Stimulation of Na+,K+-ATPase of isolated smooth muscle membranes by the Ca2+ channel inhibitors, nimodipine and nitrendipine

Pan, Mary; Janis, R.A.

doi:10.1016/0006-2952(84)90463-5

Cited by 46 publications

(10 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…We have found no effect of 1 • 10 3 M diltiazem on Ca,Mg-ATPase activity of plasma membrane-enriched fractions prepared from bovine corneal epithelium (data not shown). Variable effects of these agents have been reported on Na,KATPase activity including no change as well as stimulation of pump activity (Murphy et al, 1982;Pan & Janis, 1984). Verapamil also has been reported to inhibit K influx and efflux in cardiac Purkinje fibers (Posner et al, 1975).…”

Section: Discussionmentioning

confidence: 99%

Mechanism of inhibition of net ion transport across frog corneal epithelium by calcium channel antagonists

Huff

Reinach

1985

J. Membrain Biol.

View full text Add to dashboard Cite

In the isolated bullfrog cornea, three calcium channel antagonists had dose-dependent inhibitory effects on the Cl-originated short-circuit current (SCC). Their order of decreasing potency was bepridil, verapamil and diltiazem. One millimolar diltiazem inhibited the SCC by 98% and subsequent incubation with the calcium ionophore A23187 had no restorative effect. Increasing the bathing solution Ca concentration from 0.05 to 15 mM, however, decreased diltiazem's inhibitory efficacy. This antagonist depolarized the intracellular potential difference Vsc from -54 to -18 mV (tear:reference) and the voltage divider ratio FRo decreased from 0.58 to 0.30, suggesting an increase in basolateral membrane electrical resistance. Additional indication of a basolateral membrane effect by the drug was that preincubation with 10(-5) M amphotericin B in Cl-free Ringer's did not eliminate the inhibitory effect of the drug on the Na- and K-elicited SCC. In the absence of amphotericin B in Cl-free Ringer's (SCC = 0), 1 X 10(-3) M diltiazem depolarized the Vsc from -78 to -9 mV suggesting that the increase in basolateral membrane resistance was due to K channel blockade. Diltiazem (1 X 10(-3) M) significantly decreased cyclic AMP content; however, isoproterenol in the presence of the drug increased cyclic AMP fourfold without having any restorative effect on the inhibited SCC. Therefore, the inhibition of the Cl-originated SCC resulting from an increase in basolateral membrane K resistance is not caused by a decline in cyclic AMP content.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Section: Discussionmentioning

confidence: 99%

Mechanism of inhibition of net ion transport across frog corneal epithelium by calcium channel antagonists

Huff

Reinach

1985

J. Membrain Biol.

View full text Add to dashboard Cite

show abstract

“…It is unlikely that an increase in activity and gene expression of Na + ‐K + ‐ATPase was as a result of an increase in the blood pressure, low plasma potassium level or acid–base disturbance as both pre‐ and postadrenalectomy groups had these parameters comparable to those of the control group. In addition, it is unlikely that the changes observed were because of the use of antihypertensive agents as both nifedipine and hydralazine have been shown to have no effect on Na + ‐K + ‐ATPase subunits in the cardiac muscles of rats, 23 and nifedipine has no effect on Na + ‐K + ‐ATPase activity in isolate smooth muscle membranes from rat aorta 24 . However, we cannot totally exclude the possibility that these drugs might have some effects on skeletal muscle Na + ‐K + ‐ATPase activity.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone increases Na+-K+-ATPase activity in skeletal muscle of patients with Conn’s syndrome

Phakdeekitcharoen¹,

Kittikanokrat²,

Kijkunasathian³

et al. 2011

Clinical Endocrinology

View full text Add to dashboard Cite

show abstract

“…Kidwai [6] has demon strated that Na+ and K+ did not stimulate magnesium-dependent ATPase activity of mitochondria and endoplasmic reticulum lOpmol Pi/mg protein/h of Na,K-ATPase activity from bovine aorta, and Wolowyk et al [4] about 21 pmol Pi/mg protein/h for the rabbit aorta in the presence of a nonenzymatic factor remaining in the supernatant fraction after 10,000-g centrifugation. Re cently, Pan and Janis [32] have also demon strated about 19 pmol Pi/mg protein/h of Na,K-ATPase activity of rat aortic microsomes. In the present experiments, the mag nitude of the Na,K-ATPase activity of the sarcolemma-enriched fraction of bovine aorta was also similar to that for the cardiac muscle cell.…”

Section: Discussionmentioning

confidence: 99%

Characterization of Membrane-Bound Adenosinetriphosphatase Activity of Sarcolemma-Enriched Fraction from Vascular Smooth Muscle

Takeo¹,

Sakanashi²

1985

Enzyme

View full text Add to dashboard Cite

Membrane-bound adenosinetriphosphatase (ATPase) activities of the sarcolemma- enriched fraction from bovine aorta were characterized. The membranes, isolated by a sucrose density gradient method, were enriched about 31-fold in sodium- and potassiumstimulated, magnesium-dependent ATPase (Na,K-ATPase) activity, and about 8-fold in 5'- nucleotidase activity compared to the homogenate, suggesting that the isolated membranes were substantially enriched with the sarcolemma. The membranes exhibited about 31, 33 and 42 μmol Pi/mg protein/h of Na,K-ATPase, magnesium-dependent ATPase and calciumdependent ATPase activities, respectively, in the presence of 4 mmol/1 ATP. The sarcolemmaenriched membranes required considerably high concentrations of well-known inhibitors for Na,K-ATPase such as vanadate (more than 1 μmol/1), lanthanum (more than 1 mmol/1) and calcium (10 mmol/1), to induce a significant inhibition in the Na,K-ATPase activity. Treatments of the membrane with physical disruptions and sodium dodecyl sulfate or deoxycholate reduced the total Na,K-ATPase activity, and did not expose fully the ouabain sensitivity of the Na,K-ATPase. These results indicate that there are marked differences in the properties of the ATPase between vascular smooth muscle sarcolemma and cardiac sarcolemma.

show abstract

Stimulation of Na+,K+-ATPase of isolated smooth muscle membranes by the Ca2+ channel inhibitors, nimodipine and nitrendipine

Cited by 46 publications

References 20 publications

Mechanism of inhibition of net ion transport across frog corneal epithelium by calcium channel antagonists

Mechanism of inhibition of net ion transport across frog corneal epithelium by calcium channel antagonists

Aldosterone increases Na+-K+-ATPase activity in skeletal muscle of patients with Conn’s syndrome

Characterization of Membrane-Bound Adenosinetriphosphatase Activity of Sarcolemma-Enriched Fraction from Vascular Smooth Muscle

Contact Info

Product

Resources

About