Direct measurement of sodium influx in vascular smooth muscle. Stimulation by aldosterone.

Menard, M. R.; Friedman, Sydney M.

doi:10.1161/01.hyp.7.6.873

Cited by 8 publications

(4 citation statements)

References 21 publications

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“…This is supported by the observations that both Na permeability and transport are increased in arteries after aldosterone or DOC administration (Garwitz &Jones 1982) and that aldosterone produces those changes in the artery in vitro within 24 h (Friedman 1982;Menard & Friedman 1985). However, under these circumstances [Nali was reported to be decreased or unchanged (Friedman 1982;Menard & Friedman 1985;Friedman & Tanaka 1987). The increased influx of Na into the smooth muscle cells of the incubated rat tail artery, stimulated increased active transport of Na via the Na,K pump, which was measured as increased Na efflux (Friedman 1982;Moura & Worcel 1984).…”

Section: Discussionmentioning

confidence: 80%

“…We propose that aldosterone increases cell membrane permeability to sodium, thereby increasing the influx of Na into cardiac and vascular smooth muscle cells. This is supported by the observations that both Na permeability and transport are increased in arteries after aldosterone or DOC administration (Garwitz &Jones 1982) and that aldosterone produces those changes in the artery in vitro within 24 h (Friedman 1982;Menard & Friedman 1985). However, under these circumstances [Nali was reported to be decreased or unchanged (Friedman 1982;Menard & Friedman 1985;Friedman & Tanaka 1987).…”

Section: Discussionmentioning

confidence: 80%

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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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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 80%

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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“…With the deoxycorticosterone/salt model, changes in arterial ion transport have been described even before hypertension is induced (33), and alterations in plasma volume and electrolyte composition occur. Mineralocorticoids have been reported to increase directly the transport of sodium in tail arteries (34). Angiotensin II has been shown to act directly on cultured vascular smooth muscle cells to induce changes in intracellular calcium and in Na+/H+ exchange (35,36).…”

Section: Discussionmentioning

confidence: 99%

Hypertension induces tissue-specific gene suppression of a fatty acid binding protein in rat aorta.

Sarzani

Claffey

Chobanian

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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The effect of hypertension on the expression of a fatty acid binding protein localized in the rat aorta was studied. The presence of rat heart fatty acid binding protein (hFABP) was documented in aortic tissue by using a cJDNA probe and polyclonal antibodies. Hypertension was induced in groups of rats by implantation of deoxycorticosterone acetate in conlunction with 1% salt in the drinking water (deoxycorticosterone/salt). By the third week of this treatment a marked reduction (by a factor of 20) in the expression of hFABP mRNA in aorta was found, concomitant with a reduction in immunologically detectable protein, suggesting transcriptional regulation. This effect was tissue specific, since no change in the normal amounts of hFABP mRNA in heart, skeletal muscle, or kidney was found. This reduction in aortic hFABP mRNA was also found in mildly hypertensive uninephrectomized rats given salt but no deoxycorticosterone and in normotensive rats given deoxycorticosterone but no excess 'salt intake. A marked decrease in aortic hFABP mRNA also was observed in the Goldblatt two kidney-one clip hypertensive model, and administration of angiotensin Il for 6 days by osmotic minipump also caused a reduction. These Findings suggest that hFABP is under complex regulation in aortic tissue and is suppressed by arterial hypertension.Hypertension is an important risk factor for all cardiovascular diseases, including stroke, myocardial infarction, peripheral vascular disease, and sudden death (1). However, relatively little information is available on the nature of the cellular responses to hypertension in the arterial wall and the biochemical mechanisms mediating those responses. In the aorta, hypertension has been shown to induce alterations in connective tissue metabolism (2), lysosomal enzymes (3),'ion transport (4), and fuel metabolism (5, 6). A variety of morphologic changes involving cellular components and extracellular matrix also have been described (7)(8)(9). A consistent cellular change has been an increase in medial smooth muscle cell mass, which, depending on the animal model used or the rate of onset and severity of hypertension, has been associated with either smooth muscle cell hyperplasia, hypertrophy, or polyploidy (10)(11)(12). With the exception of a recent study showing an increase in elastin mRNA in pulmonary arteries of calves with pulmonary hypertension (13), there have been no published papers on gene expression in vascular tissue obtained directly from hypertensive animal models.We previously reported the characteristics of a fatty acid binding protein (FABP) in rat heart (14-16). In the current work, we have identified this protein in rat aorta and studied the influence of different forms of hypertension on its expression. Heart fatty acid binding protein (hFABP) is one member ofa multigene family ofintracellular proteins located in the cytosol that specifically bind fatty acids, retinol, and several other organic anions (17, 18).

