Aldosterone Secretion and Primary and Malignant Hypertension *

Laragh, John H.; Ulick, Stanley; Januszewicz, Vlodzimierz; Deming, Quentin B.; Kelly, William G.; Lieberman, Seymour

doi:10.1172/jci104124

Cited by 294 publications

(66 citation statements)

References 19 publications

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“…That is, the levels of plasma norepinephrine, which may reflect sympathetic nerve activity, in the hypertensives could depend on the endogenous renin-angiotensin axis tone. The activation of renin-angiotensin axis is known to play a very important role in the pathogenesis of accelerated or malignant hypertension (7,8). ANG II has been shown to stimulate the sympathetic nervous system both at the level of the sympathetic ganglia ( 11 ) and central nervous system (12)(13)(14) in animals as well as in humans.…”

Section: Discussionmentioning

confidence: 99%

“…The activation of the renin-angiotensin axis is known to play a very important role in the pathogenesis and pathophysiology of accelerated or malignant hypertension (7,8). Angiotensin II (ANG II) is known to stimulate the sympathetic nervous system at the level of the adrenergic nerve ending (9, 10), the sympathetic ganglia ( 11 ) and the central nervous system (12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

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Elevated sympathetic nerve activity in patients with accelerated essential hypertension.

Matsukawa¹,

Mano²,

Gotoh³

et al. 1993

J. Clin. Invest.

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To determine if an abnormality exists in the sympathetic nervous system of patients with accelerated hypertension, we recorded muscle sympathetic nerve activity (MSNA) from the tibial nerve by microneurography in eight benign essential hypertensives and seven accelerated essential hypertensives. Basal MSNA, plasma renin activity, and plasma angiotensin II levels were significantly higher in accelerated hypertensives than in benign hypertensives (P < 0.05). To clarify the relationship between the renin-angiotensin axis and sympathetic nervous system in the accelerated hypertensives, we measured the MSNA after 7 d of oral administration of captopril (75 mg/d) for antihypertensive treatment in the benign hypertensives and accelerated hypertensives. After administering captopril, the arterial pressure decreased significantly in the benign hypertensives and accelerated hypertensives with decreases in plasma angiotensin II levels, and the decreases in arterial pressure were greater in the accelerated hypertensives than in the benign hypertensives. After captopril administration, the MSNA decreased significantly in the accelerated hypertensives but did not change in the benign hypertensives. Thus, in accelerated hypertensives, sympathetic tone is elevated, and the elevated sympathetic tone is closely related to the activated renin-angiotensin axis tone. (J. Clin. Invest. 1993. 92:25-28.)

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Elevated sympathetic nerve activity in patients with accelerated essential hypertension.

Matsukawa¹,

Mano²,

Gotoh³

et al. 1993

J. Clin. Invest.

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“…This is based on morphological studies in the rat (1), on indirect assessments of adrenal secretion during metabolic studies in man (2), and on direct estimations of adrenal hormone secretion in the rat (3,4) and dog (5)(6)(7). The morphological studies of Deane and Masson (8), which indicate that renin may stimulate the adrenal cortex in the rat, the results of Genest and his colleagues (9), which suggest that arterial hypertension may be associated with an increased excretion of aldosterone in man, and the demonstration by Genest ( 10,11 ) and Laragh (12) and their colleagues that angiotensin II stimulates excretion (10,11) and secretion (12,13) of aldosterone suggest that the kidney may have some influence on the rate of secretion of adrenal hormones. Recently, Pronove, MacCardle, and Bartter (14) described a dwarfed, normotensive child who was suffering from the effects of excessive production of aldosterone.…”

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confidence: 99%

Influence of the Pituitary and the Renin-Angiotensin System on the Secretion of Aldosterone, Cortisol, and Corticosterone

