Cortical collecting duct Na-K pump in obstructive nephropathy

1990 ◽  
Vol 258 (5) ◽  
pp. F1320-F1327 ◽  
Author(s):  
H. Kimura ◽  
S. K. Mujais
Keyword(s):  
Ureteral Obstruction ◽  
Turnover Rate ◽  
Collecting Duct ◽  
Obstructive Nephropathy ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Irreversible Damage ◽  
Sprague Dawley Rats ◽  
Collecting Tubule

The present study examined the alterations in the cortical collecting tubule (CCT) Na-K pump that occur after unilateral ureteral obstruction and their consequences on electrolyte excretion. In male Sprague-Dawley rats, unilateral ureteral ligation led to a progressive decrease in intact CCT Na-K pump in situ turnover worsening with the duration of the obstruction: control, 20.1 +/- 0.4; obstructed kidney: 3 h, 14.6 +/- 0.3; 12 h, 12.7 +/- 0.6; 24 h, 12.8 +/- 0.5; 48 h, 11.6 +/- 0.5; and 96 h, 10.6 +/- 0.4 pmol Rb.mm-1.min-1 (all P less than 0.001 vs. control). CCT diameter increased with the duration of obstruction. Release of ureteral obstruction was associated with restitution of pump turnover rate. With 3 h of obstruction, recovery of pump in situ turnover was complete (19.7 +/- 0.4 pmol Rb.mm-1.min-1) by 24 h after release. With more prolonged obstruction (24 h) recovery was partial by 24 h postrelease (16.2 +/- 0.5 pmol Rb.mm-1.min-1) and complete (19.8 +/- 0.7 pmol Rb.mm-1.min-1) by 48 h, suggesting a delay in recovery without the occurrence of irreversible damage. The impairment in Na-K pump in situ turnover was paralleled by an impairment in the ability of the obstructed kidney to excrete an acute potassium load. This parallelism of functional and biochemical studies favors the notion that impairment of CCT Na-K pump in situ turnover contributes significantly to the abnormal potassium excretion that accompanies obstructive damage.

Vasopressin resistance in potassium depletion: role of Na-K pump

1992 ◽  
Vol 263 (4) ◽  
pp. F705-F710 ◽  
Author(s):  
S. K. Mujais ◽  
Y. Chen ◽  
N. A. Nora
Keyword(s):  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Pump Activity ◽  
Before And After ◽  
Directional Change ◽  
Medullary Collecting Duct ◽  
Low K ◽  
K Depletion

Resistance to the hydrosmotic effects of vasopressin has been described in K depletion. It is not clear whether other effects of vasopressin, notably its effects on the Na-K pump in the collecting duct, are similarly affected. Adrenalectomized male Sprague-Dawley rats were allocated to either a normal K (NK) or low-K (LK) diet. Na-K pump activity (pmol.mm-1.h-1) in cortical collecting duct (CCD) and medullary collecting duct (MCD) was determined at 21 days after allocation to the dietary groups before and after exogenous vasopressin (0.1 U twice daily for 3 days). In animals on NK diet, vasopressin (AVP) led to a doubling of Na-K pump activity in the CCD from 502 +/- 47 to 1,144 +/- 41 pmol.mm-1.h-1 (P < 0.01). In K-depleted animals, which had a higher baseline Na-K pump activity, an increase was also observed from 1,056 +/- 97 to 1,239 +/- 65 pmol.mm-1.h-1 (P < 0.05), but this increase was quantitatively less, with the change being 183 vs. 642 pmol.mm-1.h-1 in K-replete rats. The findings in the MCD were similar; in rats on a NK diet, AVP led to a significant increase in Na-K pump activity from 498 +/- 29 to 830 +/- 28 pmol.mm-1.h-1 (P < 0.01). With K depletion, this directional change was preserved, increasing from 1,380 +/- 49 to 1,556 +/- 45 pmol.mm-1.h-1 (P < 0.05), but was quantitatively less than in K-replete rats, the change being 176 vs. 332 pmol.mm-1.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Expression of the thiazide-sensitive Na-Cl cotransporter in rat and human kidney

