scholarly journals Calcium transport by the luminal membrane of distal tubule: II. Effect of pH, electrical potential and calcium channel inhibitors

1992 ◽  
Vol 41 (2) ◽  
pp. 289-296 ◽  
Author(s):  
Michèle G. Brunette ◽  
Johanne Mailloux ◽  
Daniel Lajeunesse
Keyword(s):  
Calcium Channel ◽  
Calcium Transport ◽  
Electrical Potential ◽  
Distal Tubule ◽  
Effect Of Ph ◽  
Luminal Membrane ◽  
Calcium Channel Inhibitors

scholarly journals Calcium transport through the luminal membrane of the distal tubule. I. Interrelationship with sodium

1992 ◽  
Vol 41 (2) ◽  
pp. 281-288 ◽  
Author(s):  
Michele G. Brunette ◽  
Johanne Mailloux ◽  
Daniel Lajeunesse
Keyword(s):  
Calcium Transport ◽  
Distal Tubule ◽  
Luminal Membrane

Characterization of three types of calcium channel in the luminal membrane of the distal nephron

2004 ◽  
Vol 82 (1) ◽  
pp. 30-37 ◽  
Author(s):  
M G Brunette ◽  
M Leclerc ◽  
D Couchourel ◽  
J Mailloux ◽  
Y Bourgeois
Keyword(s):  
Calcium Transport ◽  
Distal Tubule ◽  
Distal Nephron ◽  
High Affinity ◽  
Luminal Membrane ◽  
Kinetics Of ◽  
Substrate Concentrations ◽  
Renal Calcium Transport ◽  
Specific Inhibitors

We previously reported a dual kinetics of Ca2+ transport by the distal tubule luminal membrane of the kidney, suggesting the presence of several types of channels. To better characterize these channels, we examined the effects of specific inhibitors (i.e., diltiazem, an L-type channel; ω-conotoxin MVIIC, a P/Q-type channel; and mibefradil, a T-type channel antagonist) on 0.1 and 0.5 mM Ca2+ uptake by rabbit nephron luminal membranes. None of these inhibitors influenced Ca2+ uptake by the proximal tubule membranes. In contrast, in the absence of sodium (Na+), the three channel antagonists decreased Ca2+ transport by the distal membranes, and their action depended on the substrate concentrations: 50 µM diltiazem decreased 0.1 mM Ca2+ uptake from 0.65 ± 0.07 to 0.48 ± 0.06 pmol·µg–1·10 s–1 (P < 0.05) without influencing 0.5 mM Ca2+ transport, whereas 100 nM ω-conotoxin MVIIC decreased 0.5 mM Ca2+ uptake from 1.02 ± 0.05 to 0.90 ± 0.05 pmol·µg–1·10 s–1 (P < 0.02) and 1 µM mibefradil decreased it from 1.13 ± 0.09 to 0.94 ± 0.09 pmol·µg–1·10 s–1 (P < 0.05); the latter two inhibitors left 0.1 mM Ca2+ transport unchanged. Diltiazem decreased the Vmax of the high-affinity channels, whereas ω-conotoxin MVIIC and mibefradil influenced exclusively the Vmax of the low-affinity channels. These results not only confirm that the distal luminal membrane is the site of Ca2+ channels, but they suggest that these channels belong to the L, P/Q, and T types.Key words: renal calcium transport, calcium channels, diltiazem, mibefradil, ω-conotoxin.

scholarly journals Neuronal calcium channel inhibitors. Synthesis of omega-conotoxin GVIA and effects on 45Ca uptake by synaptosomes.

