Captopril but Not Acebutolol, Prazosin or Indomethacin Decreases Postexercise Proteinuria

Abstract

Strenuous physical exercise causes transient proteinuria and renal hemodynamic changes: decrease of renal blood flow and to a lesser extent of the glomerular filtration rate, and an increase of the filtration fraction. However, the mechanisms of these modifications are still poorly understood. In order to elucidate them we performed maximal exercise tests on 8 untrained healthy volunteers after inhibition of the renin-angiotensin system (RAS) by captopril, the sympathetic nervous system by a β-blocking drug (acebutolol) or an α-blocking drug (prazosin) and the prostaglandin system by indomethacin. Urinary albumin excretion was measured in every subject first at rest (AB) and then after exercise (AA) performed successively without and with blockade by each of theses drugs. AA-AB difference in the captopril test (12.04 ± 6.11 μg/min) compared to that in the control test (68.91 ± 25.18 μg/min) was significantly reduced (p < 0.02). This difference remained unchanged after acebutolol (59.87 ± 21.91 μg/min, p = 0.62), prazosin (35.23 ± 27.80 μg/min, p = 0.21) and indomethacin (55.21 ± 28.43 μg/min, p = 0.35). There was a negative correlation between the lowering of AA elevation and the rise in plasma renin activity in the captopril test (r = 0.64; p < 0.03). Only acebutolol decreased systolic blood pressure significantly. These results suggest that the RAS plays a major role in postexercise proteinuria. We hypothesize that stimulation of this system induces an increase of efferent glomerular artery constriction and consequently of glomerular transcapillary pressure and the filtration fraction. Captopril seems able to prevent these hemodynamic changes.

Effect of nitric oxide on exercise-induced proteinuria in rats

“…Angiotensin II, another possible effective vasoconstrictor agent in renal hemodynamics, has been investigated extensively. Angiotensin II production after renin release has been shown to cause an increase in transglomerular pressure and filtration fraction via a more prominent constriction of efferent arteriole (3,6). On the other hand, some authors did not observe an involvement of renin-angiotensin system in postexercise proteinuria (24).…”

“…It is described as a "temporary increase in protein excretion by urine in healthy individuals after exercise" (27) and was shown to occur in various exercising laboratory animals as well as in humans (5,14,27). The basic mechanisms of postexcercise proteinuria are increased glomerular permeability and/or exceeding the maximum tubular reabsorption capacity for proteins (6,29). The permeability of the glomerular capillary membrane, which does not allow the filtration of macromolecules under normal circumstances, increases because of the renal hemodynamic alterations occurring during exercise.…”

The Renin–Angiotensin System, Not the Kinin–Kallikrein System, Affects Post-Exercise Proteinuria

“…Previous studies have shown ACE inhibition might prevent post-exercise proteinuria [4, 5, 7, 10]. However, ACE inhibition also induces a rise in plasma bradykinin levels as the kininase activity is blocked as well [16].…”

“…In addition to increased activity of renal sympathetic nerves, an increase in circulating adrenaline levels also leads to cumulative vasoconstriction in the nephrons’ afferent and efferent arterioles [3]. Increased sympathetic nerve activation during exercise also induces renin release [4, 5], increasing angiotensin II (Ang II), which is a potent vasoconstrictor and has important implication for renal haemodynamics. The FF increases especially due to the vasoconstriction of the efferent arteriole [5].…”

“…Increased sympathetic nerve activation during exercise also induces renin release [4, 5], increasing angiotensin II (Ang II), which is a potent vasoconstrictor and has important implication for renal haemodynamics. The FF increases especially due to the vasoconstriction of the efferent arteriole [5]. Previous studies have shown angiotensin-converting enzyme (ACE) inhibitors reduce post-exercise proteinuria [4, 6, 7].…”