angiotensinogen and Cushing-Syndrome

Topics: 11-beta-Hydroxysteroid Dehydrogenases; ACTH Syndrome, Ectopic; Adenoma; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Angiotensinogen; Cushing Syndrome; Diagnosis, Differential; Glucocorticoids; Humans; Hydrocortisone; Hypertension; Nitric Oxide; Pituitary Neoplasms; Receptor, Angiotensin, Type 1; Sympathetic Nervous System

Topics: Adrenal Cortex Neoplasms; Adrenalectomy; Adrenocorticotropic Hormone; Angiotensinogen; Body Fluids; Captopril; Cushing Syndrome; Glucocorticoids; Humans; Hypertension; Pituitary Gland; Potassium; Renin-Angiotensin System; Saralasin; Sodium; Tomography, X-Ray Computed

Topics: Addison Disease; Angiotensinogen; Biological Assay; Cushing Syndrome; Female; Humans; Hyperaldosteronism; Liver; Male; Pregnancy; Radioimmunoassay; Reference Values; Renin-Angiotensin System

Topics: Adult; Aged; Angiotensinogen; Captopril; Cushing Syndrome; Female; Furosemide; Humans; Hyperaldosteronism; Hypertension; Liver Cirrhosis; Male; Middle Aged; Sodium Chloride

The mechanisms causing high blood pressure in patients with Cushing's syndrome were investigated by measurements of humoral factors and pharmacological maneuvers. Twelve patients with adrenal adenomas were studied. The mean systolic and diastolic pressures of the patients were 171 +/- 28 and 109 +/- 15 mm Hg (+/- SEM), respectively, which were significantly higher than those of normal subjects. PRA, plasma renin concentration, plasma renin substrate, plasma cortisol, plasma aldosterone, urinary kallikrein, and urinary prostaglandin E2 were measured as the humoral factors. PC values were markedly elevated in patients with Cushing's syndrome. Among the components of the renin-angiotensin system, only plasma renin substrate was increased. Urinary kallikrein and prostaglandin E2 were decreased in patients with Cushing's syndrome. Oral administration of captopril lowered blood pressure, but infusion of an angiotensin II analog did not. Furthermore, the pressor responses to infusion of both norepinephrine and angiotensin II were increased. We conclude that blood pressure is elevated in patients with Cushing's syndrome because they have enhanced pressor responses to vasoactive substances, suppression of depressor systems, and some abnormalities of the renin-angiotensin system.

Topics: Adenoma; Adrenal Gland Neoplasms; Adult; Aged; Aldosterone; Angiotensin II; Angiotensinogen; Captopril; Cushing Syndrome; Dinoprostone; Female; Humans; Hydrocortisone; Hypertension; Kallikreins; Male; Middle Aged; Norepinephrine; Prostaglandins E; Renin; Renin-Angiotensin System

Abnormalities of the renin-angiotensin-aldosterone system (RAAS) were observed in hypertensive patients suffering from Cushing's syndrome. In 12 patients with different etiology of Cushing's syndrome renin substrate concentration and urinary-free cortisol, as well as the circadian rhythms of plasma cortisol, aldosterone and plasma renin activity were measured. Plasma renin substrate concentrations were found elevated in all but 1 patient, while plasma renin activity was elevated, normal or lowered. Plasma aldosterone values were found in the lower normal range. A physiological rhythm of cortisol secretion was not observed in any patient with Cushing's syndrome, while plasma aldosterone was secreted episodically mostly within the normal range. We conclude that changes of the RAAS may not be predominantly responsive for hypertension in Cushing's syndrome; other factors like circulating catecholamines are probably of greater importance for the pathogenesis of blood pressure elevation in hypercortisolemic patients.

Topics: Adolescent; Adult; Aged; Aldosterone; Angiotensinogen; Blood Pressure; Child; Circadian Rhythm; Cushing Syndrome; Female; Humans; Hydrocortisone; Hypertension; Male; Middle Aged; Potassium; Renin; Renin-Angiotensin System

The renin aldosterone system was studied in 5 cases of Cushing's disease (bilateral benign hyperplasia) without medication. For a daily sodium intake of 120 mmol plasma angiotensinogen was abnormally increased, plasma renin activity (PRA) remained normal, but without significant diurnal variation. Plasma aldosterone (PA) was normal and its circadian rhythm was maintained. One hour active orthostatism and low sodium diet (20 mmol of sodium during 4 days) induced a normal PRA increase but an insufficient PA response. Positive significant correlations were found between PRA and PA and between plasma angiotensinogen and plasma cortisol. The mechanisms underlying this functional hypoaldosteronism were discussed.

Topics: Adult; Aldosterone; Angiotensinogen; Angiotensins; Cushing Syndrome; Diet, Sodium-Restricted; Female; Humans; Hydrocortisone; Middle Aged; Posture; Renin

Topics: Angiotensinogen; Angiotensins; Contraceptives, Oral; Cushing Syndrome; Diuretics; Electrophoresis, Polyacrylamide Gel; Female; Humans; Hypertension; Isoelectric Focusing; Kinetics; Liver Cirrhosis; Molecular Weight; Pregnancy; Pregnancy Trimester, Third; Radioimmunoassay; Regression Analysis; Uremia

The objective of this investigation was to determine whether heterogeneity of plasma renin substrate could be observed in states of steroid excess and various forms of hypertensive disease. In states of stimulated renin substrate production by estrogens or glucocorticoids, multiple forms of renin substrate were apparent when stimulation was excessive. Stimulation of substrate production caused by uremia associated with hypertension showed similar results. None, or only trace quantities of the additional forms of renin substrate were evident in subjects with normal or suppressed levels of plasma renin substrate. The additional forms of renin substrate could be distinguished from the normal form on the basis of cross-reactivity with a specific antiserum to the normal form, electrophoretic mobility, and kinetic rate constants. Differences in rate constants of the various forms of plasma renin substrate may account for the altered rate of the renin reaction associated with several states of hypertension. In plasma of patients with renovascular hypertension, significant quantities of a protein which cross-reacted with the antiserum but could not generate angiotensin I were observed.

Topics: Angiotensinogen; Angiotensins; Contraceptives, Oral; Cushing Syndrome; Female; Humans; Hypertension; Hypertension, Malignant; Hypertension, Renal; Pregnancy; Uremia

The blood pressure response to the angiotensin II analog 1-sar-8-ala-angiotensin II, or saralasin, was studied in five patients with clinical and laboratory evidence of Cushing's syndrome. Plasma renin activity, plasma renin substrate, and plasma renin concentration were measured in all five patients. The renin system and the response to saralasin were measured after furosemide administration. Plasma aldosterone was measured after infusion of 2 liters normal saline. All patients studied showed a hypotensive response to saralasin, the mean BP changing from 163/108 mm Hg to 130/85 mm Hg (P less than 0.02). There was a significant elevation of the plasma renin activity and plasma renin concentration in the patients compared to normal subjects, although plasma renin substrate was not significantly different from normal values. There was normal suppression of plasma aldosterone after the infusion of 0.9% saline. The findings indicate that the hypertension of these patients with Cushing's syndrome was mediated in large part by angiotensin II.

Topics: Adrenal Glands; Adrenalectomy; Adult; Aldosterone; Angiotensin II; Angiotensinogen; Blood Pressure; Cushing Syndrome; Female; Humans; Hydrocortisone; Hypertension; Male; Middle Aged; Renin; Saralasin