Altered contractility of urinary bladder in diabetic rabbits: relationship to reduced Na+ pump activity

1996 ◽  
Vol 271 (6) ◽  
pp. C2045-C2052 ◽  
Author(s):  
S. Gupta ◽  
S. Yang ◽  
R. A. Cohen ◽  
R. J. Krane ◽  
I. Saenz De Tejada
Keyword(s):  
Smooth Muscle ◽  
Muscle Tone ◽  
Bladder Smooth Muscle ◽  
Na Pump ◽  
A 23187 ◽  
Normal Bladder ◽  
Diabetic Rabbit ◽  
Pump Activity ◽  
Diabetic Rabbits ◽  
Ionophore Monensin

We studied the effect of alloxan-induced diabetes on Na+ pump activity in isolated rabbit bladder strips. In addition, the effects of diabetes and the Na+ pump inhibitor ouabain on contractions induced by carbachol (CCh) and KCl were studied. In bladder strips from diabetic rabbits, ouabain-sensitive 86Rb+ uptake (a measure of Na+ pump activity) was approximately 50% less compared with strips from normal bladder. Diabetes also reduced the maximum contractions induced by CCh and KCl. Treatment of bladder strips with ouabain alone caused an acute concentration-dependent increase in tone. In contrast, longer incubation with ouabain inhibited CCh- and KCl-induced contractions in normal and diabetic bladders. Furthermore, differences in agonist-mediated contractions observed between normal and diabetic bladders were abolished in the presence of the maximally effective concentration of ouabain (10 microM). The ability of CCh to cause contraction in normal and diabetic rabbit bladders was also significantly inhibited by the Na+ ionophore monensin but not by the Ca2+ ionophore A-23187 or by depolarization with KCl. Monensin also inhibited KCl-induced contractions in normal bladder strips. These results indicate that 1) Na+ pump activity is an important modulator of bladder smooth muscle tone, 2) diabetes diminishes Na+ pump activity and inhibits agonist-induced contractions in bladder, and 3) an increase in intracellular Na+ concentration, secondary to inhibition of bladder smooth muscle Na+ pump activity, is associated with reduced responsiveness to contractile agonists. Diminished Na+ pump activity in diabetes may, in part, contribute to the development of bladder cystopathy.

Reduced Na(+)-K+ pump activity in diabetic rabbit carotid artery: reversal by aldose reductase inhibition

1993 ◽  
Vol 265 (4) ◽  
pp. H1189-H1194 ◽  
Author(s):  
B. Tesfamariam ◽  
S. Gupta ◽  
P. J. Oates ◽  
N. B. Ruderman ◽  
R. A. Cohen
Keyword(s):  
Carotid Artery ◽  
Aldose Reductase ◽  
Group Treatment ◽  
Carotid Arteries ◽  
Diabetic Group ◽  
Free Solution ◽  
Na Pump ◽  
Diabetic Rabbit ◽  
Pump Activity ◽  
Diabetic Rabbits

This study addresses the question of whether a decrease in basal Na+ pump [Na(+)-K(+)-adenosinetriphosphatase (ATPase)] activity occurs in the carotid artery of an alloxan-diabetic rabbit and, if so, whether it is associated with altered 86Rb+ uptake and contractile response to ouabain and K(+)-free solution. Ouabain-sensitive 86Rb+ uptake, an index of Na+ pump activity, was diminished approximately 50% in carotid arteries from diabetic rabbits. Concurrent with this, contractions induced by incubating the carotid arteries in a K(+)-free solution (in the absence of phentolamine) were significantly larger in the diabetic group. Readdition of K+ (1 mM) to arteries contracted with the K(+)-free solution caused relaxations that were slower to occur and of lesser magnitude in diabetic than in control rabbits. In contrast to the contractions caused by the K(+)-free medium, contractions caused by incubation with ouabain (1 mM) in the presence of phentolamine were significantly smaller in the diabetic group. Treatment of diabetic rabbits with an aldose reductase inhibitor, zopolrestat, at both high and low doses restored the alterations in vascular reactivity toward normal. The results indicate that the Na+ pump activity is diminished in the carotid artery of diabetic rabbit, and this is associated with abnormal vascular responsiveness and increased polyol pathway flux.

