Adrenocorticosteroids in Peripheral and Adrenal Venous Blood of Man*†

Sweat, Max L.; Lipscomb, Marion D.

doi:10.1210/jcem-15-9-1043

Cited by 74 publications

(12 citation statements)

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“…§1 0- (Table III) for steroid formation by adrenal incubates from the three "normal" and eight carcinoma patients suggests that the latter do not differ greatly from those of the former, although the number of patients in the "normal" group is too small for statistical evaluation. While no comparative data on in vitro steroid formation of normal human adrenal tissue are available in the literature, Sweat (21) has obtained ratios of 2.8 to 3.0 for hydrocortisone to corticosterone in peripheral blood of normal subjects-a value similar to the averages of 2.62 for carcinoma and 3.09 for "normal" adrenal incubates in our series. b) Hypertensive group.…”

Section: Chromatographic Pattern In Adrenal Incubatessupporting

confidence: 79%

Steroid Formation by Adrenal Tissue from Hypertensives1

Cooper¹,

Touchstone²,

Roberts³

et al. 1958

J. Clin. Invest.

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The adrenal cortical hormones have been thought to play a role in the pathogenesis of hypertension for the following reasons: 1) Hypertension is a characteristic finding in Cushing's disease; 2) large doses of desoxycorticosterone (DCA) and salt administered to Addisonian patients produce hypertension (1); 3) hypertensive patients who developed Addison's disease had blood pressure falls to normal limits which were restored to previous levels with DCA (2) ; and 4) 80 per cent of the patients with severe hypertension have had significant improvement for three to seven years following 90 to 100 per cent adrenalectomy and limited sympathectomy (3). Moreover, animal experiments (4, 5) have shown that hypertension following renal artery occlusion cannot be produced in the absence of adrenal cortical steroids.Despite these observations, altered adrenal function in hypertension has not been clearly demonstrated. While mean levels of cortical steroids in blood and urine (6-9) are not elevated in hypertensive patients, disturbances in salt and water metabolism observed in early hypertension prior to the development of renal damage by Green, Johnson, Bridges and Lehmann (10) and BraunMenendez (11) indirectly support the idea that the pattern of adrenal corticoids is altered.

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Section: Chromatographic Pattern In Adrenal Incubatessupporting

confidence: 79%

Steroid Formation by Adrenal Tissue from Hypertensives1

Cooper¹,

Touchstone²,

Roberts³

et al. 1958

J. Clin. Invest.

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“…Although contributing little to the body pool of adrenocortical steroids in man, it is one of the major adrenocortical secretory products in some animals, e.g., rodents (3). In man the major glucocorticosteroid is cortisol and the major mineralocorticosteroid is probably aldosterone; nevertheless, corticosterone has been identified and measured in human adrenal tissue (4), adrenal gland perfusates (5), adrenal vein blood (6)(7)(8), and peripheral blood (9)(10)(11)(12)(13)(14)(15)(16). In all of these tissues the corticosterone concentration was found to be lower than that of cortisol, although the concentration of the biologically important aldosterone has been found to be even less than that of the corticosterone (17,18).…”

mentioning

confidence: 99%

The Metabolism of Corticosterone in Man

Peterson¹,

Pierce²

1960

J. Clin. Invest.

107

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“…In the present investigation blood ACTH and plasma corticosteroid concentrations were determined in subjects experiencing hypoxia, alone or in combination with heat. The (8). Blood was processed by the oxycellulose technique (9) and assayed for ACTH in hypophysectomized rats by the adrenal ascorbic acid depletion method.…”

mentioning

confidence: 99%

Blood Adrenocorticotrophic Hormone and Plasma Corticosteroids in men Exposed to Adverse Environmental Conditions12

Hale¹,

Sayers²,

Sydnor³

et al. 1957

J. Clin. Invest.

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Electroshock (2), surgical trauma (3), accidental trauma and acute illness (4) are associated with elevations in plasma-corticosteroids in man. It was of considerable interest to extend these observations to include adverse environmental conditions. Metabolic and hematologic changes similar to those resulting from the administration of adrenocorticotrophic hormone (ACTH) or corticosteroids have been reported to occur in human subjects experiencing hypoxia (5-7). In the present investigation blood ACTH and plasma corticosteroid concentrations were determined in subjects experiencing hypoxia, alone or in combination with heat. After 2, 15 or 45 minutes of exposure, 20 ml. of blood were drawn from an antecubital vein into a heparinized syringe for corticosteroid analyses, then 200 ml. were drawn directly into glacial acetic acid for ACTH analysis. Plasma corticosteroids were determined by the method of Sweat (8). Blood was processed by the oxycellulose technique (9) and assayed for ACTH in hypophysectomized rats by the adrenal ascorbic acid depletion method. (10). A dose of eluate equivalent to 40 ml. blood was injected into each of five test rats. An estimate of the concentration of ACTH was based on the average response of the test rats to doses of unknown and the responses induced by the administration of 1.0 and 0.25 milliunits (mU) U.S.P. ACTH per 100 Gm. rat on the same day. As an additional control, five hypophysectomized rats were injected with 0.9 per cent NaCl solution in each assay. Experiment 2. Three hour exposure; hypoxia induced by decompression in heated chamber. Five male subjects, 31 to 42 years of age, wearing shorts, were decompressed to the barometric pressure level equivalent to 14,000 feet altitude (total pressure, 446 mm. Hg; oxygen tension, 95 mm. Hg) in a chamber in which the air and wall temperatures were held at 510 C. and relative humidity at 13 per cent Air was circulated through the chamber at a constant rate, and the subjects remained seated throughout the exposure. Cardiovascular, respiratory, and body temperature determinations were made periodically, and 20 ml. blood samples (venous) for corticosteroid, hematocrit, sodium, and potassium determinations were drawn immediately before the exposure, at the end of the second and third hours of exposure, and one hour after exposure. Urine samples collected one hour after exposure were analyzed by standard methods (11) for uric acid, creatinine, sodium, and potassium, and comparison was made with samples obtained at the same 1642

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Adrenocorticosteroids in Peripheral and Adrenal Venous Blood of Man*†

Cited by 74 publications

References 0 publications

Steroid Formation by Adrenal Tissue from Hypertensives1

Steroid Formation by Adrenal Tissue from Hypertensives1

The Metabolism of Corticosterone in Man

Blood Adrenocorticotrophic Hormone and Plasma Corticosteroids in men Exposed to Adverse Environmental Conditions12

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