ISSN:1420-4096    

DOI:10.1159/000172860

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

The factors responsible for the increase in glomerular filtration rate associated with compensatory hypertrophy in Sprague-Dawley rats were studied 2 weeks following uninephrectomy. In sham-operated rats, the single nephron glomerular filtration rate (SNGFR) was 40 nl/min and the calculated glomerular plasma flow (GPF) was 138 nl/min. Proximal intratubular free-flow (Pτ) and stop-flow (PSF) hydrostatic pressures were 12 and 34 mm/Fig. respectively. The estimated glomerular capillary hydrostatic pressure (PGC) was 49 mm Hg and the estimated efferent effective ultrafiltration pressure (PufEA) was 12 mm Hg, indicating filtration pressure disequilibrium. The specific ultrafiltration coefficient was calculated to be 0.039 nl/s · mm Hg per glomerulus. In uninephrectomized rats, SNGFR increased to 61 nl/min and the calculated GPF increased to 266 nl/min. Pτ was 12 mm Hg; PGCe was 49 mm Hg and PUFEA was 15 mm Hg. Kfwas calculated to be 0.053 nl/s · mm Hg per glomerulus. These data indicate that in Sprague-Dawley rats under conditions of filtration pressure disequilibrium, the increase in GFR associated with compensatory hypertrophy is in part related to a significant change in Kf

ISSN:1420-4096    

DOI:10.1159/000172861

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Constriction of the artery to the remaining kidney of control rats uninephrectomized 24 h previously induced a sixfold rise in plasma renin level from 11 ± 1 to 60 ± 11 ng AI mh-1 h-1, a 43% decrease of renal cortical renin level, and a 21% rise of mean arterial pressure from 119 + 2 to 144 ± 3 mm Hg. Constriction of the artery to a renin-depleted kidney (with a renin level which was 5% of normal) was not followed by any significant increase in plasma renin level or mean blood pressure. Renin-depleted kidneys were produced by removing the clipped kidney from two-kidney one-clip hypertensive rats, 24 h before the experiment. Such a maneuver induces renin depletion but does not completely normalize blood pressure. When a large dose of frusemide (50 mg/kg i.p.) was injected immediately following removal of the clipped kidney, mean arterial pressure (117 ± 7 mm Hg) returned to control values 24 h later but again constriction of the remaining renal artery failed to induce a rise in plasma renin level or mean arterial pressure. By 7 days after removal of the clipped kidney, plasma renin level and mean arterial pressure were normal and clipping of the remaining kidney (in spite of the fact that kidney renin level was still low) now produced a wave of renin release and an increase in mean arterial pressure. These results suggest that the initial, rapid increase in mean arterial pressure following unilateral renal artery constriction is dependent on an increase in plasma renin level. Our results from animals with kidneys of varying renin levels suggest the existence of a cortical renin content of about 20% of normal below which the kidney is incapable of responding to renal artery constriction with significant renin release. Complete recovery of the renin (and blood pressure) response to clipping occurred when the renin content had reached about 75% of nor

ISSN:1420-4096    

DOI:10.1159/000172862

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

During the first 48 h of HgCl2-induced acute renal failure (ARF), a single intraperitoneal injection of 100–100 µg/kg of the beta-adrenergic blockers pindolol, pro-pranolol and practolol caused a significant rise in urinary sodium excretion and a decrease in plasma renin activity (PRA), renal cortical renin activity (RRA) and urinary catecholamine excretion. A single intraperitoneal injection of 3 mg/kg HgCl2 resulted in ARF characterized by progressive azotemia, a transient increase in PRA, a progressive rise in RRA and urinary catecholamine excretion. After pretreatment with these beta blockers, PRA, RRA and urinary catecholamine excretion remained unchanged and azotemia was markedly reduced; urine flow rates did not fall, and were significantly higher than control flows till after 48 h. These results indicate that pretreatment with beta blockers decreases the severity of ARF, though they cannot prevent is; that increased activity of the sympathetic nervous system is involved in ARF and that increase in RRA may be an aggravating factor in the pathomechanism of the nephrotoxic model in A

ISSN:1420-4096    

DOI:10.1159/000172863

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Carotid arterial catheters, inserted for repetitive sampling of arterial blood, were associated with frequent renal infarcts in rats. Renal infarcts were not seen with jugular venous catheters alone.

ISSN:1420-4096    

DOI:10.1159/000172864

出版商:S. Karger AG    

年代:1982

数据来源: Karger