Inhibitory effect of epinephrine on renal potassium secretion: a micropuncture study

The effect of epinephrine on renal potassium excretion was examined in the rat. In group I KCl was infused acutely to increase plasma K (PK) by 2.0 meq/liter; urinary K excretion (UKV) rose by 1.22 mueq/min. In group II rats, which received a similar dose of KCl but with epinephrine, the increase in PK (delta = 0.8 meq/liter, P less than 0.001) was blunted and UKV was reduced (delta = 0.23 mueq/min, P less than 0.001). To determine whether the reduction in UKV resulted from the smaller increase in PK or from a direct action of epinephrine on renal K transport, a third group of animals received a lower dose of KCl. Despite similar PK levels, the epinephrine group excreted significantly less K in the urine (0.61 vs. 0.93 mueq/min). In group IV propranolol was infused with KCl; UKV was modestly increased. The effects of epinephrine on UKV were unrelated to changes in glomerular filtration rate, urine flow, or UNaV. Micropuncture results showed that at comparable PK levels epinephrine had no direct effect on K secretion by the distal tubule but indirectly inhibited K secretion in this nephron segment by reducing PK. In addition, epinephrine reduced K addition at tubular sites beyond the late distal tubule, most likely in the collecting tubule.     

Absorption and secretion of potassium by rabbit descending colon

Measurements of K fluxes under a variety of conditions have provided an internally consistent set of data that demonstrate active absorption and active secretion of K by rabbit descending colon in vitro. The properties of K diffusion across the paracellular pathway are those of a free solution shunt. With Na and Cl present on both sides of short-circuited tissues the two opposing active K transport systems balance each other, so that there is no net K transport. Net K absorption results when the transcellular secretory K flux is inhibited by 1. serosal addition of ouabain, 2. serosal addition of furosemide, or 3. omission of either Na or Cl from the serosal solution. Hence basolateral K uptake appears to be mediated by a furosemide-sensitive Na–Cl–K cotransport system in addition to the Na–K exchange pump. Luminal addition of mersalyl or orthovanadate inhibits active K absorption. The adenosine analogue 5-N-ethylcarboxamide adenosine and the -adrenergic agent isoproterenol, added to the serosal solution, cause net K secretion which is inhibitable by furosemide. The secretory K fluxes, both under stimulated and non-stimulated conditions, are abolished by an opposing electrical gradient, suggesting conductive K exit across the apical cell membrane, whereas K absorption appears to be an electroneutral process.     

Production of Heymann nephritis by a chemically modified renal antigen

An autoimmune kidney disease morphologically and functionally similar to Heymann nephritis (HN) was induced in mature male Sprague Dawley rats by repeated weekly IP injections of a chemically modified azo sonicated ultracentrifuged (u/c) rat kidney fraction 3 (rKF3) antigen in an aqueous medium. The experiment was terminated 15 weeks after the first injection of the chemically altered antigen. Serum samples collected and analysed by an indirect fluorescent antibody test on normal rat kidney sections during the course of the experiment showed a gradual rise in circulating pathogenic autoantibodies directed against the proximal tubular brush border regions. Proteinuria was present and significantly increased in the urine of two of eight rats. The arising immune-complex glomerulonephritis (ICGN) revealed typical HN kidney disease lesions in 70% of the rats in histological, direct fluorescent antibody and electron-microscopical examinations. Control rats injected similarly with the an unmodified version of the same antigen did not develop the HN-characteristic morphological and functional changes. To our knowledge, this is the first time that the autoimmune kidney disease designated as an active HN has been produced by the administration of a chemically altered renal antigen in an aqueous solution and not by the usual presentation of the nephritogenic renal antigen in an adjuvant.     