1987 ◽  
Vol 262 (3) ◽  
pp. 1194-1198
Author(s):  
J Rivier ◽  
R Galyean ◽  
W R Gray ◽  
A Azimi-Zonooz ◽  
J M McIntosh ◽  
...  
Keyword(s):  
Calcium Channel ◽  
45Ca Uptake ◽  
Calcium Channel Inhibitors ◽  
Neuronal Calcium Channel

Prolactin stimulates the L-type calcium channel-mediated transepithelial calcium transport in the duodenum of male rats

2013 ◽  
Vol 430 (2) ◽  
pp. 711-716 ◽  
Author(s):  
Nitita Dorkkam ◽  
Kannikar Wongdee ◽  
Panan Suntornsaratoon ◽  
Nateetip Krishnamra ◽  
Narattaphol Charoenphandhu
Keyword(s):  
Calcium Channel ◽  
Calcium Transport ◽  
Male Rats

Effects of flow rate and potassium intake on distal tubular potassium transfer

1975 ◽  
Vol 228 (4) ◽  
pp. 1249-1261 ◽  
Author(s):  
RN Khuri ◽  
WN Strieder ◽  
G Giebisch
Keyword(s):  
Flow Rate ◽  
Electrical Potential ◽  
Isotonic Saline ◽  
Distal Tubule ◽  
Sodium Reabsorption ◽  
Electrical Potential Difference ◽  
High Potassium ◽  
Flow Rates ◽  
Potassium Intake ◽  
Potassium Secretion

Potassium transport was studied across proximal and distal tubular epithelium in rats on a normal, low- and high-potassium intake during progressive loading with isotonic saline (150 mM) or a moderately hypersomotic urea (200 mM) sodium chloride (100 mM) solution. Free-flow micropuncture and recollection techniques were used during the development of diruesis and tubular fluid (TF) analyzed for inulin-14C, potassium (K) and sodium (Na). Tubular puncture sites were localized by neoprene filling and microdissection. During the large increase in tubular flow rates (10 times): 1) fractional potassium reabsorption fell along the proximal tubule, 2) TFk along the distal tubule remained constant and independent of flow rate in control and high-k rats; thus, net potassium secretion increased in proportion to and was limited by flow rate. 3) In low-K rats TF k fell; with increasing flow rates distal K secretion was not effectively stimulated. 4) Distal tubular sodium reabsorption increased in all animals with flow rate, but tubular Na-K exchange ratios varied greatly. It is suggested that whenever sodium delivery stimulates distal tubular potassium secretion it does so by 1) increasing volume distal tubular potasssium secretion and by 2) augmenting the transepithelial electrical potential difference (lumen negative).

Luminal influences on potassium secretion: chloride, sodium, and thiazide diuretics

1992 ◽  
Vol 262 (6) ◽  
pp. F1076-F1082 ◽  
Author(s):  
H. Velazquez ◽  
D. H. Ellison ◽  
F. S. Wright
Keyword(s):  
Distal Tubule ◽  
Distal Convoluted Tubule ◽  
Thiazide Diuretics ◽  
Maximal Level ◽  
Luminal Membrane ◽  
K Secretion ◽  
Potassium Secretion

In the presence of Cl-, K+ secretion by the distal tubule saturates with increasing luminal Na+ concentration. Apparent maximal K+ secretion is attained with luminal Na+ concentrations of 40 mM. The results of the present study show that lowering the Cl- concentration of luminal fluid can increase the level of Na(+)-stimulated K+ secretion beyond the maximal level attained in the presence of Cl-. The effect of lowering luminal Cl- concentration to less than 10 mM on K+ secretion is greater with higher Na+ concentration. Under these conditions, chlorothiazide decreases K+ secretion. When chlorothiazide is present, changing the Na+ concentration does not affect K+ secretion. Because in rats a thiazide effect is attributed primarily to the distal convoluted tubule (DCT), we postulate that it is primarily DCT cells that increase K+ secretion when Na+ concentration is raised in the presence of low luminal Cl- concentration. We propose that the rat DCT cells have both an absorptive Na(+)-Cl- cotransport mechanism and a secretory K(+)-Cl- cotransport mechanism in the luminal membrane that can mediate the apparent exchange of Na+ for K+.

