Peritubular Uptake of 125I-Insulin in the Avian Kidney

Author(s):  
A. Milton ◽  
B. Odlind ◽  
L. Wibell ◽  
L. Dencker
Keyword(s):  
1980 ◽  
Vol 13 (8) ◽  
pp. 897-905 ◽  
Author(s):  
L Charest-Boulé ◽  
A.Z Mehdi ◽  
T Sandor
Keyword(s):  

1989 ◽  
Vol 119 (5) ◽  
pp. 818-828 ◽  
Author(s):  
Robert F. Wideman ◽  
William B. Roush ◽  
Joyce L. Satnick ◽  
Raymond P. Glahn ◽  
Norman O. Oldroyd

1985 ◽  
Vol 249 (6) ◽  
pp. F842-F850 ◽  
Author(s):  
J. N. Stallone ◽  
E. J. Braun

Recently developed radioimmunoassay (RIA) techniques were employed in a quantitative investigation of the renal actions of the avian antidiuretic hormone arginine vasotocin (AVT) in the conscious domestic fowl. Constant intravenous infusion of AVT at doses of 0.125-1.00 ng X kg-1 X min-1 was used to produce plasma AVT (PAVT) concentrations (verified by RIA) over the entire range of physiological PAVT levels in the domestic fowl. Comparison of the dose-response relationships between PAVT and glomerular and tubular mechanisms of antidiuresis revealed that tubular mechanisms are of primary importance and glomerular mechanisms of secondary importance in the conservation of water by the avian kidney. The greatest proportion of the total AVT-induced reduction in renal water excretion occurred at low physiological PAVT levels (less than 5 microU/ml), prior to any significant reduction in glomerular filtration rate (GFR), and appeared to be the exclusive result of tubular mechanisms of antidiuresis. At high PAVT levels (5-16 microU/ml), glomerular and tubular mechanisms overlapped, and their effects on water conservation could not be separated. Although GFR was reduced by nearly 30% at the highest dose of AVT, only minor additional amounts of water were conserved by the combined actions of glomerular and tubular mechanisms. Thus glomerular mechanisms appear to have only a minor secondary effect on water-conserving ability of the avian kidney.


1976 ◽  
Vol 231 (4) ◽  
pp. 1147-1151 ◽  
Author(s):  
RE Austic ◽  
RK Cole

Uric acid transport in renal cortical slices from a selected line of hyperuricemic chickens was investigated. Slices from the hyperuricemic (HUA) line accumulated less than half as much uric acid as slices from a control (LUA) line when uric acid in the medium varied from 0.01 to 5 mM. Uric acid uptake by both lines increased as the uric acid concentration in the medium was raised from 0.1 to 0.5 mM, but was markedly inhibited in the HUA line at 3-5 mM. Omission of sodium or potassium from the incubation medium inhibited uric acid uptake by slices from both lines. Ouabain inhibited uric acid uptake in the LUA line. The sodium and potassium requirements for initiation of uric acid uptake were higher, and the potassium requirement for maximal uptake was lower, for slices of the HUA line. No genetic differences in potassium or sodium contents of slices were observed when the potassium content of the incubation medium was altered or when the medium contained ouabain. These studies indicate that hereditary hyperuricemia in chickens may be due to a qualitative change in renal uric acid transport which involves the interaction of cations in the transport process.


2002 ◽  
Vol 283 (4) ◽  
pp. C1155-C1162 ◽  
Author(s):  
Steven M. Grassl

Membrane transport pathways mediating transcellular secretion of urate across the proximal tubule were investigated in brush-border membrane vesicles (BBMV) isolated from avian kidney. An inside-positive K diffusion potential induced a conductive uptake of urate to levels exceeding equilibrium. Protonophore-induced dissipation of membrane potential significantly reduced voltage-driven urate uptake. Conductive uptake of urate was inhibitor sensitive, substrate specific, and a saturable function of urate concentration. Urate uptake was trans-stimulated by urate and cis-inhibited by p-aminohippurate (PAH). Conductive uptake of PAH was cis-inhibited by urate. Urate uptake was unaffected by an outward α-ketoglutarate gradient. In the absence of a membrane potential, urate uptake was similar in the presence and absence of an imposed inside-alkaline pH gradient or an outward Cl gradient. These observations suggest a uniporter-mediated facilitated diffusion of urate as a pathway for passive efflux across the brush border membrane of urate-secreting proximal tubule cells.


1968 ◽  
Vol 46 (5) ◽  
pp. 471-475 ◽  
Author(s):  
Jean Leclerc ◽  
Leo Benoiton

ω-N-Acyl-diamino acids have been tested as substrates for ε-lysine acylase from animal sources. Chicken and pigeon kidney enzyme preparations hydrolyzed derivatives of lysine homologues as well as of lysine, the best substrates tested being ε-N-propionyl-lysine and ε-N-propionyl-ornithine. A modified procedure for purifying the enzyme from rat and hog kidney is presented. Some of its properties are different from those previously reported.


1983 ◽  
Vol 245 (4) ◽  
pp. H628-H634 ◽  
Author(s):  
M. E. Burrows ◽  
E. J. Braun ◽  
S. P. Duckles

The renal portal circulation of the avian kidney contains a unique smooth muscle valve that can direct blood flow from the posterior extremities to the central circulation or through the kidney. The neural control of the valve and adjacent venous tissue from Rhode Island Red roosters was characterized by measuring the isometric force developed following transmural nerve stimulation (TNS). During TNS, the valve relaxed while the iliac vein contracted. In the valve, a poststimulus contraction followed the relaxation. Propranolol and guanethidine abolished the TNS-induced relaxation of the valve, leaving a contraction that was increased by physostigmine and partially blocked by atropine or prazosin. In contrast, the TNS-induced contraction of the vein was blocked by guanethidine or prazosin. Measurement of choline acetyltransferase activity and norepinephrine content confirms that the valve is densely innervated with both cholinergic and adrenergic nerves. Thus the vein shows a predominantly adrenergic contractile response typical of most vascular smooth muscle, but the valve demonstrates a dual control, i.e., adrenergic nerves producing relaxation and cholinergic nerves causing contraction. Knowledge of the nature of neuronal control of the valve should aid in the design of experiments to determine its functional role.


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