Effects of prostaglandins on Na transport in isolated collecting tubules

1978 ◽  
Vol 373 (2) ◽  
pp. 125-132 ◽  
Author(s):  
Yasuhiko Iino ◽  
Masashi Imai
Keyword(s):  
Na Transport ◽  
Collecting Tubules

Ca2(+)-dependent inhibition of sodium transport in rabbit cortical collecting tubules

1990 ◽  
Vol 258 (3) ◽  
pp. F568-F582 ◽  
Author(s):  
G. Frindt ◽  
E. E. Windhager
Keyword(s):  
Cell Membrane ◽  
Amphotericin B ◽  
Apical Cell ◽  
Ringer Solution ◽  
Na Transport ◽  
Apical Cell Membrane ◽  
Dependent Inhibition ◽  
Collecting Tubules ◽  
Rate Limiting ◽  
Sustained Increase

Experiments were carried out to test whether maneuvers believed to increase intracellular Ca2+ concentration [( Ca2+]cell) inhibit Na transport in cortical collecting tubules (CCTs). Unidirectional Na efflux (JNa1----b) and Na influx (JNab----1) were measured isotopically in isolated perfused renal CCTs of rabbits. The animals were either untreated or pretreated with deoxycorticosterone (DOC) for 1-3 wk. To raise [Ca2+]cell, ionomycin or quinidine were added to, or [Na] reduced in, pertubular fluid. In control DOC-pretreated CCTs JNa1----b tended to saturate as luminal Na concentration was increased, reaching 22.9 +/- 1.2 pmol.cm-1.s-1 at 145 mM. In addition, in these CCTs, in contrast to non-DOC-treated tubules, the apical cell membrane was not found to be rate limiting for Na reabsorption as neither amphotericin B nor vasopressin further enhanced JNa1----b. In non-DOC-treated CCTs 10(-6) M ionomycin inhibited JNa1----b by 44.7%. When DOC-pretreated CCTs were exposed to either 10(-6)M ionomycin or 10(-4)M quinidine, JNa1----b was inhibited by 27 and 26%, respectively, while JNab----1 remained unchanged. This ionomycin-induced inhibition was Ca dependent. Exposure of DOC-pretreated CCTs to 5 mM Na-Ringer solution (Na replaced by choline or N-methyl-D-glucamine) for 30 min reduced JNa1----b by 18-30%. The inhibition of JNa1----b caused by any of the three maneuvers was fully reversed upon addition of amphotericin B to the luminal fluid. The results are consistent with the view that a sustained increase in [Ca2+]cell reduces Na transport by inhibition of the rate of Na+ entry across the apical cell membrane.

Patterns of K+ permeation following inhibition of Na+ transport in rabbit cortical collecting tubule

1986 ◽  
Vol 250 (1) ◽  
pp. F120-F126 ◽  
Author(s):  
J. B. Stokes
Keyword(s):  
Apical Membrane ◽  
Na Transport ◽  
Transcellular Pathway ◽  
Collecting Tubule ◽  
Before And After ◽  
K Secretion ◽  
Pg E2 ◽  
Collecting Tubules ◽  
K Permeability ◽  
Cortical Collecting Tubule

The passive (lumen-to-bath) K+ permeation (KK) of rabbit cortical collecting tubules was measured before and after inhibition of Na+ transport. Inhibition of the Na-K pump with ouabain reduced KK. This result contrasts sharply with the previously described increase in KK observed following inhibition of Na+ transport with amiloride. These opposite changes in KK are owing to the fact that a substantial component of the lumen-to-bath K+ permeation involves a transcellular pathway. Amiloride, because it hyperpolarizes the apical membrane, increases KK; ouabain, because it depolarizes the cell, decreases KK. Previous results have also suggested that the cell K+ permeability is secondarily altered by these agents so that the changes in voltage and permeability are additive. These patterns of changes in KK were used to evaluate the mechanism of action of two agents that partially inhibit Na+ transport: vasopressin and prostaglandin (PG) E2. Their effect on KK was qualitatively similar to that of amiloride. In amiloride-treated tubules, neither vasopressin nor PGE2 altered KK. Neither did they alter the normal reduction in KK caused by pump inhibition. Thus they did not have any direct effect on K+ permeability. These results are consistent with the thesis that vasopressin and PGE2 inhibit Na+ absorption by reducing apical membrane permeability. The relation between the regulation of Na+ absorption and K+ permeation may have important implications for the regulation of K+ secretion by the cortical collecting tubule.

