Possible role of dark cells of the collecting tubules in acidification of the urine

1974 ◽  
Vol 77 (2) ◽  
pp. 109-111 ◽  
Author(s):  
K. A. Zufarov ◽  
V. M. Gontmakher
1995 ◽  
Vol 268 (4) ◽  
pp. F569-F580 ◽  
Author(s):  
L. C. Stoner ◽  
G. E. Morley

We are able to evert and perfuse rat cortical collecting tubules (CCT) at 37 degrees C. Patch-clamp techniques were used to study high-conductance potassium channels (maxi K) on the apical membrane. Under control conditions (150 mM Na+ and 5 mM K+ in pipette and bathing solutions), the slope conductance averaged 109.8 +/- 6.6 pS (12 channels), and reversal potential (expressed as pipette voltage) was +26.3 +/- 2.4 mV. The percent of time the channel spends in the open state and unitary current when voltage was clamped to 0 mV were 1.4 +/- 0.7% and 3.12 +/- 0.42 pA, respectively. In six patches voltage clamped to 0 mV, the isosmotic solution perfused through the everted tubule (basolateral surface) was exchanged for one made 70 mosmol/kgH2O hyposmotic to the control saline. Open probability increased from 0.019 to 0.258, an increase of 0.239 +/- 0.065 (P ' 0.005). In four patches where a maxi K channel was evident, no increase in open probability was observed when a hyposmotic saline was placed on the apical surface. However, when vasopressin was present on the basolateral surface, apical application of hyposmotic saline resulted in a series of bursts of channel activity. The average increase in open probability during bursts was (0.055 +/- 0.017, P < 0.005). We conclude that one function of the maxi K channel located in the apical membrane of the rat CCT may be to release intracellular solute (potassium) during a volume regulatory decrease induced by placing a dilute solution on the basolateral surface or when the apical osmolarity is reduced in the presence of vasopressin. These data are consistent with the hypothesis that the physiological role of the channel is to regulate cell volume during water reabsorption.


1986 ◽  
Vol 251 (2) ◽  
pp. F266-F270 ◽  
Author(s):  
J. K. Kim ◽  
S. N. Summer ◽  
A. E. Erickson ◽  
R. W. Schrier

Two groups of Sprague-Dawley rats, Harlan (H) and Charles River (CR), were discovered in that the medullary thick ascending limb (MAL) had a profoundly different adenylate cyclase response to arginine vasopressin (AVP). Using these two groups of rats, we studied the correlation between AVP action on the MAL and maximal urinary concentration. AVP (10(-6) M) significantly stimulated adenylate cyclase in MAL of H rats (7.4 +/- 0.9 to 43.8 +/- 4.6 fmol cAMP formed X 30 min-1 X mm-1, P less than 0.001) but not in CR rats (10.3 +/- 1.4 to 12.7 +/- 2.0 fmol cAMP formed X 30 min-1 X mm-1, NS). In contrast, AVP significantly stimulated adenylate cyclase of cortical, outer and inner medullary collecting tubules from both H and CR rats. Glucagon (10(-6) M) significantly stimulated adenylate cyclase of MAL from both H and CR rats. After 48 h of fluid deprivation, urinary osmolality was significantly higher (P less than 0.001) in the H (4,504 +/- 399 mosmol/kg H2O, n = 14) than CR (2,840 +/- 176 mosmol/kg H2O, n = rats. This observation was not attributable to differences in creatinine clearance (CR, 1.30 +/- 0.24; H, 1.24 +/- 0.03 ml/min, NS, n = 4) or plasma AVP (CR, 12.75 +/- 1.44; H, 12.38 +/- 1.17 pg/ml, NS, n = 6) levels. These results therefore suggest that the action of AVP on the MAL, in addition to the effect on collecting tubules, is involved in maximal urinary concentration in rats.


1950 ◽  
Vol 92 (1) ◽  
pp. 11-23 ◽  
Author(s):  
Joseph J. Lalich ◽  
Seymour I. Schwartz

The effect of acid diets, fasting, and dehydration on the urine pH and the kidneys was determined in 11 control animals. Hyaline casts in the collecting tubules and interstitial medullary edema were observed in the 8 that survived. The test rabbits were subjected to the same treatment as the controls but, in addition, received 1.8 gm./kilo of intravenous homologous hemoglobin. Eleven of 18 animals died of hemoglobinuric nephrosis. The rabbits which died of hemoglobinuric nephrosis exhibited significant alterations in two or more of the following: kidney weight, pigment cast accumulation, and elevations of NPN. The theories which have been advanced to explain the pathogenesis of hemoglobinuric nephrosis are evaluated in the light of the present observations. It is proposed on the basis of them that antecedent tubular damage is of primary importance in the pathogenesis of hemoglobinuric nephrosis.


