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.

Synthesis of prostaglandin E2 in different segments of isolated collecting tubules from adult and neonatal rabbits

1985 ◽  
Vol 248 (1) ◽  
pp. F134-F144 ◽  
Author(s):  
D. Schlondorff ◽  
J. A. Satriano ◽  
G. J. Schwartz
Keyword(s):  
Arachidonic Acid ◽  
Prostaglandin E2 ◽  
Feedback Loop ◽  
Pge2 Production ◽  
Large Variability ◽  
Pge2 Synthesis ◽  
Collecting Tubule ◽  
Concentrate Urine ◽  
Collecting Tubules

Prostaglandin E2 (PGE2) inhibits the action of the antidiuretic hormone (ADH) in isolated collecting tubules. A negative feedback loop has been postulated whereby ADH stimulates PGE2 synthesis. Furthermore, lysyl-bradykinin (LBK) inhibits the antidiuretic effect of ADH, probably via PGE2. Enhanced PGE2 synthesis has also been implicated as contributing to the inability to maximally concentrate urine during the neonatal period. We investigated PGE2 synthesis in microdissected cortical (CCT), medullary (MCT), and branched cortical (BCT) collecting tubules from adult and in corticomedullary collecting tubules (CT) from newborn rabbits. Isolated BCT produced significantly less PGE2 (12 +/- 2 pg X mm-1 X 20 min-1) than CCT (65 +/- 9) or MCT (76 +/- 8) from kidneys of adult rabbits. CT from newborn rabbits produced only 19 +/- 3 pg/mm, significantly less than either CCT or MCT from adults. A large variability in basal PGE2 production and hormonal response was observed from tubule to tubule. Under either basal conditions or in the presence of 2 microM arachidonic acid, LBK enhanced PGE2 synthesis in CCT and MCT from adults. ADH enhanced PGE2 production in MCT under basal conditions and in CCT in the presence of arachidonic acid. Neither LBK nor ADH stimulated PGE2 synthesis in neonatal CT. A23187 consistently stimulated PGE2 synthesis in CCT and MCT from adults and, to a lesser extent, in CT from newborn rabbits. Our results support the hypothesis that ADH and LBK enhance PGE2 synthesis in the collecting tubule. This response is, however, subject to large variations from tubule to tubule and depends on the in vitro incubation conditions.

A Simple Dichromatic Stain for Plastic Embedded Tissues

1970 ◽  
Vol 28 ◽  
pp. 296-297 ◽  
Author(s):  
G. R. Mackay ◽  
M. L. Mead
Keyword(s):  
Electron Microscopy ◽  
Toluidine Blue ◽  
Biological Material ◽  
Good Reproducibility ◽  
Routine Work ◽  
Staining Techniques

Color contrasting of 1 to 2 micron sections of plastic embedded biological material is an important adjunct to electron microscopy. The procedures in general use today are simple and rapid giving monochromatic results, e.g., toluidine blue. Although many di- and polychromatic histologic staining techniques have been modified to obtain a counterstaining effect with plasticembedded tissue, the methods are usually undesirable for routine work because they are time consuming, complicated and often defy good reproducibility.

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.

Time course of sodium-induced Na(+)-K(+)-ATPase recruitment in rabbit cortical collecting tubule

1992 ◽  
Vol 263 (1) ◽  
pp. C61-C68 ◽  
Author(s):  
N. Coutry ◽  
M. Blot-Chabaud ◽  
P. Mateo ◽  
J. P. Bonvalet ◽  
N. Farman
Keyword(s):  
Time Course ◽  
Sucrose Solution ◽  
Sodium Concentration ◽  
Rabbit Kidney ◽  
Ouabain Binding ◽  
Kinase C ◽  
Short Period ◽  
Intracellular Sodium Concentration ◽  
Collecting Tubule ◽  
Collecting Tubules