Effect of ADH on Rat Renal Papilla, an Ultrastructural and Cytochemical Study

1973 ◽  
Vol 31 ◽  
pp. 410-411
Author(s):  
C. N. Sun ◽  
H. J. White ◽  
E. J. Towbin
Keyword(s):  
Electron Microscopy ◽  
Diabetes Insipidus ◽  
Renal Papilla ◽  
Milk Diet ◽  
Intercellular Spaces ◽  
Cytochemical Study ◽  
Collecting Tubule ◽  
Concentrate Urine ◽  
Staining Techniques ◽  
Collecting Tubules

Diabetes insipidus and compulsive water drinking are representative of two categories of antidiuretic hormone (ADH) lack. We studied a strain of rats with congenital diabetes insipidus homozygote (DI) and normal rats on an isocaloric fortified dilute milk diet. In both cases, the collecting tubules could not concentrate urine. Special staining techniques, Alcian Blue-PAS for light microscopy and lanthanum nitrate for electron microscopy were used to demonstrate the changes in interstitial mucopolysaccharides (MPS). The lanthanum staining was done according to the method of Khan and Overton.Electron microscopy shows cytoplasmic lesions, vacules, swelling and degenerating mitochondria and intercellular spaces (IS) in the collecting tubule cells in DI and rats on milk diet.

A Scanning Electron Microscopic Study of the Uriniferous Tubules

1973 ◽  
Vol 31 ◽  
pp. 622-623
Author(s):  
Peter M. Andrews
Keyword(s):  
Electron Microscopy ◽  
Scanning Electron Microscopy ◽  
Renal Glomerulus ◽  
Electron Microscopic ◽  
Vascular Perfusion ◽  
Scanning Electron Microscopic Study ◽  
Scanning Electron Microscopic ◽  
Collecting Tubules ◽  
Bowman's Capsule ◽  
Scanning Electron

Although there have been a number of recent scanning electron microscopic reports on the renal glomerulus, the advantages of scanning electron microscopy have not yet been applied to a systematic study of the uriniferous tubules. In the present investigation, scanning electron microscopy was used to study the ultrastructural morphology of the proximal, distal, thin loop, and collecting tubules. Material for observation was taken from rat kidneys which were fixed by vascular perfusion, sectioned by either cutting or fracturing technigues, and critically point dried.The brush border characterising proximal tubules is first detected on the luminal surface of Bowman's capsule adjacent to the urinary pole orifice. In this region one frequently finds irregular microvilli characterized by broad and flattened bases with occasional bulbous structures protruding from their surfaces.

Ultrastructural and chemical evidences of heterogeneity and hormone dependence of certain glycocalyces

1978 ◽  
Vol 36 (2) ◽  
pp. 322-323
Author(s):  
B. Monis ◽  
D. Lis ◽  
I. Parlanti ◽  
A. R. Eynard ◽  
M. A. Valentich ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Concanavalin A ◽  
Ruthenium Red ◽  
Transitional Epithelium ◽  
Membrane Material ◽  
Hormone Dependence ◽  
Cellulose Acetate Electrophoresis ◽  
Electrophoretic Data ◽  
Fat Globule ◽  
Collecting Tubules

We are gathering evidences which indicate ultrastructural variations and chemical heterogeneity of certain glycocalyces as well as hormone dependence of some of them. Thus, in the lumenal glycocalyx of renal collecting tubules of the guinea-pig granular and filamentous structures were seen (1, fig. 1). By isolation, chemical analysis and cellulose acetate electrophoresis in various buffers of tubular membrane material, glycopeptides and glycosaminoglycans were identified (fig. 2).Guinea-pig and rat transitional epithelium of urinary tract showed a filamentous lumenal glycocalyx demonstrable with ruthenium red (fig. 3) but which only in part stained with concanavalin A. Chemical and electrophoretic data indicated that urothelium contains glycoproteins, glycosaminoglycans and glycolipids.The glycocalyx of the fat globule membrane of milk of several species has a granular appearance as shown by cationic dyes and by concanavalin A (2, 3, fig. 4 and 5). Also, several glycoproteins were isolated and identified on polyacrilamide gel electrophoresis (fig. 6). Glycosaminoglycans and certain glycolipids such as sulfatides were chemically identified in this glycocalyx.