1995 ◽  
Vol 269 (6) ◽  
pp. F900-F910 ◽  
Author(s):  
N. Obermuller ◽  
P. Bernstein ◽  
H. Velazquez ◽  
R. Reilly ◽  
D. Moser ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Human Kidney ◽  
Protein Band ◽  
Distal Region ◽  
Thick Ascending Limb ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Nephron Segments ◽  
Collecting Tubule

An electroneutral thiazide-sensitive Na-Cl cotransport pathway (TSC) has been localized functionally to the distal convoluted tubule (DCT), although the TSC has also been detected in the connecting tubule (CNT), the cortical collecting duct, and the medullary collecting tubule as well. The present experiments were designed to localize expression of message for the TSC in rat and human kidney. A riboprobe, generated from the mouse TSC, was used for in situ hybridization. Simultaneous immunocytochemistry, using antibodies to Tamm-Horsfall protein, band 3, and the Na+/Ca2+ exchanger, permitted delineation of specific nephron segments. In rat, message for the TSC was highly expressed in DCT cells but not elsewhere. The transition from thick ascending limb to DCT was abrupt, whereas the transition to CNT was gradual. In the more distal region of rat DCT (DCT-2), which contained few intercalated cells, both TSC message and Na+/Ca2+ exchanger immunoreactivity were present. Treatment of rats with furosemide for 5 days increased expression of TSC message within the DCT but did not induce its expression elsewhere. In humans, expression of TSC message was also highest in cells of the DCT. In humans, however, expression extended well into the CNT. These experiments indicate that the TSC is expressed predominantly by DCT cells in both rat and humans, although expression extends into the CNT cells in humans. They also show that the TSC and Na+/Ca2+ exchanger are coexpressed by a subpopulation of DCT cells near the junction with the CNT.

Abstract 344: Intrarenal Ghrelin Receptors Mediate Sodium Reabsorption via an ENaC-Dependent Pathway

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Brandon A Kemp ◽  
Nancy L Howell ◽  
John J Gildea ◽  
Susanna R Keller ◽  
Shetal H Padia
Keyword(s):  
Collecting Duct ◽  
Sodium Reabsorption ◽  
Na Channel ◽  
Cortical Collecting Duct ◽  
Distal Nephron ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Nephron Segment ◽  
Ghrelin Receptors ◽  
Excretion Rates

Intrarenal ghrelin infusion stimulates distal nephron-dependent sodium (Na+) reabsorption in normal rats, but the mechanism is unknown. The main Na+ transporters of the distal nephron segment are the Na+-Cl- co-transporter (NCC) and the epithelial Na+ channel (ENaC). To determine which of these transporters is involved in the antinatriuretic actions of intrarenal ghrelin receptors, uninephrectomized Sprague-Dawley rats received 3 cumulative 1h renal interstitial (RI) infusions of ghrelin (0.3-3 μg/min, N=8) or vehicle (5% dextrose in water, D5W, N=8), prior to harvesting the infused kidney for determination of NCC and ENaC protein expression. Ghrelin-infused rats demonstrated significantly reduced Na+ excretion rates (UNaV) compared to D5W-infused rats (66.7±7.1% of baseline, P<0.01) and significantly increased cortical collecting duct ENaC expression (2.46±0.17 and 1.56±0.19 densitometric units respectively, P<0.01). Renal NCC expression did not change in response to either ghrelin or D5W infusion (4.21±0.58 and 4.13±0.44 densitometric units respectively, P=NS). To test whether the ghrelin-induced increase in collecting duct ENaC expression was responsible for the antinatriuretic actions of ghrelin, we infused ghrelin into the kidney in the presence of amiloride, a selective inhibitor of ENaC activity. Following uninephrectomy, rats were implanted with either a subcutaneous osmotic minipump which systemically delivered amiloride (1.4 ng/min) for 72h to block ENaC activity (N=6), or a minipump that was filled with D5W (N=6). On the day of the study, RI ghrelin (0.3-3 μg/min) or D5W infusion was initiated. RI ghrelin infusion (in the absence of amiloride) significantly reduced UNaV to 58.9±7.2% of baseline, P<0.01; however, in the presence of amiloride, RI ghrelin failed to reduce UNaV, demonstrating values identical to rats that did not receive RI ghrelin. In contrast, studies carried out in the presence of chlorothiazide pumps (to block NCC activity, 1.1 μg/min, N=6), continued to demonstrate ghrelin-induced antinatriuresis (UNaV decreased to 65.3±8.8% of baseline, P<0.01). Mean arterial pressures did not change during any of the acute RI infusions. Thus, intact ENaC function is necessary for ghrelin-induced Na+ reabsorption.

