Relationship of vascular sodium-potassium pump activity to intracellular sodium in hypertensive rats.

Brock, Tommy A.; Smith, Jeffrey B.; Overbeck, Henry W.

doi:10.1161/01.hyp.4.3_pt_2.43

Cited by 15 publications

(4 citation statements)

References 27 publications

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“…These relaxation responses are blocked by ouabain and by K +free solution. These observations, along with those of Brock et al, (1982), suggest that the results that we have observed with the dog LAD may be a generalized effect of monensin on vascular smooth muscle.…”

Section: Discussionsupporting

confidence: 82%

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Mechanism of canine coronary artery relaxation by monensin.

Anderson

Winquist

Webb³

et al. 1983

Circulation Research

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Monensin is a monocarboxylic sodium ionophore which causes increased myocardial contractility and increased coronary blood flow in the anesthetized dog. The current experiment investigated the mechanism by which monensin produces relaxation of smooth muscle from the canine coronary artery. Helical strips of coronary artery were mounted in a muscle chamber and made to contract by stimulation with 5-hydroxytryptamine. First, concentration-response curves were established for the relaxant effect of added monensin. Then the following agents were evaluated for their effects on the monensin-induced inhibition of contraction to 5-hydroxytryptamine: aminophylline, indomethacin, propranolol, ouabain, and a potassium-free solution. Finally, the effect of added monensin on potassium-induced relaxation of denervated coronary artery strips was used to further characterize this relaxant effect. The results demonstrate that monensin causes coronary smooth muscle relaxation at the same concentrations reported to cause a positive inotropic effect in isolated myocardial preparations. The monensin-induced inhibition of contraction of the isolated coronary artery was not blocked by aminophylline, propranolol, or indomethacin, demonstrating that the inhibition is not mediated by adenosine, by /3-adrenergic receptors, or by prostaglandins. The inhibition of coronary smooth muscle contraction was completely blocked by ouabain or by a potassium-free solution. Monensin also potentiated potassiuminduced relaxation of both innervated and denervated coronary artery strips; both the potassiuminduced relaxation and the potentiation of this relaxation by monensin were ouabain-blocked. We conclude that monensin produces coronary relaxation by stimulation of Na + ,K + -ATPase. This stimulation may result from a monensin-induced increase in intracellular sodium ion concentration similar to the change that, paradoxically, mediates the positive inotropic effect in the myocardium. (CircRes 53: 168-175, 1983)

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Section: Discussionsupporting

confidence: 82%

“…Ouabain blocked the hyperpolarization in both experiments. Recently Brock et al (1982) have measured Na + ,K + -ATPase activity in rat aorta using the ouabain-sensitive ^Rb" 1 " uptake method. They found that monensin increased 86 Rb + uptake in rat aortic smooth muscle by increasing total cell sodium.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of canine coronary artery relaxation by monensin.

Anderson

Winquist

Webb³

et al. 1983

Circulation Research

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“…1980;Songu-Mize el al. 1982), increased (Friedman & Nakashima 1978;Brock et al 1982) and others have found no change (Stern et al 1984) in vascular Na,K ATPase activity. Stern et al ( 1 984) have suggested that these conflicting data probably reflect the opposing effects of sodium loading induced inhibition of Na,K ATPase activity and DOCAmediated stimulation of the enzyme.…”

Section: Discussionmentioning

confidence: 89%

Digoxin Enhances the Pressor Response to Aldosterone Administration in Conscious Sheep

Spence

Coghlan

Whitworth

et al. 1989

Clin Exp Pharma Physio

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1. This study examined the hypothesis that inhibition of Na,K ATPase with digoxin would enhance the pressor response to aldosterone infusion in conscious sheep. 2. While intravenous infusion of digoxin (10 micrograms/kg per day for 5 days) had no effect on blood pressure and aldosterone infusion (6 micrograms/kg per day for 5 days) increased blood pressure by 7 mmHg, combined infusion of digoxin and aldosterone increased blood pressure by 17 mmHg. 3. The metabolic effects of the combined digoxin and aldosterone infusion were similar to those for aldosterone alone, suggesting that digoxin did not enhance the mineralocorticoid action of aldosterone. 4. The results of this study suggest that changes in Na influx (aldosterone-dependent) and efflux (digoxin-dependent) are important in the genesis of aldosterone-induced hypertension.

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“…Increasing intracellular Ca2+ was recently shown to augment passive Na+ influx in cultured human fibroblasts and MDCK cells (Rindler et al, 1979;Villereal, 1981). An increase in Na+ influx in turn increases Na+/K+ pump activity, as was recently shown with Na+ ionophores in both cultured cells and intact arterial tissue (Smith and Rozengurt, 197813;Brock and Smith, 1982;Brock et al, 1982a). The stimulation of the pump would be expected to hyperpolarize the cell membrane, which might help to reestablish the Na+ gradient.…”

Section: Discussionmentioning

confidence: 78%

Analysis of angiotensin‐stimulated sodium transport in cultured smooth muscle cells from rat aorta

Smith

Brock

1983

Journal Cellular Physiology

129

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Angiotensin peptides (AI, AII, AIII) increased the rate of Na+ accumulation by smooth muscle cells (SMC) cultured from rat aorta. The stimulatory effect of AII on Na+ uptake was observed when Na+ exodus via the Na+/K+ pump was blocked either by ouabain or by the removal of extracellular K+. AII was at least ten times more potent than AIII and about 100 times more potent than AI in stimulating Na+ uptake. Saralasin had little effect on Na+ uptake by itself but almost completely blocked the increase caused by AII. The stimulation of net Na+ entry by AI, but not AII, was prevented by protease inhibitors. The stimulation of Na+ uptake was almost completely blocked by amiloride. Tetrodotoxin, which prevented veratridine from increasing Na+ uptake, had no effect on the response to AII. Angiotensin increased the rate of ouabain-sensitive 86Rb+ uptake (Na+/K+ pump activity) but had no effect on ouabain-sensitive ATPase activity in frozen-thawed SMC or in microsomal membranes isolated from cultured SMC. The stimulation of ouabain-sensitive 86Rb+ uptake by AII was blocked by saralasin. Omitting Na+ from the external medium prevented AII from increasing 86Rb+ uptake. AII had no effect on cell volume or cyclic AMP levels in the cultured SMC. These results suggest that angiotensin peptides activate an amiloride-sensitive Na+ transporter which supplies the Na+/K+ pump with more Na+, its rate-limiting substrate.

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Relationship of vascular sodium-potassium pump activity to intracellular sodium in hypertensive rats.

Cited by 15 publications

References 27 publications

Mechanism of canine coronary artery relaxation by monensin.

Mechanism of canine coronary artery relaxation by monensin.

Digoxin Enhances the Pressor Response to Aldosterone Administration in Conscious Sheep

Analysis of angiotensin‐stimulated sodium transport in cultured smooth muscle cells from rat aorta

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