Efferent renal sympathetic nerve stimulation in vivo. Effects on regional renal haemodynamics in the Wistar rat,studied by laser-Doppler technique

Intrarenal blood flow regulation probably affects long-term blood pressure homeostasis. We have previously shown that 5 Hz renal sympathetic stimulation inhibits a humoral renal depressor mechanism, otherwise activated when increasing perfusion pressure to an isolated kidney in a cross-circulation set-up. This inhibition was suggested to occur as a result of a reduction of renomedullary blood flow. Little is known about nervous blood flow regulation within the medulla. Therefore in this study, total renal (RBF), cortical (CBF) and papillary (PBF) blood flows were separately measured by ultrasonic and laser-Doppler techniques in Wistar rats during graded renal sympathetic stimulations. Periods of 15 min stimulation at 0.5, 2 and 5 Hz were performed in random order. RBF decreased at 0.5 Hz by 1%, at 2 Hz by 16% (P < 0.001) and at 5 Hz by 49% (P < 0.001). In a similar fashion (r = 0.73, P < 0.001), CBF decreased by 1%, 10% (P < 0.001) and 37% (P < 0.001), respectively. By contrast, PBF increased by 2% at 0.5 Hz and 4% at 2 Hz, while it decreased at 5 Hz, by 4% (P < 0.05, compared with 2 Hz). It seems therefore, that superficial renocortical and total renal blood flows are closely regulated by renal sympathetic nerves with increasing vasoconstriction at higher frequencies, while medullary blood flow, on the other hand, seems to be under strong local control, tending to offset neurogenic flow restrictions.     

Age-related occurrence of simple renal cysts studied by ultrasonography

Summary Three hundred forty-eight outpatients without evidence of renal disease were examined by ultrasound. Their ages ranged from 18 to 83 years. Unexpected renal cysts of more than 1 cm were found in 47 patients (13.5%). No cysts were demonstrated in patients less than 23 years old; thereafter the number of patients with cysts increased significantly with age. The cyst diameter also tended to increase with age, but the correlation with age was not significant. There was no statistical difference of cyst occurrence between the right and left kidney, or between males and females. The upper portion of the kidney was most often affected in the equally divided three portions along the long axis. These results confirm that the development of simple renal cysts is age-related.Abbreviations CT computed tomography - RCE renal central echoes     

Distribution of intracerebrally injected dopamine as studied by a punch-scintillation modeling technique.

Three-dimensional distribution gradients of intracerebrally injected tritiated dopamine were calculated on the basis of concentrations in multiple punch-samples from sequential sections of Macaca fascicularis brain tissue. The monkey was pretreated systemically with a monoamine oxidase inhibitor to retard elimination. Gradients were best fit by cubic exponential equations relating concentration to distance from the center of the site. The concentration at the center, total amount of label, and total extent of the site injected just before perfusion were consistent with initial distribution in the extracellular space, if the volume fraction of the latter is estimated at 20%. The extent of distribution was distinctly greater in the mediolateral and dorsoventral dimensions than in the anteroposterior dimension. The total amount of label near the site decreased rapidly in the first few minutes after injection, then much more slowly, reaching about 30% of the injected amount after 2 h. Its distribution within the site changed steadily, the outer boundary gradually expanding and the peak at the center gradually decreasing. This pattern was consistent with an initial rapid dispersion by injection pressure and an initial loss of tritiated dopamine due to disruption of the blood-brain barrier at the center of the site, followed by a steady expansion of the site driven by diffusion and bulk flow.     

The dynamics of mast cell secretion studied by vital berberine staining

The fluorescent cationic dye berberine in combination with histamine release studies have been used to explore the different steps of the mast cell secretory process. We have previously shown that quantitation of heparin release by the binding of berberine to fixed mast cells can be used as a direct measure of release of granules. This report summarizes recent work using berberine as a vital stain demonstrating the secretory activity of mast cells. After membrane stabilization with polyethylene glycol (PEG) normal mast cells exclude the dye while mast cells stimulated to secretion with polymyxin B show a strongly fluorescent dye binding to individual cytoplasmic granules. The mean fluorescence intensity of the cell populations after vital berberine staining was compared both to heparin and histamine release. The results strongly suggest that berberine, under the vital staining conditions used, is a marker of intracellular granules that have released histamine. The vital staining method was also used to study membrane events following a polymyxin B-induced secretion. The mean fluorescence intensity decreased by 75% during the first hour after the termination of a polymyxin B stimulation while the mast cell content of histamine and heparin remained constant. The findings support the idea that the membranes are rapidly restored after mast cell secretion, permitting a selective amine release without accompanying release of heparin or other matrix components of the granules.