Role of Ammonium Ion in Adenosine Triphosphate Consumption of the Rat Medullary Thick Ascending Limb

2015 ◽  
pp. 149-159
Author(s):  
Hitoshi Endou ◽  
Kyu Yong Jung ◽  
Yasuhiro Komatsu ◽  
Kweon Haeng Lee
Keyword(s):  
Adenosine Triphosphate ◽  
Ammonium Ion ◽  
Thick Ascending Limb ◽  
Medullary Thick Ascending Limb

Role of arginine vasopressin in medullary thick ascending limb on maximal urinary concentration

1986 ◽  
Vol 251 (2) ◽  
pp. F266-F270 ◽  
Author(s):  
J. K. Kim ◽  
S. N. Summer ◽  
A. E. Erickson ◽  
R. W. Schrier
Keyword(s):  
Adenylate Cyclase ◽  
Arginine Vasopressin ◽  
Urinary Concentration ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
Urinary Osmolality ◽  
Medullary Thick Ascending Limb ◽  
Sprague Dawley Rats ◽  
Collecting Tubules

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.

Stimulation of Na+/K+-ATPase activity by polyamines in the rat renal medullary cells of the thick ascending limb of Henle's loop

1990 ◽  
Vol 127 (3) ◽  
pp. 377-382 ◽  
Author(s):  
J. A. Charlton ◽  
P. H. Baylis
Keyword(s):  
Atpase Activity ◽  
Arginine Vasopressin ◽  
Thick Ascending Limb ◽  
Stimulus Response ◽  
Spermine Synthase ◽  
Medullary Thick Ascending Limb ◽  
Henle's Loop ◽  
Specific Inhibitors ◽  
Stimulation Of

ABSTRACT Previous studies have indicated that ornithine decarboxylase (ODC) may be involved in the stimulation of Na+/K+-ATPase activity by arginine vasopressin (AVP) in the rat renal medullary thick ascending limb of Henle's loop. The present study was aimed at establishing the role of the polyamines, the conversion products of ODC activity, in the stimulation of Na+/K+-ATPase by AVP. Using cytochemical methods, we have demonstrated an increase in Na+/K+-ATPase activity after stimulation with putrescine, spermidine and spermine (each 1 mmol/l) for 2·5,2 and 1·5 min respectively. The specific inhibitors of spermidine and spermine synthase, bis-cyclohexylammonium sulphate and N-alkylated-1,3-diaminopropane respectively, inhibited the stimulation of Na+/K+-ATPase by AVP, this inhibition being reversed by spermine. These findings suggest that polyamines are involved in the stimulus-response coupling of the hormone-mediated response. Journal of Endocrinology (1990) 127, 377–382

scholarly journals Role of 20-HETE in mediating the effect of dietary K intake on the apical K channels in the mTAL

2001 ◽  
Vol 280 (2) ◽  
pp. F223-F230 ◽  
Author(s):  
Ruimin Gu ◽  
Yuan Wei ◽  
Houli Jiang ◽  
Michael Balazy ◽  
Wenhui Wang
Keyword(s):  
Gas Chromatography Mass Spectrometry ◽  
K Channel ◽  
Thick Ascending Limb ◽  
Patch Clamp Technique ◽  
Open Probability ◽  
Deficient Diet ◽  
K Channels ◽  
Medullary Thick Ascending Limb ◽  
High K

