摘要:

Renal functional adaptation to additional nephrons was studied in rats in which a third kidney was transplanted isogeneically. Total renal function did not increase when an extra kidney was added. Quantitation of the contribution of each kidney, by means of a 99mTc-DTPA scan, showed that the glomerular filtration rate of the native kidneys had decreased to counterbalance the added function. The glomerular filtration rate of the transplanted kidney as well as its number of glomeruli were 20% less than that of the intact native kidneys. The present findings once again illustrate the kidney’s remarkable capacity for functional adaptation to a change in the total number of nephron

ISSN:1420-4096    

DOI:10.1159/000173045

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Autoradiography showed that 3H-labelled alcian blue injected into the rat renal artery was concentrated in the glomeruli. To test if the uptake could be used as a measure of local glomerular plasma flow, the one-pass extraction was measured in 19 rats. The average extraction was 31.9% (SD 8.0%). Impurities and heterogeneity of the tracer as well as reversible binding to erythrocytes may have contributed to the low estimated extraction. The average extraction of 103Ru-ruthenium red was 26.3%. We conclude that neither of these dyes are suitable for measurement of glomerular plasma flow.

ISSN:1420-4096    

DOI:10.1159/000173046

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The response of plasma renin activity (PRA) to stepwise reductions in renal arterial pressure (RAP) induced by suprarenal aortic constriction (SAC) or hydralazine (0.1–30 mg/kg i.v.), and the effect of indomethacin (5 mg/kg i.v.) or propranolol (1.5 mg/kg s.c.) on the PRA response were examined in anesthetized rats whose right kidneys had been removed 6–7 days earlier. The stepwise reduction of RAP by SAC or hydralazine produced a steep increase in PRA when RAP was below approximately 100 mmHg. Above this level, PRA was unaffected by changes in RAP. The SAC-induced increase in PRA was nearly abolished by indomethacin. On the other hand, propranolol failed to affect the SAC-induced increase in PRA. The hydralazine-induced renin release was remarkably suppressed by either indomethacin or propranolol. These results suggest that SAC-induced renin release is mainly dependent on the prostaglandin system, whereas hydralazine-induced renin release is dependent on the prostaglandin and the adrenergic nervous system. We estimated the threshold pressure for increasing renin release is approximately 100 mm

ISSN:1420-4096    

DOI:10.1159/000173047

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Renal catecholamine concentrations and urinary dopamine excretion from the isolated perfused kidney were measured in intact and peripherally sympathectomized rats. Urinary dopamine excretion was not diminished by sympathectomy, was increased by l-dopa (but not tyrosine or dopamine 4-O-sulphate) in the perfusate and was virtually abolished by prior treatment with the dopa decarboxylase inhibitor, carbidopa. These results confirm the importance of renal extraneuronal dopamine production, from circulating l-dopa, as a contributor to urinary dopamine excretion.

ISSN:1420-4096    

DOI:10.1159/000173048

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effect of a continuous intra-aortal infusion of prostaglandin E2 (PGE2) (0.03 µg· min-1 • kg-1) on the course of postischemic renal failure (180 min cessation of blood flow by inflation of a pneumatic cuff) has been investigated in 11 conscious sodium-replete dogs. The glomerular filtration rate (51Cr-EDTA; endogenous creatinine clearance) was less decreased in the PGE2 group (group B, n = 6) than in the control group (group A, n = 5; 13 ml·min-1 vs. 22 ml min-1; p < 0.05). Renal blood flow (electromagnetic flow probe) was markedly lower in the control group (82 ml •min-1) than in the PGE2 group (130 ml • min-1; p < 0.05), even exceeding baseline levels in the latter group. Accordingly, the excessive rise in renal vascular resistance in the control group (+ 277%) was abolished in the PGE2 group (-20%) (ρ < 0.05). Nitrogen retention was also markedly improved. Plasma renin activity, which was markedly raised initially (25.8 ng angiotensin I·ml-1 h-1) was not significantly further increased during the subsequent 7 days. Urinary excretion of PGE2 was diminished in the control group and elevated following PGE2 infusion. It is suggested that the beneficial effects of PGE2 are mediated by preservation of renal perfusion. Additional effects of prostanoids on the ultrafiltration coefficient (KF) and cytoprotection by reduction of intracellular calcium accumulation must also be taken into con

ISSN:1420-4096    

DOI:10.1159/000173049

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

To examine the PGE2 and renin release during autoregulatory dilation of preglomerular vessels, experiments were performed in three groups of anesthetized dogs. [1] By reducing the arterial perfusion pressure from 113 + 3 to 78 ± 3 mm Hg, renin release rose to 20 + 5% and PGE2 release to 74 + 12% of the maximal values attained at two perfusion pressures below the range of autoregulation. [2] During ureteral occlusion, PGE2 and renin release rose to maximal values already at control blood pressure and remained unaltered as the arterial perfusion pressure was reduced from 124 + 7 to 68 + 2 mm Hg. Renal blood flow fell in proportion to the perfusion pressure indicating abolished autoregulation. [3] At a perfusion pressure below the range of autoregulation, saline infusion restored sodium excretion and reduced renin release but did not alter PGE2 release. We conclude that PGE2 release is raised by autoregulatory dilation of preglomerular arteries. Prostaglandins enhance renin release when afferent arterioles are dilated. Renin release mediated by a macula densa mechanism is not PGE2 dependent

ISSN:1420-4096    

DOI:10.1159/000173050

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effect of lithium on p-aminohippurate (PAH) transport was studied using slices and basolateral membrane vesicles prepared from rat kidney cortex. The addition of lithium in concentrations ranging from 0.5 to 5 mM caused a concentration-dependent inhibition of PAH accumulation in the slices. Lithium inhibited PAH accumulation in the slices, not only during the rapid uptake period (after 10 min) but also during the approach to equilibrium (after 30 min). The effect of lithium (2 mM) in the slices was irreversible. The inhibitory effect of lithium was not the result of changes in the water distribution and the concentrations of ATP, sodium and potassium in the slices during incubation. The effect of lithium on the kinetic parameters for PAH accumulation was to decrease Vmax, while apparent Km remained constant. There was no lithium effect on the efflux of PAH from the slices back into the incubation medium, indicating that lithium inhibited PAH influx to the kidney cells. No evidence was obtained to indicate that lithium (1 mM) directly affected PAH uptake by isolated basolateral membrane vesicles. These results suggest that lithium seems to affect metabolism linked to the carriers for PAH transport other than ATP production and sodium gradient and then seems to decrease the mobility of the carriers in the membranes.

ISSN:1420-4096    

DOI:10.1159/000173051

出版商:S. Karger AG    

年代:1985

数据来源: Karger