Pressor Hyporeactivity to Angiotensin in Addison's Disease

Kuchel, O; Horký, K; Pazourek, M; Gregorová, I

doi:10.1016/s0140-6736(64)91107-9

Cited by 25 publications

(7 citation statements)

References 8 publications

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“…The mean overall blood flow response to A,, was 49 ml/min before and 40 ml/min after the cyclo-oxygenase inhibitor had been infused (difference NS, Table IIIB (2,(7)(8)(9). Decreases in the pressor response to All have also been documented in a variety of diseases in which the renin-angiotensin system is activated (7,9,(13)(14)(15)(16)(17).…”

Section: Resultsmentioning

confidence: 94%

“…The influenice of sodium balance on the vascular action of A11 has been studied primiarily by monitoring the blood pressuire rise produced by an intravenous infusion of the hormiione (6)(7)(8)(9)(13)(14)(15)(16)(17). This approach, however, is complicated by the fact that All, in addition to its direct actioni to produce vasoconstrictio(n of arteriolar smooth muscle, also influences blood pressure indirectly through actions on the central and sympathetic nervous systems (32,33), on the adrenal medulla (33), the heart (34), and possibly also on the systemic veins (4).…”

Section: Resultsmentioning

confidence: 99%

“…All to normal women receiving estrogein-containing oral contraceptives (52). Similarly, it may explain the blunted pressor sensitivity to All in a variety of diseases (7,9,(14)(15)(16)(17). For example, the blunted pressor response to A11 observed in patients with the syndrome ofjuxtaglomerular cell hyperplasia (Bartter's syndrome) is significantly enhanced when peripheral plasma renin activity is suppressed by saline infusion (53) or administration of propranolol or indomethacin (16).…”

Section: Resultsmentioning

confidence: 99%

“…Differences in the pressor responsiveness to Al have also been reported in a variety of diseases including cirrhosis with ascites (9,13,14), nephrosis (14), malignant and reniovascular hypertension (7), Bartter's syndrome (15,16), and Addison's disease (17). The mechanisms underlying these variations have not been clarified.…”

Section: Introductionmentioning

confidence: 99%

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The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

Oliver¹,

Cannon²

1978

J. Clin. Invest.

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A B S T R A C T The mechanism whereby the vasoconstrictor response to angiotensin II (A,,) is influenced by sodium balance or disease is unclear. To explore this question, the renal vascular responses (RVR) to intrarenal injections of subpressor doses of A,, and norepinephrine were studied in dogs with an electromagnetic flowmeter. Acute and chronic sodium depletion increased plasma renin activity (PRA) and blunted the RVR to A,,, while acute sodium repletion and chronic sodium excess plus desoxycorticosterone acetate decreased PRA and enhanced the RVR to All.The magnitude of the RVR to Al1 was inversely related to PRA. The RVR to norepinephrine was unaffected by sodium balance and was not related to PRA. Inhibition of the conversion of angiotensin I to Al, by SQ 20,881 during sodium depletion lowered mean arterial blood pressure (MABP), increased renal blood flow (RBF), and enhanced the RVR to Al, but not to norepinephrine. Administration of bradykinin to chronically sodium-depleted dogs also lowered the MABP and increased RBF but had no effect on the RVR to A11. SQ 20,881 had no effect on MABP, RBF, or the RVR to Al1 in the dogs with chronic sodiuni excess and desoxycorticosterone acetate. Administration of indomethacin to chronically sodium-depleted dogs lowered RBF but did not influence the RVR to A,,.The results indicate that the RVR to A,, is selectively influenced by sodium balance and that the magnitude of the response is inversely related to the availability of endogenous AII The data did not suggest that the variations in the RVR to A,, were because of direct effects of sodium on vascular contraction, changes in

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Section: Resultsmentioning

confidence: 94%

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

Oliver¹,

Cannon²

1978

J. Clin. Invest.

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“…Thus, sodium depletion of normal rats decreases and sodium loading increases the blood pressure response to a standard dose of exogenous angiotensin II (16). Reduced pressor responsiveness to angiotensin II has also been demonstrated in adrenalectomized rats (17), in patients with Addison's disease (18), in nephrosis (19), and in cirrhosis (19,20). Furthermore, patients with primary aldosteronism exhibit an increased pressor responsiveness to angiotensin II (21).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II Vascular Receptors: Their Avidity in Relationship to Sodium Balance, the Autonomic Nervous System, and Hypertension

Brunner¹,

Chang²,

Wallach³

et al. 1972

J. Clin. Invest.

197

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A B S T R A C T During intravenous administration of varying doses of angiotensin II antibody to anesthetized rats, apparently specific vascular receptors were characterized. These receptors compete with administered antibody to bind circulating angiotensin. This competitive phenomenon was used to evaluate the affinity of these receptors for angiotensin. Apparent vascular receptor affinity was defined by the amount of antibody required to block the blood pressure response to exogenous angiotensin. It was found that this receptor affinity varies directly with sodium intake so that the amount of antibody required to block was eightfold greater in normal animals on a high sodium intake, as compared with those on a low sodium intake. Sodium dependence of receptors was also demonstrated in nephrectomized animals, in desoxycorticosterone (DOC)-treated rats, and in chronic renal hypertension. Thus the observed changes in receptor affinity were usually inversely related to measured endogenous angiotensin II levels. Ganglionic blockade increased antibody requirement eightfold. All of these changes were consistent, with no overlap observed in response of individual animals from different groups. These results may explain the variation in pressor activity of angiotensin associated with changes in salt balance and ganglionic blockade.In general, when sufficient antibody was injected to block the effect of exogenous angiotensin a blood pressure lowering effect was also observed. Two exceptions were the nephrectomized and the one-kidney renal hypertensive animals, in both of which antibody administration had no effect on blood pressure.Additional results suggest that changes in receptor affinity are involved in the pathogenesis of various types of experimental hypertensions because the amount of

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Six Year Follow-up of a Child With Bartter Syndrome

Ramanathan¹

1973

Arch Pediatr Adolesc Med

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Renal and metabolic studies were performed on a 4-year-old Negro girl with dwarfism, polyuria, polydipsia, salt craving, hyposthenuria, and hypokalemic alkalosis. Hypertrophy and hyperplasia of the juxtaglomerular apparatus were seen on renal biopsy. The aldosterone secretion was elevated. The serum renin concentration was unusually high and an inadequate elevation of blood pressure occurred in response to infusions of angiotensin, vasopressin, and levarterenol. Treatment with potassium salts, spironolactone, and liberal salt intake for a period of six years improved the hypokalemia and dwarfism in this girl.The recent demonstration of the interrelationship among the re¬ nal juxtaglomerular cells, renin, an-

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Pressor Hyporeactivity to Angiotensin in Addison's Disease

Cited by 25 publications

References 8 publications

The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

The effect of altered sodium balance upon renal vascular reactivity to angiotensin II and norepinephrine in the dog. Mechanism of variation in angiotensin responses.

Angiotensin II Vascular Receptors: Their Avidity in Relationship to Sodium Balance, the Autonomic Nervous System, and Hypertension

Six Year Follow-up of a Child With Bartter Syndrome

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