Key result
Administration of quinapril restored intrarenal hemodynamics toward normal in aortocaval fistula rats, supporting a pathophysiological role of the renin-angiotensin system in this model of cardiac failure.
Why the study?
Does quinapril improve intrarenal hemodynamics in aortocaval fistula rats?
Does quinapril improve intrarenal hemodynamics in aortocaval fistula rats?
ACE inhibition with quinapril restores intrarenal hemodynamics toward normal in a rat model of AV fistula-induced heart failure, supporting the pathophysiological role of the renin-angiotensin system.
Animal data preclude clinical recommendations; leaves open translation of quinapril effects to human HF-related renal hemodynamics.
To investigate intrarenal hemodynamics of aortocaval, arteriovenous (AV)-fistula rats and the effect of angiotensin-converting-enzyme (ACE) inhibition, micropuncture studies were obtained before and after administration of quinapril (100 micrograms.kg-1 x min-1), an ACE inhibitor. AV fistula produced by needle multipuncture was characterized by elevated left ventricular end-diastolic pressure (LVEDP), lower mean arterial pressure, and increased left and right ventricular weights. Effective renal plasma flow was lower in AV-fistula rats, and single-nephron glomerular filtration rate (SNGFR) and plasma flow (SNPF) were reduced. Single-nephron filtration faction (SNFF), stop-flow pressure, and glomerular pressure (PG) were increased. The lower SNGFR and SNPF and higher PG and SNFF were associated with higher afferent and efferent arteriolar resistances (RA and RE) and lower ultrafiltration coefficient (Kf). LVEDP correlated positively with with RA, RE, and SNFF (all P < 0.01) and negatively with SNGFR (P < 0.05) and SNPF (P < 0.01). After quinapril these variables returned toward normal. Thus this method for producing AV fistula was useful in creating mild and moderately severe cardiac failure (CHF). Intrarenal hemodynamics of AV were characterized by increased PG and SNFF and lower SNGFR and SNPF associated with increased RA and RE and lower Kf and SNPF correlated and with severity of CHF. Restoration of intrarenal hemodynamics to or toward normal with quinapril supports an important pathophysiological role of renin-angiotensin system in this CHF.
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Nishikimi et al. (1993) studied Cardiac failure (aortocaval fistula). Quinapril vs. Baseline (before administration) was evaluated on Intrarenal hemodynamics (SNGFR, SNPF, SNFF, PG, RA, RE, Kf). Administration of quinapril restored intrarenal hemodynamics toward normal in aortocaval fistula rats, supporting a pathophysiological role of the renin-angiotensin system in this model of cardiac failure.
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