Na+-K+ regulation in cultured vascular smooth muscle cell of the spontaneously hypertensive rat

1986 ◽  
Vol 250 (6) ◽  
pp. C939-C947 ◽  
Author(s):  
H. Tamura ◽  
L. Hopp ◽  
M. Kino ◽  
A. Tokushige ◽  
B. M. Searle ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Vascular Smooth Muscle Cells ◽  
Rate Constants ◽  
Washout Rate ◽  
Spontaneously Hypertensive ◽  
Na Pump ◽  
Deficient Medium ◽  
Pump Activity ◽  
Na Uptake

Na+-K+ passive transport and activity of the Na+ pump were examined in serially passed cultured vascular smooth muscle cells originating from spontaneously hypertensive (SH), Wistar-Kyoto (WKY), and Wistar (W) rats. Measurements included 22Na+ and 86Rb+ (K+ analogue) uptake and washout rate constants as well as intracellular Na+ and K+ levels. The aforementioned variables were studied in cells subjected to either 2 mM Ca2+ or Ca2+-deficient media. In 2 mM Ca2+ medium, SH rat cells demonstrated the highest exchange (uptake and washout) rate constants for Na+ and Rb+ (K+) among cells of the three rat strains. At this extracellular Ca2+ concentration, the Na+ pump activity of SH rat cells was higher than that of WKY rat cells and was not different from that of W rat cells. Incubation in Ca2+-deficient medium resulted in increased magnitudes of Rb+ washout and Na+ uptake rate constants in all cell preparations associated with elevated intracellular Na+ concentrations and augmented activity of the Na+ pump. Under this condition, cells derived from SH rats showed the highest Na+ uptake and Rb+ washout rate constants associated with the highest Na+ pump activity. The increase in intracellular Na+ level in Ca2+-deficient medium was the highest in SH rat cells. These findings show that innate membrane defects and the response of the Na+ pump to these abnormalities can be demonstrated in in vitro-grown vascular smooth muscle cells of the SH rat.

Effect of short-term cyclic stretch on sodium pump activity in aortic smooth muscle cells

2001 ◽  
Vol 281 (5) ◽  
pp. H2072-H2078 ◽  
Author(s):  
Emel Songu-Mize ◽  
Nancy Sevieux ◽  
Xiang Liu ◽  
Mary Jacobs
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cyclic Stretch ◽  
Short Term ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Na Pump ◽  
Baseline Activity ◽  
Pump Activity

We previously demonstrated that expression of both the α1- and α2-subunits of Na+-K+-ATPase is elevated after a 2- to 4-day cyclic stretch in aortic smooth muscle cells. In this study, we determined the effect of short-term (2–30 min) cyclic stretch on the activity of the Na pump and investigated possible mechanisms that may be involved in the action of stretch. Na pump activity was significantly increased above the baseline activity between 2 and 30 min of stretch. This effect of stretch was reversible within 1 h. Intracellular Na was also elevated at corresponding time points. Blocking the entry of Na with Gd and amiloride did not affect the stretch-induced increase in Na pump activity. Inhibition of protein kinase A (PKA) activity attenuated the effect of stretch on the Na pump. Furthermore, inhibition of polymerization of actin and phosphatidylinositol 3-kinase (PI3K) activity prevented the action of stretch on Na pump activity. We conclude that the stimulation of the Na pump in response to cyclic stretch requires the integrity of the actin cytoskeleton as well as the activity of PI3K, which has a role in intracellular vesicular trafficking. PKA may also be involved in this effect of stretch on Na pump.

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