1982 ◽  
Vol 243 (4) ◽  
pp. F364-F371
Author(s):  
M. Cruz-Soto ◽  
D. Batlle ◽  
S. Sabatini ◽  
J. A. Arruda ◽  
N. A. Kurtzman

A distal acidification defect is said to exist in rabbits because this species does not achieve a normal urine minus blood (U-B) PCO2 gradient in response to sodium bicarbonate infusion. This observation contrasts with data derived from studies in isolated rabbit cortical collecting tubules that have shown an acidifying capacity when the tubules were obtained from acidotic animals. The present study was designed to examine the role of diet and blood pH on distal acidification in the rabbit. Maximal alkalinization of the urine by acute sodium bicarbonate infusion was associated with a low U-B PCO2 gradient (0.7 +/- 2.1 mmHg). Rabbits made acidotic by ammonium chloride administration for 1 wk achieved a substantial U-B PCO2 gradient (29 +/- 5 mmHg) in response to neutral sodium phosphate infusion. To further evaluate the role of blood pH on the ability to raise U-B PCO2 gradient, rabbits and rats made acidotic by chronic ammonium chloride administration were studied. Neutral sodium phosphate was then infused to stimulate distal acidification. At comparable levels of urinary phosphate concentration and blood pH, acidotic rabbits were able to achieve a U-B PCO2 (50 +/- 7 mmHg) comparable with that of acidotic rats (48 +/- 8.3 mmHg). These data show that the failure of rabbits to raise U-B PCO2 gradient can be partially corrected by prior exposure to acid in the diet and further corrected by maintaining the blood pH within the acidotic range.


1980 ◽  
Vol 28 (11) ◽  
pp. 1175-1182 ◽  
Author(s):  
K Tanahashi ◽  
S H Hori

Distribution of hexose 6-phosphate dehydrogenase in various organs of the rat has been studied by a peroxidase-labeled antibody method in order to find some clue to elucidating the, as yet unclear, function of this enzyme. As a result, the following cells were found to contain this enzyme in relative abundance: hepatic parenchymal cells, ovarian lutein and theca interna cells, testicular interstitial cells, striated ducts and serous tubular portions of the submandibular gland, plasma cells and the P3 segment of proximal convolutions, and collecting tubules of the cortex and inner medulla of the kidney. Although the role of this enzyme in salivary glands and in plasma cells is unclear at present, the results obtained with steroidogenic cells, liver cells, and renal tubules appear to suggest the possibility that this enzyme might be involved in drug and steroid metabolism.


1961 ◽  
Vol 9 (1) ◽  
pp. 157-170 ◽  
Author(s):  
Fritz Miller

The light and, to a lesser extent, the dark cells of the cortical collecting tubules in mouse kidney contain a great number of granules which according to histochemical tests are composed of phospholipids and proteins. These granules are bounded by a triple-layered membrane measuring approximately 75 A across, and contain one or several crystals with a hexagonal or square lattice. These crystals are built up of rod-shaped units, which appear dense after osmium fixation, measure about 48 A in diameter, and are separated by a light interspace of similar dimensions. The mean center-to-center distance of the rods is about 96 A. The structure is explained as a lipoprotein crystallized within a membrane-bounded vacuole. No relationship between these granules and mitochondria was found. The physiological significance of the granules remains unknown.


1976 ◽  
Vol 22 (3) ◽  
pp. 617-622
Author(s):  
R. Paniagua ◽  
J.J. Vazquez

A special structural pattern of the smooth endoplasmic reticulum (SER) has been observed in the kidney of the snail Cryptomphalus aspersa. Two types of cells (clear and dark) cover the foldings of the renal sac; the dark cells are by far the most numerous. A cisterna of SER enveloping the nucleus appears invariably in both types of cells, with no disruptions, or small ones (from 50 to 90 nm) along its profile. The layer of cytoplasm lodged between the external nuclear membrane and this cisterna is found invariably to be from 0-20 to 0-25 mum in width. Glycogen is abundant in the cytoplasm as alpha particles, and also in the nucleus, but as beta particles. It is noteworthy that absolutely no glycogen is present in the layer of cytoplasm lodged between the nuclear membrane and the surrounding SER envelope. Long profiles of SER are also observed closely approaching and parallel to the plasma membrane of the dark cells. Considering the role of SER in glycogen metabolism in the kidney of the snail, the possible function of these cisternae as a support system ofr enzymes involved in the metabolism of glucides is discussed.


1991 ◽  
Vol 261 (6) ◽  
pp. F921-F932 ◽  
Author(s):  
K. L. Goetz

The discovery of the natriuretic peptide, urodilatin, in human urine, together with data from renal cell cultures, immunocytochemistry, radioimmunoassays, and other techniques, strongly indicates that distal tubules in the kidney produce a natriuretic prohormone that may be identical to the 126-residue prohormone of atrial natriuretic peptide [proANP-(1-126)] produced by cardiac atria. The 32-residue peptide, urodilatin [ANP-(95-126)], is found in urine but not in plasma; its natriuretic potency equals or exceeds that of atriopeptin [ANP-(99-126)]. It is still unclear whether urodilatin is the only, or even the primary, renal natriuretic peptide. Circumstantial evidence suggests that natriuretic peptide produced in connecting and collecting tubules may be a principal physiological ligand for more distal "ANP" receptors, but this issue is far from settled. Evidence that the kidneys produce their own natriuretic peptide may partly explain why investigations of the effects of endogenous atriopeptin on renal sodium excretion often have yielded inconsistent results. This inconsistency has led to a gradual evolution of opinion concerning the functional role of atriopeptin. Based on current data, it is postulated that atriopeptin is primarily a regulator of the cardiovascular system and that renal natriuretic peptide participates in the intrarenal regulation of sodium and chloride transport.


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