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“…This suggestion is based on two observations: 1) a transmembrane redistribution of Na and K consistent with increased permeability to Na is observable within 6 hours after the administration of DOCA-saline 29 and 2) aldosterone directly increases Na permeability in the incubated rat tail artery. 30 This sets in train an enhancement of protein synthetic activity, either as a direct action of the mineralocorticoid on nuclear DNA or as the indirect consequence of the increased presentation of Na to or suppression of the transport enzyme. 31 More protein is synthesized for transport, more for intrinsic cell functions, and more for export as paracellular matrix.…”

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confidence: 99%

Prehypertensive changes in sodium transport induced by deoxycorticosterone acetate in incubated rat tail artery.

Friedman¹,

McIndoe²,

Tanaka³

1986

Hypertension

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SUMMARY The transport and distribution of sodium, potassium, and water were examined in tail arteries of rats treated with deoxycorticosterone acetate (DOCA)-saline for 10 days, a time that marks the earliest onset of a rise of blood pressure in the strain (Wistar) used. The arteries were incubated for more than 20 hours to ensure that any change observed was sufficiently built in so that it could not readily be washed out. Three distinct changes were observed. First, the steady state transmembrane sodium gradient (operationally [NaVfNa],) was increased. Second, the amount of sodium excluded from participation in the sodium gradient, and hence probably bound, was increased. Third, after prolonged potassium depletion, the ouabain-insensitive loss of cell water and sodium that follows the readmittance of potassium was increased. These results suggest that fundamental embedded changes in sodium transport occur well before the blood pressure rises in response to DOCA-saline. (Hypertension 8: 592-599, 1986) KEY WORDS • hypertension deoxycorticosterone acetate sodium cell water vascular smooth muscle S TRUCTURAL changes have long been known to play an important role in the development and perhaps the initiation of the hypertensive process. 1 In general, only the physical aspects of these changes as they determine the geometry and hence the reactivity of the vascular wall have been denned. It is clear, however, that structural changes include the chemical configuration of the cell membrane and the cytoplasm and that, as determinants of ion permeability and distribution, these warrant equal consideration. Such changes should be sufficiently embedded to be discernible in the blood vessel maintained in vitro under artificial conditions. The present study was undertaken to examine this possibility insofar as it affects the transport and distribution of Na in the tail artery taken from rats treated with deoxycorticosterone acetate (DOCA)-saline for 10 days and incubated in various modified physiological salt solutions for 18 to 24 hours before analysis. Received April 16, 1985; accepted January 5, 1986. Materials and Methods Adult male rats of an inbred Wistar strain (Charles River Canada, Montreal, Quebec), weighing 300 g or more were used throughout in batches of 18 or 36 rats for each experiment. These batches were unilaterally nephrectomized under pentobarbitone sodium anesthesia; 3 to 7 days later, half of each batch was set aside as controls and half were injected subcutaneously with 0.5 ml of saline containing 12.5 mg of DOC A as a microcrystalline suspension. A second and third injection of 6.25 mg each were given on Days 4 and 7. Vehicle alone was administered to controls on the same schedule to ensure equal handling. The DOCAtreated rats were given 1 % saline as drinking water so that the effective agonist was the DOCA-saline combination. At the 1% level, saline alone has no significant eifect on blood pressure or on conventional indices of Na transport.

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Direct measurement of sodium influx in vascular smooth muscle. Stimulation by aldosterone.

Cited by 8 publications

References 21 publications

Digoxin Enhances the Pressor Response to Aldosterone Administration in Conscious Sheep

Digoxin Enhances the Pressor Response to Aldosterone Administration in Conscious Sheep

Hypertension induces tissue-specific gene suppression of a fatty acid binding protein in rat aorta.

Prehypertensive changes in sodium transport induced by deoxycorticosterone acetate in incubated rat tail artery.

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