAS) in the
autoregulation of GFR in SHR. Wistar rats seem to autoregulate GFR ind
ependently of the PAS. An activation of the sympathetic nervous system
might take part in the rightward shift of the R.BF- and GFR-autoregul
ation curve in SHR. The role of this altered autoregulatory pattern in
the development of genetic hypertension remains to be investigated.