scholarly journals Chronic lithium treatment induces novel patterns of pendrin localization and expression

2018 ◽  
Vol 315 (2) ◽  
pp. F313-F322
Author(s):  
Nathaniel J. Himmel ◽  
Yirong Wang ◽  
Daniel A. Rodriguez ◽  
Michael A. Sun ◽  
Mitsi A. Blount
Keyword(s):  
Collecting Duct ◽  
Lithium Treatment ◽  
Urine Osmolality ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Cell Plasticity ◽  
Acid Base ◽  
Sprague Dawley Rats ◽  
Medullary Collecting Duct

Prolonged lithium treatment is associated with various renal side effects and is known to induce inner medullary collecting duct (IMCD) remodeling. In animals treated with lithium, the fraction of intercalated cells (ICs), which are responsible for acid-base homeostasis, increases compared with renal principal cells (PCs). To investigate the intricacies of lithium-induced IMCD remodeling, male Sprague-Dawley rats were fed a lithium-enriched diet for 0,1, 2, 3, 6, 9, or 12 wk. Urine osmolality was decreased at 1 wk, and from 2 to 12 wk, animals were severely polyuric. After 6 wk of lithium treatment, approximately one-quarter of the cells in the initial IMCD expressed vacuolar H+-ATPase, an IC marker. These cells were localized in portions of the inner medulla, where ICs are not normally found. Pendrin, a Cl−/[Formula: see text] exchanger, is normally expressed only in two IC subtypes found in the convoluted tubule, the cortical collecting duct, and the connecting tubule. At 6 wk of lithium treatment, we observed various patterns of pendrin localization and expression in the rat IMCD, including a novel phenotype wherein pendrin was coexpressed with aquaporin-4. These observations collectively suggest that renal IMCD cell plasticity may play an important role in lithium-induced IMCD remodeling.

Intracellular EDEMA does not adversely affect the ability to cryopreserve intact hearts

1993 ◽  
Vol 51 ◽  
pp. 278-279
Author(s):  
CL Hastings ◽  
RD Carlton ◽  
FG Lightfoot ◽  
AF Tryka
Keyword(s):  
Cell Injury ◽  
Median Sternotomy ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Hypoxic Cell ◽  
Free Wall ◽  
Sprague Dawley ◽  
Left Ventricular Free Wall ◽  
Sprague Dawley Rats

The earliest ultrastructural manifestation of hypoxic cell injury is the presence of intracellular edema. Does this intracellular edema affect the ability to cryopreserve intact myocardium? To answer this guestion, a model for anoxia induced intracellular edema (IE) was designed based on clinical intraoperative myocardial preservation protocol. The aortas of 250 gm male Sprague-Dawley rats were cannulated and a retrograde flush of Plegisol at 8°C was infused over 90 sec. The hearts were excised and placed in a 28°C bath of Lactated Ringers for 1 h. The left ventricular free wall was then sliced and the myocardium was slam frozen. Control rats (C) were anesthetized, the hearts approached by median sternotomy, and the left ventricular free wall frozen in situ immediately after slicing. The slam frozen samples were obtained utilizing the DDK PS1000, which was precooled to -185°C in liguid nitrogen. The tissue was in contact with the metal mirror for a dwell time of 20 sec, and stored in liguid nitrogen until freeze dry processing (Lightfoot, 1990).

Activated Kupffer cells cause a hypermetabolic state after gentle in situ manipulation of liver in rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1076-G1082 ◽  
Author(s):  
Peter Schemmer ◽  
Nobuyuki Enomoto ◽  
Blair U. Bradford ◽  
Hartwig Bunzendahl ◽  
James A. Raleigh ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Kupffer Cells ◽  
Cell Function ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypermetabolic State ◽  
Hypoxia Marker ◽  
Factor Α ◽  
Necrosis Factor

