Kinetics of active sodium transport in aortas from control and deoxycorticosterone hypertensive rats.

Jones, Allan W.

doi:10.1161/01.hyp.3.6.631

Cited by 49 publications

(15 citation statements)

References 30 publications

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“…18 " 21 However, changes in red blood cell cation transports in response to mineralocorticoid treatment have not been as extensively studied. Duhm et al 22 described enhanced sodium and rubidium diffusional leaks in deoxycorticosterone enanthate NaCl hypertensive rat erythrocytes but did not assess lithium movements.…”

Section: Discussionmentioning

confidence: 99%

Erythrocyte lithium transport changes induced by deoxycorticosterone acetate treatment in pigs.

Weder¹,

Torretti

1985

Hypertension

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Section: Discussionmentioning

confidence: 99%

Erythrocyte lithium transport changes induced by deoxycorticosterone acetate treatment in pigs.

Weder¹,

Torretti

1985

Hypertension

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“…Increased permeability and sodium transport have been described in blood vessels maintained in artificial media. 29 '…”

Section: Discussionmentioning

confidence: 99%

Rat thymocyte sodium transport. Effects of changes in sodium balance and experimental hypertension.

Bradlaugh¹,

Heagerty²,

Bing³

et al. 1984

Hypertension

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SUMMARY The wide range of membrane electrolyte transport abnormalities associated with experimental, genetic, and essential hypertension may either reflect an underlying global change in the cell membrane or may be directly related to the underlying disturbance that causes hypertension or to changes in sodium balance. To investigate this further, we studied sodium transport and intracellular electrolyte composition in the thymocytes of normal rats undergoing salt loading or depletion, and in rats with renovascular, mineralocorticoid, or spontaneous hypertension compared to appropriate age-matched normotensive control rats. In normotensive rats, although there was no significant difference between the blood pressures at the two extremes of sodium balance, sodium loading caused a nonsignificant rise in sodium transport, whereas sodium depletion was associated with a significant fall in sodium transport and intracellular sodium. When cells from salt-loaded or normal animals were incubated in a medium containing their own serum, sodium transport was slightly stimulated in both, but there was no significant difference in the sodium efflux-rate constant of thymocytes obtained from rats on the normal as opposed to the high salt intake. Compared to normotensive rats, there was no significant change in the sodium efflux-rate constant in any of the hypertensive rat models studied. However, the sodium efflux-rate constant fell with age in both the spontaneously hypertensive and Wistar-Kyoto normotensive rats. The present studies show that dietary sodium intake and aging had considerable effects on rat thymocyte sodium transport, but neither of these changes was related to a change in blood pressure. Moreover, the raised blood pressure that developed in genetic, renovascular, and mineralocorticoid hypertension was not associated with a significant change in sodium transport. These experiments suggest that the currently described changes in membrane electrolyte transport of cells not directly involved in blood pressure control, in association with hypertension, probably reflect a fundamental change in the cell membrane. This change may not necessarily be related to the raised blood pressure. Further, sodium depletion, rather than sodium loading, produces inhibition of active sodium pumping in this cell. (Hypertension 6: 454-459, 1984)

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“…58 - 59 These effects have been shown for both in vitro and in vivo situations so they cannot be dismissed. Our results with multidimensional response surface modeling that show the importance of aldosterone in control of salt-sensitive blood pressure changes as well as the laboratory investigations of Friedman and Jones provide an explanation for the depressor effects of aminoglutethimide reported by Woods et al 38 and Taylor et al 39 The cumulative results of the studies relating adrenal cortical abnormalities to hypertension are but another step in defining the role of the adrenal cortex, and they provide support for Dr. Corcoran's intuition of the importance of that role.…”

Section: Aldosterone As Determinant Of Salt-sensitive Hypertensionmentioning

confidence: 99%

Corcoran lecture: the case for or against salt in hypertension. Arthur Curtis Corcoran, MD (1909-1965). Tribute and prelude to Corcoran Lecture of 1988.

Dustan

Kirk

1989

Hypertension

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Salt intake in excess of body needs has long been considered a factor in the genesis and maintenance of human hypertension; the mechanism is salt retention due to faulty renal excretory efficiency. This discussion reviews clinical studies that make a case either for or against the salt hypothesis. Included is a summary of recent experiences with 4 days of salt depletion and 3 days of salt loading in 96 normotensive control subjects and 40 hypertensive patients. These studies were done to test the hypothesis that salt-sensitive blood pressure changes are quantitatively related to sodium balance. However, we found no statistically significant relation between arterial pressure changes and sodium lost during salt depletion or retained during salt loading. The failure of that hypothesis prompted a study of the known factors that control arterial pressure by using multidimensional response surface modeling for changes produced by salt loading. The analysis indicated that in these experiments salt-sensitive blood pressure changes of hypertensive patients were controlled differently than those of normotensive subjects. In the hypertensive group, the changes were highly predictable by combinations of variables, which featured plasma aldosterone, norepinephrine, and epinephrine. In the normotensive group, the changes were less predictable; fewer of the factors were involved, and plasma renin activity was the featured variable. These findings and results of studies done over the past 50 years indicate that salt-dependent hypertension is controlled by many factors and is not a strict correlate of salt intake.

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Kinetics of active sodium transport in aortas from control and deoxycorticosterone hypertensive rats.

Cited by 49 publications

References 30 publications

Erythrocyte lithium transport changes induced by deoxycorticosterone acetate treatment in pigs.

Erythrocyte lithium transport changes induced by deoxycorticosterone acetate treatment in pigs.

Rat thymocyte sodium transport. Effects of changes in sodium balance and experimental hypertension.

Corcoran lecture: the case for or against salt in hypertension. Arthur Curtis Corcoran, MD (1909-1965). Tribute and prelude to Corcoran Lecture of 1988.

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