The role of kidneys in the breakdown of plasma albumin was investigated. The rate of iodoalbumin breakdown by bilaterally nephrectomized rats and in isolated perfused rabbit kidney were studied. Homologous I131-labeled plasma albumin was used. To remove denatured components, the iodoalbumin was ‘screened,’ that is, it was injected into animals which were bled several days later, and whole plasma was used as the iodoalbumin substrate. It was found that bilateral nephrectomy reduced unscreened iodoalbumin breakdown by about 20% but had no effect on the breakdown of screened iodoalbumin. Unscreened iodoalbumin was broken down at an appreciable rate by perfused kidney, but with screened iodoalbumin the breakdown rate was greatly reduced. It is concluded that, at most, 10% of the turnover of native plasma albumin in the body may occur in kidneys.
The effects of splenectomy, partial and complete gastrectomy, partial and subtotal hepatectomy, and evisceration on the catabolism of I131-labeled screened and unscreened plasma albumin in rats was studied. Splenectomy and removal of jejunum and ileum had no effect, but complete enterectomy, hepatectomy, and evisceration depressed plasma albumin breakdown as compared to sham-operated controls. Plasma albumin breakdown was found to proceed at an appreciable rate in eviscerated rats, and it appears that up to half of albumin breakdown in the rat occurs in nonvisceral sites. In perfused rat liver unscreened iodoalbumin is rapidly degraded, but the breakdown of screened albumin is low, accounting for about 15% of total plasma albumin catabolism in vivo.
The intrarenal mechanisms of renin release were studied in the isolated perfused rabbit kidney during stimulation by isoproterenol, 0.01 mug/kg per min, and by theophylline, 0.87 mg/kg per min. In the absence of urinary flow during the early stages of perfusion, isoproterenol caused a 17% increase of renal vein serum renin concentration (RVSRC) (P less than 0.001) without changing renal blood flow, renal vascular resistance, or serum potassium. dl-Propranolol, 2.0 mg/kg per min. abolished this isoproterenol-induced renin release. A moderate reduction in perfusion pressure prior to the infusion of isoproterenol resulted in a marked additional stimulation of renin release. Studies during and following ureteral occlusion demonstrated that theophylline stimulates renin release by decreasing renal vascular resistance, whereas the concomitant increase in sodium transport to the macula densa exerted an opposite effect. dl-Propranolol did not affect theophylline-induced renin secretion. It is concluded that single exogenous stimuli may activate more than one intrarenal mechanism simultaneously. Isoproterenol has a direct renin-stimulatory effect on intrarenal beta-adrenergic receptors that may be reinforced by baroreceptor stimulation. Theophylline stimulates renin via a baroreceptor mechanism, with simultaneous renin suppression via a sodium-macula densa effect.
HYDRONEPHROSIS IN THE RATin the duct epithelium of submaxillary gland, whereas activity in the clamped kidney is higher than normal. Simultaneously there is a widening of ducts in the salivary gland comparable to that seen in cortical tubular system in the kidney. Adrenalectomy is followed by increased G6PD activity in the macula densa and a high normal activity in the submaxillary gland.
Normal renal function has been maintained in an isolated artificial heart-lung, whole-blood perfused rabbit kidney for periods of 2–4 hr. The isolated kidney responds to changes in perfusion pressure, changes in plasma protein concentration, and exposure to a 10-min period of ischemia, in a manner similar to that described for the kidney of the normal intact animal. Elevation of the plasma protein concentration produces a fall in the rate of urine flow, sodium excretion, and creatinine clearance, and a marked proteinuria. The administration of renin produces a marked diuresis, natriuresis, and proteinuria. This effect is also produced by the exposure of the isolated kidney to a 10-min period of ischemia, suggesting that this response may be mediated by a renin mechanism. The responses of the kidney to these two procedures differ only in that ischemia produces an increase in renal blood flow and renin produces a slight reduction in renal blood flow and a more pronounced proteinuria.
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