Studies of the urinary acidification defect induced by lithium

1982 ◽  
Vol 242 (1) ◽  
pp. F23-F29 ◽  
Author(s):  
N. Bank ◽  
P. D. Lief ◽  
H. S. Aynedjian ◽  
B. F. Mutz
Keyword(s):  
Proximal Tubule ◽  
Renal Tubular Acidosis ◽  
Electrical Potential ◽  
Distal Renal Tubular Acidosis ◽  
Distal Nephron ◽  
Luminal Membrane ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Convoluted Tubules

Experiments were carried out in rats and isolated turtle bladders to study the defect in H+ transport induced by LiCl. After 3-4 days of intraperitoneal LiCl, rats developed urinary findings of "distal" renal tubular acidosis. Proximal tubular fluid pH measured in situ by glass microelectrodes was higher in lithium-treated rats than in acidotic controls. Proximal fluid total CO2 [tCO2] was also higher, and the fraction of tCO2 leaving the proximal tubule was 14 vs. 7% (P less than 0.001). Impaired acidification was also apparent beyond distal convoluted tubules, as judged by normal distal tCO2 reabsorption but increased HCO3(-) in the urine. During NaHCO3 loading, the proximal defect was ameliorated but not the distal. Turtle bladder studies showed that mucosal lithium inhibits H+ secretion secondary to reducing transepithelial electrical potential, presumably by hyperpolarization of the luminal membrane. A similar mechanism may be responsible for lithium's effect on the distal nephron. Inhibition of proximal tubular HCO3(-) reabsorption is probably not attributable to electrical potential changes but might be due to interference of luminal membrane Na+ entry by Li+ and reduced (Na+ + Li+)-H+ exchange.

Stimulation of distal potassium secretion by low lumen chloride in the presence of barium

1985 ◽  
Vol 248 (5) ◽  
pp. F638-F649 ◽  
Author(s):  
D. H. Ellison ◽  
H. Velazquez ◽  
F. S. Wright
Keyword(s):  
Chloride Concentration ◽  
Distal Tubule ◽  
Perfusion Fluid ◽  
Transport Pathway ◽  
Luminal Membrane ◽  
Potassium Secretion ◽  
Transepithelial Voltage ◽  
Tubule Fluid ◽  
Stimulation Of

Potassium secretion into the renal distal tubule is increased when chloride in the tubule fluid is replaced by another anion. The present experiments were done to determine whether this increment in transported potassium traverses a conductive pathway from cell to lumen. Transport rates of potassium, sodium, chloride, and fluid by the renal distal tubule of rats were examined in vivo by continuous microperfusion. The effects of substituting gluconate for chloride in the presence and absence of 5 mM barium in the perfusion fluid were determined. When gluconate replaced chloride in the perfusion solutions, potassium secretion increased (by 44%) without a significant change in transepithelial voltage. Barium in the lumen increased the magnitude of the lumen-negative transepithelial voltage (by 30%) and reduced potassium secretion (by 56%) by inhibiting conductive potassium movement. Barium also decreased both sodium (by 51%) and chloride (by 37%) absorption. Barium did not reduce the stimulation of potassium secretion caused by reducing lumen chloride concentration. Potassium secretion increased (by 77%) when lumen chloride was reduced in the presence of 5 mM barium. We interpret these results by postulating that a cotransport mechanism linking potassium and chloride is present in the luminal membrane of distal tubule cells, that this mechanism operates in parallel with a conductive transport pathway for potassium, and that the K-Cl cotransport mechanism is not inhibited by barium.

Effects of calcium channel inhibitors on the hypothermic response to oxotremorine in normo and hypercholinergic rats

1991 ◽  
Vol 43 (6) ◽  
pp. 436-439 ◽  
Author(s):  
OLGIERD PUCILOWSKI ◽  
DAVID H. OVERSTREET ◽  
AMIR H. REZVANI ◽  
DAVID S. JANOWSKY
Keyword(s):  
Calcium Channel ◽  
Hypothermic Response ◽  
Calcium Channel Inhibitors

Two New Classes of T-Type Calcium Channel Inhibitors with New Chemical Scaffolds from Ganoderma cochlear

2015 ◽  
Vol 17 (12) ◽  
pp. 3082-3085 ◽  
Author(s):  
Feng-Jiao Zhou ◽  
Yin Nian ◽  
Yongming Yan ◽  
Ye Gong ◽  
Qi Luo ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Inhibitors
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