We have used the patch-clamp technique to study the effect of dietary K intake on the apical K channels in the medullary thick ascending limb (mTAL) of rat kidneys. The channel activity, defined by the number of channels in a patch and the open probability ( NP o), of the 30- and 70-pS K channels, was 0.18 and 0.11, respectively, in the mTAL from rats on a K-deficient diet. In contrast, NP o of the 30- and 70-pS K channels increased to 0.60 and 0.80, respectively, in the tubules from animals on a high-K diet. The concentration of 20-hydroxyeicosatetraenoic acid (20-HETE) measured with gas chromatography-mass spectrometry was 0.8 pg/μg protein in the mTAL from rats on a high-K diet and increased significantly to 4.6 pg/μg protein in the tubules from rats on a K-deficient diet. Addition of N-methylsulfonyl-12,12-dibromododec-11-enamide (DDMS) or 17-octadecynoic acid (17-ODYA), agents that inhibit the formation of 20-HETE, had no significant effect on the activity of the 30-pS K channels. However, DDMS/17-ODYA significantly increased the activity of the apical 70-pS K channel from 0.11 to 0.91 in the mTAL from rats on a K-deficient diet. In contrast, inhibition of the cytochrome P-450 metabolism of arachidonic acid increased NP o from 0.64 to 0.81 in the tubules from animals on a high-K diet. Furthermore, the sensitivity of the 70-pS K channel to 20-HETE was the same between rats on a high-K diet and on a K-deficient diet. Finally, the pretreatment of the tubules with DDMS increased NP o of the 70-pS K channels in the mTAL from rats on a K-deficient diet to 0.76. We conclude that an increase in 20-HETE production is involved in reducing the activity of the apical 70-pS K channels in the mTAL from rats on a K-deficient diet.

Regulation of renal Na-K-ATPase in the rat: effect of uninephrectomy

1986 ◽  
Vol 251 (3) ◽  
pp. F506-F512 ◽  
Author(s):  
S. K. Mujais ◽  
N. A. Kurtzman
Keyword(s):  
Enzyme Activity ◽  
Adrenal Gland ◽  
Atpase Activity ◽  
Thick Ascending Limb ◽  
Medullary Thick Ascending Limb ◽  
Collecting Tubule ◽  
Pars Recta ◽  
Intact Rats ◽  
Cortical Collecting Tubule

This study has examined the temporal profile and the segmental localization along the rat nephron of the increase in Na-K-ATPase produced by uninephrectomy, and the role of the adrenal gland in the generation of the increase in enzyme activity. In adrenal-intact rats, an increase in Na-K-ATPase activity in the cortical collecting tubule (CCT) was observed at 1 wk (140 +/- 13% of sham, P less than 0.05) and sustained at 2 wk (140 +/- 8% of sham, P less than 0.05). In contrast, the enhancement of enzyme activity in the proximal convoluted tubule (PCT) was transient (at 1 wk: 164 +/- 20% of sham, P less than 0.05; and at 2 wk: 97 +/- 9% of sham, P greater than 0.5). No changes in Na-K-ATPase activity were observed in the other nephron segments studied: pars recta, medullary thick ascending limb, cortical thick ascending limb, distal convoluted tubule, and medullary collecting tubule. In adrenalectomized rats, CCT enzyme activity was lower than in adrenal-intact rats (761 +/- 84 vs. 1,984 +/- 276 pmol X mm-1 X h-1, P less than 0.001) and was not altered by uninephrectomy (849 +/- 91 pmol X mm-1 X h-1, NS). We conclude that the increase in Na-K-ATPase activity following uninephrectomy is restricted to two segments of the nephron and follows a distinctive pattern in each. In the PCT a transient enhancement in enzyme activity is observed, whereas in the CCT the increase in Na-K-ATPase is sustained and requires the presence of an intact adrenal gland.

Transepithelial HCO3− absorption is defective in renal thick ascending limbs from Na+/H+ exchanger NHE1 null mutant mice

2004 ◽  
Vol 287 (6) ◽  
pp. F1244-F1249 ◽  
Author(s):  
David W. Good ◽  
Bruns A. Watts ◽  
Thampi George ◽  
Jamie W. Meyer ◽  
Gary E. Shull
Keyword(s):  
Rat Kidney ◽  
Basolateral Membrane ◽  
Thick Ascending Limb ◽  
Wild Type ◽  
Medullary Thick Ascending Limb ◽  
Transepithelial Voltage ◽  
Regulatory Defect ◽  
Null Mutant Mice

