Tubuloglomerular feedback and glomerular morphology in Goldblatt hypertensive rats on varying protein diets

Schnermann, J…gen; Gokel, Michael; Weber, Peter C.; Schubert, Gisela; Briggs, Josephine P.
February 1986
Kidney International;Feb1986, Vol. 29 Issue 2, p520
Academic Journal
The present experiments were performed to examine the effect of variation in protein intake on renal function and morphology in the non-clipped kidneys of Goldblatt hypertensive rats. After renal artery clipping, rats were put on diets containing 5 (LP), 17.5 (NP), or 51% (HP) protein. After 4 to 5 weeks, all rats had developed hypertension. GFR was directly correlated with protein intake (1.47 ± 0.15 in HP, 1.19 ± 0.14 in NP, and 0.93 ± 0.08 ml/min in LP), as was SNGFR (44.2 ± 1.89. 39.1 ± 2.23, and 27.9 ± 0.86 nl/min in HP, NP, and LP rats). The response of SNGFR to changes in loop of Henle flow rate was attenuated in NP and HP rats: the maximum decrease was reduced (30.0 ± 5.2% in NP, 22.1 ± 4.2% in HP) and higher tubular flow rates were required to elicit responses (V̇1/2, the flow rate at which the response is half-maximum, was 28.9 ± 2.6 nl/min in NP and 28.2 ± 1.4 nl/min in HP). In LP rats, the maximum response was a decrease of 47.7 ± 2.5%, and (V̇1/2 was 18.1 ± 1.2 nl/min, values similar to those found in normal control rats. The weights of the non-clipped kidneys were 0.96 ± 0.04 g (LP), 1.06 ± 0.05 g (NP), and 1.36 ± 0.06 g (HP). In the LP rats there was no difference between the non-clipped and clipped kidneys. Light microscopic evaluation showed a high incidence of focal glomerulosclerosis in non-clipped kidneys of HP rats, but no glomerular lesions in the non-clipped kidneys of LP rats. These results show that a low-protein diet prevents the elevation of filtration rate and the impairment of feedback regulation observed in the non-clipped kidneys of Goldblatt hypertensive rats. Likewise, it prevents the rapid development of glomerulosclerosis found in these kidneys when protein intake is high. It is possible that the protection from glomerular damage is causally related lo the intact tubuloglomerular feedback mechanism.


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