Harvesting trauma to the graft dramatically decreases survival after liver transplantation. Since activated Kupffer cells play a role in primary nonfunction, the purpose of this study was to test the hypothesis that organ manipulation activates Kupffer cells. To mimic what occurs with donor hepatectomy, livers from Sprague-Dawley rats underwent dissection with or without gentle organ manipulation in a standardized manner in situ. Perfused livers exhibited normal values for O2 uptake (105 ± 5 μmol · g−1 · h−1) measured polarigraphically; however, 2 h after organ manipulation, values increased significantly to 160 ± 8 μmol · g−1 · h−1 and binding of pimonidazole, a hypoxia marker, increased about threefold ( P < 0.05). Moreover, Kupffer cells from manipulated livers produced three- to fourfold more tumor necrosis factor-α and PGE2, whereas intracellular calcium concentration increased twofold after lipopolysaccharide compared with unmanipulated controls ( P < 0.05). Gadolinium chloride and glycine prevented both activation of Kupffer cells and effects of organ manipulation. Furthermore, indomethacin given 1 h before manipulation prevented the hypermetabolic state, hypoxia, depletion of glycogen, and release of PGE2 from Kupffer cells. These data indicate that gentle organ manipulation during surgery activates Kupffer cells, leading to metabolic changes dependent on PGE2 from Kupffer cells, which most likely impairs liver function. Thus modulation of Kupffer cell function before organ harvest could be beneficial in human liver transplantation and surgery.

Evidence of corticosteroid action along the nephron

1984 ◽  
Vol 246 (2) ◽  
pp. F111-F123 ◽  
Author(s):  
D. Marver
Keyword(s):  
Collecting Duct ◽  
Type I ◽  
Type Ii ◽  
Cortical Collecting Duct ◽  
Distal Nephron ◽  
Type Iii ◽  
Collecting Ducts ◽  
Collecting Tubule ◽  
Cortical Collecting Tubule

The kidney contains three classes of corticosteroid-binding proteins receptors. They include a mineralocorticoid-specific (Type I), a glucocorticoid-specific (Type II), and a corticosterone-specific (Type III) site. The Type I and Type III sites roughly parallel each other along the nephron, with maximal binding occurring in the late distal convoluted or connecting segment and the cortical and medullary collecting ducts. Type II sites occur throughout the nephron, with maximal concentrations appearing in the proximal tubule and the late distal convoluted-cortical collecting duct region. The function of the Type I sites in the connecting segment is unclear since chronic mineralocorticoid therapy does not influence the potential difference in this segment as it does in the cortical collecting tubule. Furthermore, the specific role of Type II versus Type III sites in the distal nephron is unknown. Finally, the possible influence of sodium on both latent and steroid-induced renal cortical and medullary Na-K-ATPase is discussed.

Distribution of kallikrein-binding protein mRNA in kidneys and difference between SHR and WKY rats

1994 ◽  
Vol 267 (2) ◽  
pp. F325-F330 ◽  
Author(s):  
T. Yang ◽  
Y. Terada ◽  
H. Nonoguchi ◽  
M. Tsujino ◽  
K. Tomita ◽  
...  
Keyword(s):  
Blot Analysis ◽  
Binding Protein ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Sd Rats ◽  
Medullary Collecting Duct ◽  
Wistar Kyoto

We investigated kallikrein-binding protein (KBP) mRNA distribution in the kidney of Sprague-Dawley (SD) rats, spontaneously hypertensive rats (SHR), and Wistar-Kyoto strain (WKY) rats. Northern blot analysis revealed that KBP mRNA was located mainly in the medulla and with lower amounts in SHR than in WKY rats. KBP mRNA in microdissected nephron segments was detected by reverse transcription and polymerase chain reaction (RT-PCR) followed by Southern blot analysis. In SD rats, the most abundant signals were consistently found in inner medullary collecting duct (IMCD), with small amounts in outer medullary collecting duct, proximal convoluted tubule, and glomerulus. No signals were found in connecting tubule and cortical collecting duct. The nephron distribution of KBP mRNA was similar in WKY and SD rats. Only a small amount of signal was found, however, in IMCD of SHR. In conclusion, 1) KBP mRNA was predominantly distributed in the medullary segments of the distal nephron, downstream from the known kallikrein activity site in the collecting duct, and 2) KBP mRNA expression was significantly decreased in the kidney of SHR.

