Prolonged Infusions of Angiotensin II and Norepinephrine and Blood Pressure, Electrolyte Balance, and Aldosterone and Cortisol Secretion in Normal Man and in Cirrhosis with Ascites*

Ames, Richard P.; Borkowski, Abraham; Siciński, A; Laragh, John H.

doi:10.1172/jci105224

Cited by 336 publications

(129 citation statements)

References 42 publications

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“…Several studies in man, immediately relevant to the assessment of the role of salt intake as a determinant of adrenal responsiveness to angiotensin, have been performed (6,22,27). In this study we have demonstrated an unequivocal sensitization of the adrenal's response to angiotensin II with sodium restriction in normal man.…”

Section: Discussionsupporting

confidence: 51%

“…The results are not in accord with the conclusions of earlier studies, but examination of the other reports may account for the difference. Ames, Borkowski, Sicinski, and Laragh did not document an enhanced adrenal response with sodium restriction in normal subjects on a low salt diet when aldosterone secretion rate was used as the index of the adrenal response (27). In their study, the blood pressure increase was used to adjust the angiotensin dose; therefore a variable amount of angiotensin was infused.…”

Section: Discussionmentioning

confidence: 95%

“…Implicit approach is the assumption that the restriction of salt intake does not modify the adrenal's responsiveness to angiotensin II. In contrast to the broad agreement on the effect of salt restriction on vascular responses to angiotensin II, there has been considerable disagreement concerning the adrenal's responsiveness (3,5,6,(22)(23)(24)(25)(26)(27) perhaps reflecting the greater difficulty of assessing this system. Ganong and Boryczka first demonstrated an enhanced adrenal response to angiotensin in the dog on a low salt diet (5); they further demonstrated that this alteration in sensitivity could be reproduced in sodium-replete dogs by the administration of homologous renin for 5 days (23).…”

Section: Discussionmentioning

confidence: 99%

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Reciprocal Influence of Salt Intake on Adrenal Glomerulosa and Renal Vascular Responses to Angiotensin II in Normal Man

Hollenberg¹,

Chenitz²,

Adams³

et al. 1974

J. Clin. Invest.

326

145

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A B S T R A C T The adrenal glomerulosa cell and the renal vasculature respond to similar arterial angiotensin II (A II) levels. We have assessed the effect of decreased sodium intake on their responses to A II in man. Studies were performed in 42 normal subjects in balance on a daily intake of 100 meq potassium and either 200 or 10 meq sodium/day. Renal blood flow was measured with AXe and arterial A II, renin and aldosterone concentrations by radioimmunoassay. A II was infused intravenously (1, 3, or 10 ng/kg/min) for 40-60 min; 14 subjects received graded doses. The A II level increased linearly with dose and plateaued within 3 min; blood pressure and renal vascular resistance showed a similar time-course. Aldosterone rose within 10 and plateaued within 20 min. Dose-response relationships were established between the rate of A II infusion and the adrenal, the renal vascular, and -pressor responses. Sodium restriction reduced the pressor (P <0.01) and the renal vascular response (P < 0.01), but potentiated the adrenal response to A II (P < 0.01). An excellent correlation was found between the plasma A II and aldosterone levels, but the slope of their regression relationship on a high (y = 0.13x + 6) and low salt intake (y = 0.32x + 14) differed significantly (P < 0.0005).Thus, sodium intake reciprocally influences vascular and adrenal responses to A II: salt restriction blunts the vascular response and potentiates the adrenal's, a physiologically important influence in view of aldosterone's role in sodium conservation.

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Section: Discussionsupporting

confidence: 51%

Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

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Reciprocal Influence of Salt Intake on Adrenal Glomerulosa and Renal Vascular Responses to Angiotensin II in Normal Man

Hollenberg¹,

Chenitz²,

Adams³

et al. 1974

J. Clin. Invest.

326

145

View full text Add to dashboard Cite

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“…During sodium depletion the already increased activity of the renin-angiotensin axis of early tetraplegics is still more active. The rise in renin caused by postural changes such as tilt or wheelchair may then be too small to be effective in patients with decreasing sodium stores and therefore less vascular sensitivity to angiotensin and norepinephrine (Ames et al, 1965) and inadequate homeostatic mechanisms. Similar mechanisms are probably involved in the reduced tolerance to acceleration caused by hydrochlorothiazides in normotensive man (Pfaff and Newberry, 1972).…”

Section: Discussionmentioning

confidence: 99%

Metabolic effects of sodium restriction and thiazides in tetraplegic patients

et al. 1977

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Abstract. The metabolic effects of sodium restriction, alone or with thiazide, were studied in 12 healthy subjects, in 24 tetraplegics during the initial 8 months of paralysis (early) and in 16 others during the subsequent period (late). The diuresis caused by both treatments led to more haemoconcentration in early than in late patients. In contrast with the healthy subjects on low sodium, the tetraplegics had a delayed urinary sodium retention and no fall in calciuria. During thiazide, urinary sodium depletion occurred early and the urine calcium fell after 3 days in all tetraplegics. During both treatments, aldosterone and renin increased more in early patients than in the other groups. The clinical implications of inducing dehydration and a sustained stimulation of the renin angiotensin-aldosterone axis in recently injured tetraplegics with severe orthostatic hypotension are discussed.

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“…The slow pressor response needs 5-10 h to develop, reaching a maximum peak 3-5 days after the onset of the infusion (8). The important characteristic of the slow pressor response is that it is not specific for any particular animal species since it has been demonstrated in man (11), rats (12), rabbits (6), and dogs (7). In our laboratory we have demonstrated similar responses in the swine model (13).…”

Section: The Vasoconstrictor Effects Of Normal Levels Of Angiotensinmentioning

confidence: 99%

Oxidative stress may explain how hypertension is maintained by normal levels of angiotensin II

Romero

Reckelhoff

2000

Braz J Med Biol Res

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It is well known that essential hypertension evolves in most patients with near normal levels of plasma renin activity. However, these levels appear to be responsible for the high levels of arterial pressure because they are normalized by the administration of angiotensin II converting inhibitors or angiotensin receptor antagonist. In experimental animals, hypertension can be induced by the continuous intravenous infusion of small doses of angiotensin II that are not sufficient to evoke an immediate pressor response. However, this condition resembles the characteristics of essential hypertension because the high levels of blood pressure exist with normal plasma levels of angiotensin II. It is suggested that small amounts of angiotensin whose plasma levels are inappropriate for the existing size of extracellular volume stimulate oxidative stress which binds nitric oxide forming peroxynitrite. The latter compound oxidizes arachidonic acid producing isoprostaglandin F2a (an isoprostane) which is characterized by a strong antinatriuretic vasoconstrictor renal effect. In this chain of reactions the vasoconstrictor effects derived from oxygen quenching of nitric oxide and increased isoprostane synthesis could explain how hypertension is maintained with normal plasma levels of renin. Correspondence

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Prolonged Infusions of Angiotensin II and Norepinephrine and Blood Pressure, Electrolyte Balance, and Aldosterone and Cortisol Secretion in Normal Man and in Cirrhosis with Ascites*

Cited by 336 publications

References 42 publications

Reciprocal Influence of Salt Intake on Adrenal Glomerulosa and Renal Vascular Responses to Angiotensin II in Normal Man

Reciprocal Influence of Salt Intake on Adrenal Glomerulosa and Renal Vascular Responses to Angiotensin II in Normal Man

Metabolic effects of sodium restriction and thiazides in tetraplegic patients

Oxidative stress may explain how hypertension is maintained by normal levels of angiotensin II

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