In the medullary thick ascending limb (MTAL) of rat kidney, inhibiting basolateral Na+/H+ exchange with either amiloride or nerve growth factor (NGF) results secondarily in inhibition of apical Na+/H+ exchange, thereby decreasing transepithelial HCO3− absorption. To assess the possible role of the Na+/H+ exchanger NHE1 in this regulatory process, MTALs from wild-type and NHE1 knockout (NHE1−/−) mice were studied using in vitro microperfusion. The rate of HCO3− absorption was decreased 60% in NHE1−/− MTALs (15.4 ± 0.5 pmol·min−1·mm−1 wild-type vs. 6.0 ± 0.5 pmol·min−1·mm−1 NHE1−/−). Transepithelial voltage, an index of the NaCl absorption rate, did not differ in wild-type and NHE1−/− MTALs. Basolateral addition of 10 μM amiloride or 0.7 nM NGF decreased HCO3− absorption by 45–49% in wild-type MTALs but had no effect on HCO3− absorption in NHE1−/− MTALs. Inhibition of HCO3− absorption by vasopressin and stimulation by hyposmolality, both of which regulate MTAL HCO3− absorption through primary effects on apical Na+/H+ exchange, were similar in wild-type and NHE1−/− MTALs. Thus the regulatory defect in NHE1−/− MTALs is specific for factors (bath amiloride and NGF) shown previously to inhibit HCO3− absorption through primary effects on basolateral Na+/H+ exchange. These findings demonstrate a novel role for NHE1 in transepithelial HCO3− absorption in the MTAL, in which basolateral NHE1 controls the activity of apical NHE3. Paradoxically, a reduction in NHE1-mediated H+ extrusion across the basolateral membrane leads to a decrease in apical Na+/H+ exchange activity that reduces HCO3− absorption.

Role of calcium in insulin-stimulated NaC1 transport in medullary thick ascending limb

1995 ◽  
Vol 269 (2) ◽  
pp. F236-F241 ◽  
Author(s):  
O. Ito ◽  
Y. Kondo ◽  
N. Takahashi ◽  
K. Omata ◽  
K. Abe
Keyword(s):  
Thick Ascending Limb ◽  
Dependent Manner ◽  
Tetraacetic Acid ◽  
Acetoxymethyl Ester ◽  
Maximal Inhibition ◽  
Nacl Transport ◽  
Medullary Thick Ascending Limb ◽  
Direct Measurements

It has been reported that insulin stimulates directly NaCl transport in the rabbit medullary thick ascending limb (MTAL) [O. Ito, Y. Kondo, N. Takahashi, K. Kudo, Y. Imai, K. Omata, and K. Abe. Am. J. Physiol. 267 (Renal Fluid Electrolyte Physiol. 36): F265-F270, 1994]. In the present investigation, we evaluated the role of Ca2+ in insulin-stimulated NaCl transport in rabbit MTAL by in vitro microperfusion methods. In control experiments, insulin increases transepithelial voltage (Vte) and net lumen-to-bath Cl-flux (JCl). The effects of insulin on Vte and JCl in a Ca2+ -free solution containing ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N' -tetraacetic acid did not differ from those in a Ca2+ -containing control solution. Direct measurements of cytosolic free Ca2+ ([Ca2+]i) with fura 2 fluorescence showed that insulin caused no detectable change in [Ca2+]i in MTAL cells. Chelation of intracellular Ca2+ with the acetoxymethyl ester of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid inhibited the actions of insulin in Vte and JCl without affecting basal values. We examined further whether calmodulin is also involved in insulin-stimulated NaCl transport in MTAL using two dissimilar inhibitors of calmodulin, trifluoperazine (TFP) and N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7). TFP and W-7 inhibited the action of insulin in a dose-dependent manner, with maximal inhibition of both agents of > 90%. The half-maximal inhibition by TFP and W-7 was approximately 50 and 100 microM, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Na-K-ATPase in nephron segments of rats developing spontaneous hypertension