Резекция печени изменяет механизмы выведения аммиака почками крыс с хроническим тетрахлорметановым гепатитом

2018 ◽  
pp. 72-79
Author(s):  
П.Н. Савилов ◽  
Д.В. Молчанов
Keyword(s):  
Body Weight ◽  
Toxic Hepatitis ◽  
Ammonia Excretion ◽  
Left Lobe ◽  
Free Form ◽  
Sham Operation ◽  
White Rats ◽  
Urea Reabsorption ◽  
Ambiguous Effect ◽  
Collecting Tubules

Цель исследования - изучение влияния резекции печени (РП) на аммиакэкскретирующую функцию почек при хроническом тетрахлорметановом гепатите. Методика. Опыты выполнены на 265 беспородных белых крысах (самках) массой 180-220 г. Хронический гепатит воспроизводили подкожным введением 50% раствора тетрахлорметана (CCl) на оливковом масле (0,1 мл/100 г массы тела, через сутки, c двумя двухнедельными перерывами между 6, 7 и 13-14 инъекциями). На 65-е сут. (последние) введения тетрахлорметана, удаляли часть левой доли печени (15-20% массы органа). На 3-и, 7-е и 14-е сут. после РП или лапаротомии («ложнооперированные» животные) в почках, артериальной и венозной крови, моче исследовали содержание аммиака, глутамина и мочевины. Результаты. Прогрессирование эндогенной аммиачной интоксикации после РП на фоне тетрахлорметанового гепатита сопровождается повышенной экскрецией аммиака почками. Однако это не устраняет артериальную гипераммониемию и не предотвращает накопление почками аммиака. Инкреция глютамина из почек в кровоток прекращается. К 14-м сут. послеоперационного периода возрастает потребление глютамина из артериальной крови, что приводит к его накоплению в почках. Стимулируя выведение мочевины из организма с мочой, РП одновременно активирует её образование в почках, с дальнейшим поступлением как в кровоток, так и в мочу. В зависимости от сроков послеоперационного периода это сопровождается изменением скорости реабсорбции мочевины в почках. Заключение. Полученные результаты свидетельствуют, что при РП на фоне тетрахлорметанового гепатита почки не предотвращают прогрессирование эндогенной аммиачной интоксикации, патологическое накопление аммиака и глутамина её клетками, но сохраняют способность принимать участие в регуляции повышенного содержания мочевины в артериальной крови. Mechanical (resection) or toxic (hepatitis) liver damage alone has an ambiguous effect on renal ammonia excretion during development of endogenous ammonia intoxication. The aim. The study investigated the effect of liver resection (LR) on renal ammonia excretion in chronic tetrachlorocarbon (CCl)-induced hepatitis. Methods. Experiments were conducted on 240 mongrel white rats (females) weighing 180-220 g. Chronic hepatitis was induced by subcutaneous injection of 50% solution of carbon tetrachloride (CCl) in olive oil (0.1 ml/100g body weight per day with two two-week breaks between injections 6-7 and 13-14). LR with removal of a part of the left lobe (15-20% of body weight) was performed on the 65th (last) day of CCl injections. The animals were examined on the 3rd, 7th and 14th day after LR or laparotomy (sham operation). Contents of ammonia (AM), glutamine (GN), and urea were measured in the kidney, arterial (AB) and venous ( v.renlis ) blood, and urine. Results. Progression of endogenous ammonia intoxication after LR associated with CCl-induced hepatitis and increased renal excretion of Am involves three mechanisms: 1) excretion of Am that is delivered to kidneys in the free form with AB; 2) stimulation of renal tubule secretion of Am that had formed in kidneys by deamidation of «arterial» Gn; and 3) contrary to rules, partial reabsorption of Am from collecting tubules into the blood. However, this does not eliminate arterial hyperammonemia or prevent accumulation of Am in kidneys. The stimulatory effect of LR in CCl-induced hepatitis on Gn incretion from kidneys to the circulation stops by the 14 day after surgery, and the accompanying increased consumption of Gn from AВ results in Gn accumulation in kidneys. LR stimulates urea excretion with urine and simultaneously activates kidney formation of urea, which further enters the bloodstream and urine. Depending on the postoperative period this is associated with changes in the rate of urea reabsorption in kidneys. Conclusions. In RP associated with CCl-induced hepatitis, kidneys cannot prevent progression of endogenous ammonia intoxication and pathological accumulation of ammonia and glutamine in kidney cells but retain the ability to participate in the regulation of the increased urea level in AB.

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