In cortical collecting tubules (CCD) of aldosterone-repleted rabbit kidney, an increase in intracellular sodium concentration (Nai) induces the recruitment and/or activation of latent Na(+)-K(+)-ATPase pumps (Blot-Chabaud et al., J. Biol. Chem. 265: 11676-11681, 1990). The present study was addressed to determine the time course of this Nai-dependent pump recruitment and to examine some of the factors possibly involved in this phenomenon. CCD from adrenalectomized rabbits complemented with aldosterone and dexamethasone were incubated at 4 degrees C either in a K(+)-free saline solution (Na(+)-loaded CCD) or in a sucrose solution (control CCD) and then rewarmed for various time periods to allow pump recruitment to occur. The number of pumps in the membrane was determined by specific [3H]ouabain binding; Nai was measured using 22Na. A rise in Nai induced a threefold increase in the number of basolateral pumps, which was fully achieved within 1-2 min. This pump recruitment was reversible within 15 min after restoration of low Nai. It was unaffected by inhibitors of cytoskeleton and Ca2+ ionophore A 23187. The blocker of the Na(+)-H+ antiporter, amiloride, did not prevent it. The protein kinase C activator, phorbol 12-myristate 13-acetate, did not induce it in the absence of Na+. We conclude that Nai is a major determinant of pump recruitment and/or activation, which occurs over a very short period of time. It may constitute a rapid adaptative response to an increase in the cell Na+ load.

The morphogenesis of avian tendon

1956 ◽  
Vol 144 (917) ◽  
pp. 556-572 ◽  
Keyword(s):  
Electron Microscopy ◽  
Average Diameter ◽  
Relative Volume ◽  
Morphological Features ◽  
Collagen Fibrils ◽  
Intercellular Spaces ◽  
Intercellular Substance ◽  
Thin Sections ◽  
Cellular Components ◽  
Development Proceeds

Observations by electron microscopy on thin sections of the metatarsal tendon of embryonic fowls show that in the 8-day embryo the earliest definable collagen fibrils of 80 Å in diameter are intimately associated with the cytoplasm of the compact, apparently syncytial, cells of which the tendon rudiment is composed. As development proceeds, some intracytoplasmic groups of fibrils are distinguishable, but intercellular spaces also develop and these gradually become filled with fibrils; finally, bundles are formed and lie packed between the adjacent cells. Soon the extracellular organization predominates until at 20days the average diameter of the fibrils is 400 Å and the normal 640 Å periodicity of collagen has been achieved. The morphological features demonstrated have been correlated with histochemical data, and the possible function of the various cellular components in the formation of the intercellular substance has been discussed. By the use of sections in which fibrils have been cut exactly transverse to the bundle axis it has been shown that each fibril is invested by interfibrillar material. As the diameter of the fibrils increases with age the relative volume of interfibrillar material within a bundle diminishes; it is therefore concluded that this material must contain either collagen or the necessary precursors in order to account for the enlargement of the fibrils. Thus the interfibrillar material is of fundamental importance to the formation and growth of the collagen fibrils.

Na+-K+-ATPase-dependent sodium flux in cortical collecting tubule

1988 ◽  
Vol 255 (4) ◽  
pp. F605-F613 ◽  
Author(s):  
M. Blot-Chabaud ◽  
F. Jaisser ◽  
M. Gingold ◽  
J. P. Bonvalet ◽  
N. Farman
Keyword(s):  
Special Device ◽  
Instantaneous Rate ◽  
Sodium Flux ◽  
Na Efflux ◽  
Collecting Tubule ◽  
Pump Activity ◽  
Total Capacity ◽  
Collecting Tubules ◽  
Kinetics Of ◽  
Cortical Collecting Tubule

The instantaneous rate of efflux of intracellular Na was studied in rabbit isolated cortical collecting tubules (CCT) as a function of temperature and intracellular Na concentration ([Na]i). [Na]i of microdissected CCT was increased by cold and K-free exposure in the presence of 22Na and the extracellular tracer [3H] sorbitol. [Na]i rose rapidly to 40 mM at 30 min, after which it rose more slowly, reaching 120-140 mM at 6 h. Kinetics of Na efflux were studied after rapid rewarming, using a special device allowing measurements at 20-s intervals. Under control conditions, the total Na load was extruded in less than 8 min, whereas, in the presence of 10(-4) M ouabain, only 50% of the load was extruded during this period of time. Ouabain-sensitive Na efflux was first evident at 13 degrees C and gradually increased between 13 and 35 degrees C. At 37 degrees C, Na+-K+-ATPase-dependent Na efflux was dependent on [Na]i. This efflux gradually increased, from 0.05 to 0.5 peq.nl tubular volume-1.s-1 as a function of [Na]i and reached a plateau at 70 mM [Na]i. It is concluded that [Na]i is a major modulator of the pump activity in CCT; at normal levels of [Na]i, the pump is operating at only a small fraction of its total capacity.

