Sodium and the Renin-Angiotensin System in Essential Hypertension and Mineralocorticoid Excess

Lebel, Marcel; Brown, J. J.; Kremer, D.; Robertsc, J.I.S.; Schalekamp, M. A. D. H.; Davies, David; Lever, A. F.; Tree, N.M.; Beevers, D. G.; Fraser, Robert; Morton, J. J.; Wilson, Ana Maria Miranda Martins

doi:10.1016/s0140-6736(74)91690-0

Cited by 84 publications

(24 citation statements)

References 29 publications

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“…This condition appears to differ from syndromes known to involve such steroids (2)(3)(4)(5)(6), in that hypokalemia. although infrequently present (49), has not been a prominent feature of the disease (3, 8-11.…”

Section: Discussionmentioning

confidence: 76%

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Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states.

Baxter¹,

Schambelan²,

Matulich³

et al. 1976

J. Clin. Invest.

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A B S T R A C T Aldosterone receptors from rat kidney slices were utilized in a competitive binding technique to analyze the contribution of various steroids to plasma "mineralocorticoid" activity and to assess their possible role in hypertension. To consider simultaneously the plasma binding, steroids were incubated with slices in undiluted plasma; competitor activities for [3H]aldosterone binding were aldosterone, 100%; deoxycorticosterone, 16.2%; cortisol, 0.4%; and 18-hydroxy-deoxycorticosterone and 18-hydroxy-corticosterone, 0.1%. These steroids were more active in buffer than plasma, suggesting that they bind to plasma and that this reduces their receptor binding. Analysis of the competition data suggests that at normal plasma concentrations, aldosterone occupies the receptors to a major extent, cortisol occupies some of the receptors, and deoxycorticosterone and 18-hydroxydeoxycorticosterone contribute little to receptor occupancy. Two steroids implicated in low-renin essential hypertension, 16i#-hydroxy-dehydroepiandrosterone and 16-oxoandrostenediol, did not have significant competitor activity.Competitor activity in plasmas from normal subjects taken at 12 noon (upright) was greater than that in those taken at 8 a.m. (supine). Since the 12 noon samThis work has been published in abstract form: 1975.

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Section: Discussionmentioning

confidence: 76%

“…6). the earlier suggestion that this exists in low-renin essential hypertension (15) has not been confirmed (6). Finally, other studies suggest that plasma and extracellular fluid volume are also normal in low-renin essential hypertension (49).…”

Section: Discussionmentioning

confidence: 89%

Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states.

Baxter¹,

Schambelan²,

Matulich³

et al. 1976

J. Clin. Invest.

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“…17 Much of the available experimental evidence seems to support a role for AVP, since several types of experimental hypertension that are volume-dependent either will not develop or will be ameliorated by different modes of AVP inhibition. 35 There is, however, some doubt whether extracellular volume 36 37 or exchangeable sodium 38 is actually increased in the low renin, so-called volume-dependent hypertension. This variety mostly occurs in the relatively older hypertensive patient, who is not typically hyperkinetic but rather tends to have increased peripheral resistance.…”

Section: Discussionmentioning

confidence: 99%

Increased plasma vasopressin in low renin essential hypertension.

Os¹,

Kjeldsen²,

Skjøtø³

et al. 1986

Hypertension

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SUMMARY Baseline plasma vasopressin concentrations were measured in 48 men (all 50 years old) with decreased plasma renin concentration and untreated, sustained essential hypertension and in 29 healthy normotensive men. Mean hypertensive plasma vasopressin concentration was more than twice as high as the corresponding normotensive level (15.7 ± 2.2 [SE] vs 7.5 ± 1.0 pg/ml; p < 0.001). Plasma renin concentration in the hypertensive group was reduced compared with that in the normotensive group (0.28 ± 0.04 vs 0.46 ± 0.06 Goldblatt units X 10 4 /ml). These differences appeared despite virtually identical serum osmolality, creatinine clearance, and urinary sodium excretion in the two groups. In the first 38 hypertensive subjects, arterial plasma epinephrine concentrations were significantly increased over those of the first 28 control subjects (99 ± 12 vs 68 ± 6 pg/ml; p < 0.025). In contrast to those with low renin essential hypertension, 35 men with normal renin essential hypertension (all 40 years old) had normal plasma vasopressin levels that were not significantly different from those in a comparable normotensive control group (3.7 ± 0.8 vs 3.5 ± 0.4 pg/ml). Arterial epinephrine concentrations were not significantly different between normal renin subjects and the control group. After 6 weeks of treatment with the nonselective /3-adrenergic receptor blocker oxprenolol in 11 subjects with low renin hypertension, blood pressure was reduced and the plasma vasopressin concentration fell from 27.6 ±6.4 to 13.5 ±4.2 pg/ml (p < 0.01). After 6 weeks of treatment with the /3,-selective agent atenolol in another 11 men with low renin hypertension, plasma vasopressin level fell from 16.3 ± 3.3 to 13.1 ±3.1 pg/ml, but this reduction was not significant. In pooled groups treated with /3-adrenergic blockade, plasma vasopressin level decreased more the higher its initial concentrations (r= 0.79, p< 0.001, n = 22). These findings suggest that plasma vasopressin is increased in low renin essential hypertension and may be related to sympathetic adrenal overactivity. (Hypertension 8: 506-513, 1986) KEY WORDS • blood pressure • catecholamines • sodium • osmolality • /3-adrenergic blockade • pituitary • antidiuretic hormone A RGININE vasopressin (AVP) may increase /\ blood pressure primarily by volume reten-A. \. tion, but it is also a powerful vasoconstrictive agent, even more potent than angiotensin.1 It may also participate in cardiovascular regulation, both centrally 2 and peripherally, 3 and stimulate the gain of baroreceptor reflexes. 4 Potentiation of the vasoconstrictor effect of catecholamines has been established. with mineralocorticoid excess. 6 -9 "" Deoxycorticosterone-salt hypertension will not develop in the Brattleboro rat, which lacks AVP because of a genetic defect. Blockade by either specific antiserum or competitive antagonists of AVP substantially attenuates both the development and severity of preexisting deoxycorticosterone-salt hypertension. Most recently, observations by Hay wood et al.12 point to the sy...

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“…Renin is then suppressed by the sodium retention (Carey et al, 1972). Against the idea is the absence in our experience of sodium retention and volume expansion (Table 1; see also Lebel et al, 1974;, and the failure, so far, to demonstrate excess mineralocorticoid in more than a small proportion of patients. …”

Section: • Essential Hypertension With Normal Reninmentioning

confidence: 77%

Are Idiopathic Hyperaldosteronism and Low-Renin Hypertension Variants of Essential Hypertension?

Brown

Lever²,

Robertson³

et al. 1979

Ann Clin Biochem

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Sodium and the Renin-Angiotensin System in Essential Hypertension and Mineralocorticoid Excess

Cited by 84 publications

References 29 publications

Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states.

Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states.

Increased plasma vasopressin in low renin essential hypertension.

Are Idiopathic Hyperaldosteronism and Low-Renin Hypertension Variants of Essential Hypertension?

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