In situ localization of renin and its mRNA in neonatal ureteral obstruction

1990 ◽  
Vol 258 (4) ◽  
pp. F854-F862 ◽  
Author(s):  
S. S. el-Dahr ◽  
R. A. Gomez ◽  
M. S. Gray ◽  
M. J. Peach ◽  
R. M. Carey ◽  
...  
Keyword(s):  
Ureteral Obstruction ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Renin Angiotensin ◽  
Renal Vasoconstriction ◽  
Renin Mrna ◽  
Renin Content

Angiotensin II is an important mediator of renal vasoconstriction resulting from chronic unilateral ureteral obstruction (UUO). Distribution of renin mRNA and immunoreactive renin (IR) was examined in kidneys of 1-mo-old Sprague-Dawley rats subjected to either sham operation (n = 21), left complete UUO (n = 21), or right uninephrectomy (UNX, n = 16) at 2 days of age. There were no differences among the three groups in mean arterial pressure or plasma renin activity. Unlike sham kidneys, in which IR was detected in less than 55% of juxtaglomerular apparatuses (JGA) and was confined to a juxtaglomerular location, IR in both kidneys of animals with UUO appeared in greater than 75% of JGA and extended along most of the length of the afferent arteriole (P less than 0.01). In contrast, IR in kidneys of UNX rats was localized to the JGA as in sham-operated animals. Compared with sham-operated kidneys, renal renin content was increased in the obstructed kidneys (P less than 0.01) but decreased in the intact opposite kidneys of UUO rats and in the remaining kidneys of UNX rats (P less than 0.05). Renin mRNA, detected by in situ hybridization histochemistry, was localized to the JGA in kidneys of all groups. However, the fraction of JGA containing detectable renin mRNA was higher in obstructed kidneys than in intact opposite, UNX, or sham kidneys (P less than 0.05). In conclusion, UUO alters intrarenal renin independent of the systemic renin-angiotensin system. The greater distribution of IR, increased renin content, and renin gene expression of kidneys with ipsilateral UUO are consistent with a role for renin-angiotensin in mediating the vasoconstriction resulting from UUO.

scholarly journals Influence of Therapeutic Hypothermia on Matrix Metalloproteinase Activity after Traumatic Brain Injury in Rats

2005 ◽  
Vol 25 (11) ◽  
pp. 1505-1516 ◽  
Author(s):  
Jessie S Truettner ◽  
Ofelia F Alonso ◽  
W Dalton Dietrich
Keyword(s):  
Brain Injury ◽  
Therapeutic Hypothermia ◽  
Brain Injuries ◽  
Brain Temperature ◽  
Sprague Dawley ◽  
Beneficial Effects ◽  
Sprague Dawley Rats ◽  
In Situ Zymography ◽  
Metalloproteinase Activity

Recent evidence suggests that matrix metalloproteinases (MMPs) contribute to acute edema and lesion formation following ischemic and traumatic brain injuries (TBI). Experimental and clinical studies have also reported the beneficial effects of posttraumatic hypothermia on histopathological and behavioral outcome. The purpose of this study was to determine whether therapeutic hypothermia would affect the activity of MMPs after TBI. Male Sprague-Dawley rats were traumatized by moderate parasagittal fluid-percussion (F-P) brain injury. Seven groups ( n = 5/group) of animals were investigated: sham-operated, TBI with normothermia (37°C), and TBI with hypothermia (33°C). Normothermia animals were killed at 4, 24, 72 h and 5 days, and hypothermia animals at 24 or 72 h. Brain temperature was reduced to target temperature 30 mins after trauma and maintained for 4 h. Ipsilateral and contralateral cortical, hippocampal, and thalamic regions were analyzed by gelatin and in situ zymography. In traumatized normothermic animals, TBI significantly ( P<0.005) increased MMP-9 levels in ipsilateral (right) cortical and hippocampal regions, compared with contralateral or sham animals, beginning at 4 h and persisting to 5 days. At 1, 3, and 5 days after TBI, significant increases in MMP-2 levels were observed. In contrast to these findings observed with normothermia, posttraumatic hypothermia significantly reduced MMP-9 levels. Hypothermic treatment, however, did not affect the delayed activation of MMP-2. Clarifying the mechanisms underlying the beneficial effects of posttraumatic hypothermia is an active area of research. Posttraumatic hypothermia may attenuate the deleterious consequences of brain trauma by reducing MMP activation acutely.

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