What is the clinical evidence from this study?

Study design: Other. Population: Altered renal hemodynamics induced by low protein diet (n=64). Intervention: Captopril vs. Untreated low protein diet. Primary outcome: Glomerular filtration rate (GFR) (p=<0.05).

October 1, 1987Open Access

Effects of angiotensin-converting enzyme inhibition on altered renal hemodynamics induced by low protein diet in the rat.

Q: What are the key findings of this study?

Treatment with captopril (30 mg/kg per d) normalized glomerular filtration rate (1.6 vs 0.76 ml/min) and renal plasma flow in rats fed a low protein diet.

Key Result

Treatment with captopril (30 mg/kg per d) normalized glomerular filtration rate (1.6 vs 0.76 ml/min) and renal plasma flow in rats fed a low protein diet.

Structured PICO

Does captopril improve altered renal hemodynamics in rats fed a low protein diet?

Population

64 male Wistar-Furth rats weighing 90±10 g fed a low or normal protein diet for 2 weeks to assess renal hemodynamics.

Intervention

Captopril 30 mg/kg per day administered by gavage for 6 days during the second week of a 2-week low protein (6% casein) diet

Comparator

Untreated rats fed a low protein diet, and untreated or captopril-treated rats fed a normal (23% casein) diet

Outcome

Renal hemodynamics including glomerular filtration rate (GFR), renal plasma flow (RPF), and renal vascular resistance (RVR)surrogate

Intrarenal angiotensin II mediates the changes in intrarenal hemodynamics induced by protein deprivation, which can be reversed by ACE inhibition with captopril.

Main Result

Absolute Event Rate: 1.6% vs 0.76%

p-value: p=<0.05

Limitations

Short-term study duration (2 weeks)
Animal model (rats), which may not fully translate to human physiology
The potential role of bradykinin in restoring GFR could not be evaluated from the results

Abstract

We assessed the role of angiotensin II in mediating the alterations in renal hemodynamics known to result from low protein feeding to normal rats by examining the effect of the angiotensin-converting enzyme (ACE) inhibitor captopril. 2 wk of low protein (6% casein) diet resulted in decreased glomerular filtration rate (normal protein NP, 1.82 +/- 0.17 vs. low protein LP, 0.76 +/- 0.01 ml/min; P less than 0.05) and renal plasma flow (NP, 6.7 +/- 0.2 vs. LP, 3.3 +/- 0.3 ml/min; P less than 0.05); renal vascular resistance rose (NP, 8.7 +/- 0.4 vs. LP, 19.8 +/- 1.4 dyn . s per cm5; P less than 0.05). These changes were accompanied by a significant decrease in plasma renin activity (NP, 7.0 +/- 0.7 vs. LP, 4.4 +/- 0.8 ng A I/ml per h; P less than 0.05), plasma aldosterone concentration (NP, 7.0 +/- 0.6 vs. LP, 4.1 +/- 0.7 ng/dl; P less than 0.05), and urinary PGE2 excretion (NP, 3,120 +/- 511 vs. LP, 648 +/- 95 pg/mgCr; P less than 0.05); by contrast renal renin content was significantly increased (NP, 2,587 +/- 273 vs. LP, 7,032 +/- 654 ng A I/mg protein; P less than 0.05). Treatment with captopril (30 mg/kg per d) raised glomerular filtration rate (GFR; LP + capt, 1.6 +/- 0.2 ml/min) and renal plasma flow (RPF; LP + capt, 6.7 +/- 0.7 ml/min), and reduced renal vascular resistance (LP + capt, 9.2 +/- 0.5 dyn/s per cm5) in low protein-fed animals. These values were not different from those measured in untreated and captopril-treated rats fed a normal (23%) protein diet. There were no changes in systemic mean arterial pressure in any group of rats. These data provide evidence that intrarenal angiotensin II mediates the changes in intrarenal hemodynamics induced by protein deprivation. The effects of low protein feeding may be partly potentiated by the reduction in PGE2 synthesis. However, the normalization of GFR and RPF in view of only modest increases in PGE2 excretion after captopril (LP, 648 +/- 95 vs. LP + capt, 1,131 +/- 82 pg/mgCr; P less than 0.05) suggests that if PGE2 is involved in these changes, it plays a permissive but not essential role in the increased renovascular resistance.

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