scholarly journals MON-LB65 Lithium: The Culprit of Multiple Endocrinopathies

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Alice Yau ◽  
Gul Bahtiyar ◽  
Giovanna Rodriguez ◽  
Jose R Martinez Escudero
Keyword(s):  
Bipolar Disorder ◽  
Diabetes Insipidus ◽  
Mental Status ◽  
Nephrogenic Diabetes Insipidus ◽  
Kidney Injury ◽  
Urine Osmolality ◽  
Altered Mental Status ◽  
Clinical Findings ◽  
Volume Depletion ◽  
Collecting Tubules

Abstract Background: Lithium, commonly used to treat various psychiatric disorders such as bipolar disorder, can cause acute toxicity that presents with nausea, vomiting and diarrhea. Lithium can also cause life-threatening endocrine abnormalities, including hypercalcemia, hypernatremia, and both hypo- and hyperthyroidism. Clinical Case: A 61-year old female with hypothyroidism, bipolar disorder, hyperparathyroidism with two-gland parathyroidectomy on lithium for over 30 years presented with altered mental status. Initial labs revealed elevated creatinine 1.92 mg/dL (0.8-2.00mg/dL) compared to baseline 0.82 mg/dL, sodium 154 mg/dL (135-147 mg/dL), Corrected calcium 11.7 mg/dL (8.5-10.5 mg/dL), PTH 96 pg/mL (15-65 pg/mL), and high lithium levels 1.45 mmol/L (0.60-1.20 mmol/L). Further studies showed hypotonic polyuria with no increase in urine osmolality after desmopressin, consistent with nephrogenic diabetes insipidus. Lithium was held and she was treated with aggressive intravenous hydration with dextrose 5% water. Hypercalcemia is thought to result from increased secretion of PTH due to an increased set point at which calcium suppresses PTH release; this often resolves once lithium is stopped. Lithium can also unmask previously unrecognized mild hyperparathyroidism, and/or raise serum PTH concentrations independent of calcium levels.1 The drug interferes with the kidneys’ ability to concentrate urine in the collecting tubules by desensitizing response to antidiuretic hormone, causing diabetes insipidus. The resulting volume depletion from excessive urinary water loss in turn lead to acute kidney injury and hypernatremia.2 Hypothyroidism results from lithium-inhibited synthesis and release of thyroid hormones and decreases iodine trapping. Conclusion: Although these are infrequent complications of lithium use, they remain pertinent clinical findings to consider due to their morbidity. In this case, our patient may have avoided multiple chronic electrolyte abnormalities leading to altered mental status if lithium toxicity had been recognized earlier. References:1. García-Maldonado, Gerardo, and Rubén de Jesús Castro-García. “Endocrinological Disorders Related To The Medical Use Of Lithium. A Narrative Review”. Revista Colombiana De Psiquiatría (English Ed.), vol 48, no. 1, 2019, pp. 35-43. Elsevier BV, doi:10.1016/j.rcpeng.2018.12.005. 2. Tasci, E. “Lithium-Induced Nephrogenic Diabetes Insipidus Responsive To Desmopressin”. Acta Endocrinologica (Bucharest), vol 15, no. 2, 2019, pp. 270-271. ACTA Endocrinologica Foundation, doi:10.4183/aeb.2019.270.

Nephrogenic Diabetes Insipidus

1996 ◽  
Vol 17 (4) ◽  
pp. 145-146
Author(s):  
Corrine Benchimol
Keyword(s):  
Diabetes Insipidus ◽  
Nephrogenic Diabetes Insipidus ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Duct Cell ◽  
Cell Binding ◽  
Luminal Membrane ◽  
Concentrate Urine ◽  
V2 Receptor ◽  
Final Effect

Nephrogenic diabetes insipidus (NDI) is a disorder, either congenital or acquired, in which antidiuretic hormone (ADH) secretion is normal, but the ability to concentrate urine is reduced because of insensitivity of the collecting tubule to ADH. The antidiuretic action of arginine vasopressin requires binding of the hormone to the renal type V2 receptor on the basolateral membrane of the collecting duct principal cell. Binding results in activation of adenylate cyclase, generation of cAMP, and increased reabsorption of water across the apical membrane of the renal collecting duct cell. The defect in NDI may be located at any of the steps from binding of vasopressin to the final effect of the hormone on the luminal membrane.

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