Absence of renin suppression by deoxycorticosterone acetate in rats

Fj, Goodwin; Ai, Knowlton; Jh, Laragh

doi:10.1152/ajplegacy.1969.216.6.1476

Cited by 29 publications

(20 citation statements)

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“…In the present experiment these high levels of dietary sodium appeared to exert a K+-depleting effect which may ultimately have been the cardinal influence in producing the paradoxical or seemingly inappropriate hyperreninemia observed in these three groups. Failure of the higher sodium diet to suppress plasma renin levels beyond that observed with normal salt intake is also in keeping with a previous report (18). Such observations raise the possibility that, in the rat at least, plasma renin cannot be reduced below a certain minimum level by sodium administration.…”

Section: Discussionsupporting

confidence: 90%

“…In a previous report it was found that, in the rat, administration of large excess of sodium chloride did not suppress plasma renin levels below what was observed with moderate amounts of sodium in the diet (18). In this regard it is of interest to note that in the present study all three groups of animals given the high sodium intake exhibited serum renin levels of the same order of magnitude as the corresponding groups given only the medium dietary sodium intake.…”

Section: Resultssupporting

confidence: 53%

“…However, it is not at all likely that the changes in plasma renin produced by changes in dietary potassium described herein could be secondary to induced changes in aldosterone secretion. This is because a number of studies have indicated that the suppression of renin secretion by mineralocorticoids such as deoxycorticosterone or aldosterone is entirely secondary to the sodium retention induced by these steroids (18)(19)(20). Furthermore, in the present study, the effects of potassium on plasma renin often occurred in the face of changes in sodium balance which would be expected to have the opposite effect on renin secretion.…”

Section: Discussionmentioning

confidence: 64%

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Potassium balance and the control of renin secretion

Sealey¹,

Clark²,

Bull³

et al. 1970

J. Clin. Invest.

156

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Section: Discussionsupporting

confidence: 90%

Section: Resultssupporting

confidence: 53%

Section: Discussionmentioning

confidence: 64%

See 1 more Smart Citation

Potassium balance and the control of renin secretion

Sealey¹,

Clark²,

Bull³

et al. 1970

J. Clin. Invest.

156

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“…The present study confirms that rats with DOG-salt hypertension are significantly hyper-responsive to angiotensin and noradrenaline compared to matched normotensive controls, and that both DOC and salt are necessary for the development of such hypertension (Goodwin, Knowlton & Laragh, 1969). Our studies further show that hyper-responsiveness is not dependent on the presence of hypertension.…”

Section: Discussionsupporting

confidence: 87%

Effect of sodium, deoxycorticosterone and duration of hypertension on pressor responses in rats

Bing

Russell

Swales

et al. 1982

The Journal of Physiology

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SUMMARY1. Enhanced pressor responsiveness to angiotensin II and noradrenaline has been demonstrated in the hypertension that follows deoxycorticosterone (DOC) and salt administration in the rat. The present studies were carried out to assess the importance of factors common to both pressor agents and those specific to individual agents such as receptor availability.2. Accordingly pressor reponses to angiotensin II and noradrenaline have been studied in normotensive salt-loaded and sodium depleted rats with and without DOC, and in rats with DOC-salt hypertension of short and long duration. These responses have been related to the plasma renin levels in the animals studied.3. Pressor reponses to angiotensin II were increased, dose-response curve (d.r.c.) shifted to the left, in salt-loaded rats and the administration of DOC produced a further increase. DOC-salt hypertension of short duration was associated with an even greater responsiveness. Sodium depletion, however, reduced responsiveness (d.r.c. shifted to the right) and concurrent DOC administration did not alter this.Angiotensin II responses were closely correlated with plasma renin concentration over a wide range of values (p.r.c, r = -0 77, P < 0-001). The differences between the groups could be explained therefore by the number of unoccupied angiotensin II receptors available.4. On the other hand only sodium loaded rats that were also receiving DOC showed any change in noradrenaline responsiveness, when the dose-response curve was shifted to the left. Noradrenaline responses showed no linear relationship to plasma renin concentration.5. The presence of hypertension did not significantly alter noradrenaline responses and the increase observed in angiotensin II responsiveness could be explained by the greater suppression of plasma renin in this group. Duration of hypertension had no effect on responsiveness to either agent.6. These results point to important differences in the pressor responsiveness to angiotensin II and noradrenaline with variation of salt intake and DOC administration. 384 R.

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“…However, aldosterone excretion was increased to the same extent whether (group I) or not (group II) plasma renin was suppressed. Furthermore, there is a large body of evidence to indicate that aldosterone or other mineralocorticoids do not, by themselves, suppress plasma renin because the suppression produced by these hormones was found to be entirely consequent to induced sodium retention (21)(22)(23).…”

Section: Potassium Administration and Plasma Renin In Manmentioning

confidence: 99%

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

Brunner¹,

Baer²,

Sealey³

et al. 1970

J. Clin. Invest.

223

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A B S T R A C T The effect of potassium administration and of dietary potassium deprivation on plasma renin activity and aldosterone excretion has been studied in 10 normal subjects and in 12 hypertensive patients maintained on a constant dietary regimen.Potassium administration reduced plasma renin activity in 18 of 28 studies of both normal and hypertensive subjects. Suppression of renin often occurred despite sodium diuresis induced by potassium administration. The renin suppression was related to induced changes in plasma potassium concentration and urinary potassium excretion.The failure of suppression of plasma renin in 10 studies could be accounted for by the smaller amounts of potassium administered to these subjects, together with a possibly overriding influence of an induced sodium diuresis.In six studies potassium deprivation invariably increased plasma renin activity even though a tendency for sodium retention often accompanied this procedure.The data indicate that both the suppression of plasma renin activity induced by potassium administration and the stimulation of renin activity which follows potassium depletion occur independently of associated changes in either aldosterone secretion or in sodium balance. However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance.These interactions between potassium and plasma renin could be mediated by an ill-defined extrarenal pathway. But the findings are more consistent with an

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Absence of renin suppression by deoxycorticosterone acetate in rats

Cited by 29 publications

References 0 publications

Potassium balance and the control of renin secretion

Potassium balance and the control of renin secretion

Effect of sodium, deoxycorticosterone and duration of hypertension on pressor responses in rats

The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects

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