1985 ◽  
Vol 249 (6) ◽  
pp. F863-F869 ◽  
Author(s):  
L. C. Garg ◽  
N. Narang ◽  
S. McArdle
Keyword(s):  
Enzyme Activity ◽  
Atpase Activity ◽  
Collecting Duct ◽  
Thick Ascending Limb ◽  
Spontaneously Hypertensive ◽  
Nephron Segments ◽  
Medullary Thick Ascending Limb ◽  
Abnormal Pattern ◽  
Wistar Kyoto

Na-K-ATPase activity was determined in seven specific nephron segments of 5- and 12-wk-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) controls. The enzyme activity in proximal convoluted tubule (PCT) and proximal straight tubule (PST) was significantly higher in 5-wk-old SHR than in WKY. However, Na-K-ATPase activity in medullary thick ascending limb (MTAL), cortical thick ascending limb (CTAL), and distal convoluted tubule (DCT) was significantly lower in 5-wk-old SHR than in WKY. There were no significant differences in the enzyme activity in PCT, PST, MTAL, CTAL, and DCT in 12-wk-old SHR and WKY. Furthermore, there were no significant differences in Na-K-ATPase activity in collecting duct segments of 5- or 12-wk-old SHR and age-matched WKY. The possible role of the abnormal pattern of Na-K-ATPase activity in PCT, PST, MTAL, CTAL, and DCT in 5-wk-old SHR in generation of hypertension in this strain remains to be determined.

Calcium signaling in cell volume regulation

1992 ◽  
Vol 72 (4) ◽  
pp. 1037-1061 ◽  
Author(s):  
N. A. McCarty ◽  
R. G. O'Neil
Keyword(s):  
Cell Volume ◽  
Volume Regulation ◽  
Cell Volume Regulation ◽  
Cell Types ◽  
Thick Ascending Limb ◽  
Medullary Thick Ascending Limb ◽  
Complex Process ◽  
Ehrlich Ascites ◽  
Cl Channels

It is evident from the present analysis that although a role for Ca2+ in controlling hypertonic cell volume regulation and RVI mechanisms has not been shown, Ca2+ plays a central role in activating and controlling hypotonic cell volume regulation and RVD mechanisms in most cells. However, this Ca2+ dependency is highly variable among cell types and tissues. Cells can be grouped into three general categories based on the relative dependency of RVD on Ca2+: 1) cells that are highly dependent on extracellular Ca2+ and the activation of Ca2+ influx, supposedly reflecting activation of Ca2+ channels, such as observed for the renal PST cells and osteosarcoma cells; 2) cells that are not dependent on extracellular Ca2+ and Ca2+ influx but that require at least a certain basal intracellular Ca2+ level or transient release of Ca2+ from internal stores, such as observed for the Ehrlich ascites tumor cells and medullary thick ascending limb cells; and 3) cells that display little if any Ca2+ dependency, such as the lymphocytes. There is initial evidence that this variable dependency of RVD on Ca2+ may reflect, in large part, a variable Ca2+ threshold of RVD processes, although this notion has not been fully investigated. The site and mechanism of Ca2+ dependency of RVD are poorly understood. Initial studies pointed to a possible direct control of K+ and/or Cl- channels by Ca2+ to modulate KCl efflux and, hence, RVD. This view appears to be too simplistic, however, as it is increasingly evident that the ion channels involved in RVD may not be directly Ca2+ dependent and that some other regulatory process controlling the channels, perhaps a phosphorylation step, may be the Ca(2+)-dependent event. Given the added complexity of the time-dependent variability of the action of Ca2+, i.e., the Ca2+ window, coupled with the variability of the RVD mechanisms among cell and tissue types, it is likely that the RVD mechanism is a highly complex process involving events and biochemical pathways throughout the cell rather than events simply localized to the inner face of the plasma membrane. It remains for future studies to determine the exact biochemical events that underly the RVD mechanism and its control, and the Ca2+ dependency of each step, before a full understanding will be attained of the role of Ca2+ in modulating RVD.

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