Slater¹,

Barbour²,

Henderson³

et al. 1963

J. Clin. Invest.

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There is evidence suggesting that the control of aldosterone secretion is relatively independent of the pituitary gland. This is based on morphological studies in the rat (1), on indirect assessments of adrenal secretion during metabolic studies in man (2), and on direct estimations of adrenal hormone secretion in the rat (3, 4) and dog (5-7). The morphological studies of Deane and Masson (8), which indicate that renin may stimulate the adrenal cortex in the rat, the results of Genest and his colleagues (9), which suggest that arterial hypertension may be associated with an increased excretion of aldosterone in man, and the demonstration by Genest ( 10, 11 ) and Laragh (12) and their colleagues that angiotensin II stimulates excretion (10, 11) and secretion (12, 13) of aldosterone suggest that the kidney may have some influence on the rate of secretion of adrenal hormones. Recently, Pronove, MacCardle, and Bartter (14) described a dwarfed, normotensive child who was suffering from the effects of excessive production of aldosterone. This was associated with a remarkable hypertrophy and hyperplasia of the juxtaglomerular apparatus in the kidney. The syndrome has been found subsequently in two other patients with hyperaldosteronism (15, 16). The observations suggested that the kidney itself was in some way responsible for the overproduction of aldosterone. The present experiments, performed in the dog, were designed to test the hypothesis that the normal kidney contains material capable of stimulating the adrenal cortex. This was found to be so (17,18), in agreement with results simultaneously obtained by Mulrow, Ganong, Cera, and Kuljian (19) and by Davis and associates (20,21). Accordingly, further studies were designed to see whether the pattern of response of the three important adrenocortical steroid hormones (aldosterone, cortisol, and corticosterone) was such as to suggest that this renal stimulus is involved in the mediation of aldosterone secretion physiologically. MATERIAL AND METHODSThe effects of hypophysectomy in unanesthetized dogs were tested in eight dogs fed a diet containing 9 mEq of sodium and 186 mEq of potassium for 13 to 21 days. On day 1, the lumbo-adrenal vein was cannulated, and the right kidney was removed under Nembutal or ether anesthesia. On day 2, two adrenal blood samples were collected without anesthesia with the animal lying quietly. The pituitary was then removed under Nembutal or halothane anesthesia. The next morning (about 18 hours after hypophysectomy), two adrenal blood samples were again collected without anesthesia, with the animal lying quietly. All animals received 100 mg cortisone acetate intramuscularly on the day of hypophysectomy.Infusion studies. Male mongrel dogs weighing between 16.4 and 26.5 kg were anesthetized with Nembutal, and the pituitary was removed by a buccal approach 2 to 4 hours before the beginning of each experiment, except as otherwise indicated. Both kidneys were removed between double ligatures on the renal pedicles, and a cannula was inserted in...

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“…It was observed that the hypertensive with renal damage secreted aldosterone in larger amounts and that hypertensive dogs of Goldblatt type showed a hypertrophy of zona glomerulosa and hypersecretion of aldosterone Donomae et al, 1962). Thus, it seems reasonable to conclude that a renal aldosterone stimulating factor is produced from the damaged kidney in such a great amount that it causes hypersecretion of aldosterone (Laragh et al, 1960;Venning et al, 1961).…”

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confidence: 99%

STUDIES ON THE <I>IN VITRO</I> PRODUCTION OF ALDOSTERONE AND OTHER CORTICOIDS IN THE ADRENAL ADENOMA OF A PRIMARY ALDOSTERONISM

et al. 1963

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Aldosterone Secretion and Primary and Malignant Hypertension *

Cited by 294 publications

References 19 publications

Elevated sympathetic nerve activity in patients with accelerated essential hypertension.

Elevated sympathetic nerve activity in patients with accelerated essential hypertension.

Influence of the Pituitary and the Renin-Angiotensin System on the Secretion of Aldosterone, Cortisol, and Corticosterone

STUDIES ON THE <I>IN VITRO</I> PRODUCTION OF ALDOSTERONE AND OTHER CORTICOIDS IN THE ADRENAL ADENOMA OF A PRIMARY ALDOSTERONISM

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