The Effect of Angiotensin II on the Blood Pressure in Humans with Hypertensive Disease*

Kaplan, Norman M.; Silah, Jack G.

doi:10.1172/jci104951

Cited by 267 publications

(93 citation statements)

References 17 publications

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“…Vascular sensitivity to angiotensin II falls significantly when sodium intake is restricted. While most frequently documented as a reduction in the pressor response (12)(13)(14), the reduction in sensitivity has also been defined in the vessels of the rabbit leg (15) and is especially marked in the case of the human kidney (4). It is even demonstrable in the rabbit aorta, where the implications for cardiovascular homeostasis must be minor (15).…”

Section: Discussionmentioning

confidence: 99%

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: Discussionmentioning

confidence: 99%

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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“…The vascular sensitivity to angiotensin II was determined according to the method of Kaplan and Silah [7] at the age of one year and 5 months, 3 years and 5 months, and 16 years. The responses of PA and PRA to exogenous angiotensin II were examined at the age of 3 years and 5 months and 16 years.…”

Section: Methodsmentioning

confidence: 99%

Long-Term Follow-Up of a Girl with the Neonatal Form of Bartter's Syndrome.

et al. 1997

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Abstract.We followed up a girl with the neonatal form of Bartter's syndrome for sixteen years and determined the sensitivity to angiotensin II before and during the indomethacin treatment.A 4-monthold girl was admitted to our hospital, because of severe hypokalemia and growth retardation. Initially we treated her with spironolactone and potassium supplements. This treatment increased plasma potassium levels and her growth. At the age of one year she was diagnosed as having Bartter's syndrome.Since then she has been treated with indomethacin at an initial dose of 3 mg/kg/day combined with spironolactone and potassium. After the start of the indomethacin treatment, her growth increased dramatically, and her final height was normal adult height. Her puberty developed normally and menarche occurred at the age of 12 years. Levels of serum sodium, chloride, plasma aldosterone and urinary prostaglandin E2 were also normalized. Levels of angiotensin I and II were improved but not within the normal range, but plasma potassium levels slightly decreased after plasma aldosterone levels were normalized and did not change during the treatment period. Plasma renin activity remained high until about the age of 8 years, after which it decreased to almost within the normal range. At 5 months after the start of indomethacin (3 mg/kg/day), her vascular sensitivity to angiotensin II had been improved, and after 2 years and 5 months, her vascular sensitivity was further improved. At this time renin activity had decreased after angiotensin II infusion, but plasma aldosterone did not change. At the age of 16 years (dose of indomethacin: 0.5 mg/kg/day), plasma aldosterone increased after angiotensin II infusion. These data suggest that indomethacin and spironolactone are effective treatments for the neonatal form of Bartter's syndrome, especially during childhood.

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“…Thus, sodium depletion stimulates renin secretion, and sodium loading suppresses renin release. However, under circumstances of body fluid volume depletion, during which increased renin levels are found, pressor reactivity to exogenous angiotensin becomes markedly impaired (3)(4)(5)(6)(7). Conversely, when sodium is given in excess, especially if a mineralocorticoid is also administered, the pressor response to angiotensin infusion is enhanced (6).…”

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confidence: 99%

Prior receptor occupancy as a determinant of the pressor activity of infused angiotensin II in the rat.

Thurston¹,

Laragh²

1975

Circulation Research

131

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The pressor responsiveness to angiotensin II and norepinephrine was examined in rats before and during blockade of converting enzyme activity with the nonapeptide SQ 20881. Responses to angiotensin II were impaired by sodium deprivation but enhanced by sodium loading or bilateral nephrectomy. During the period of converting enzyme blockade, a twofold increase in the angiotensin II pressor response was observed in the salt-restricted rats, whereas only a small change occurred in the salt-loaded rats. Infusion of the inhibitor produced a profound fall in the blood pressure of the salt-depleted rats with a relatively minor fall in the sodium-loaded rats. Norepinephrine pressor responses were slightly potentiated in the salt-restricted rats after administration of SQ 20881, but no change occurred in the salt-loaded or the nephrectomized rats. These observations support the view that the decrease in angiotensin II pressor activity during salt deprivation is the result of a prior occupancy of receptor sites by endogenous hormone. Therefore, a change in the number or the affinity of receptors consequent to changes in sodium balance need not be postulated to explain the phenomenon. KEY WORDS pressor responsesodium depletion and loading blood pressure norepinephrine coverting enzyme blockade bilateral nephrectomy• Most studies of the renin-angiotensin system depend on measurements of the circulating levels of renin and angiotensin II. A reciprocal relationship between plasma renin activity and sodium balance has been well documented (1, 2). Thus, sodium depletion stimulates renin secretion, and sodium loading suppresses renin release. However, under circumstances of body fluid volume depletion, during which increased renin levels are found, pressor reactivity to exogenous angiotensin becomes markedly impaired (3-7). Conversely, when sodium is given in excess, especially if a mineralocorticoid is also administered, the pressor response to angiotensin infusion is enhanced (6). Thus, angiotensin pressor reactivity appears to correlate directly with sodium balance but in-

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The Effect of Angiotensin II on the Blood Pressure in Humans with Hypertensive Disease*

Cited by 267 publications

References 17 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

Long-Term Follow-Up of a Girl with the Neonatal Form of Bartter's Syndrome.

Prior receptor occupancy as a determinant of the pressor activity of infused angiotensin II in the rat.

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