saralasin and Cushing-Syndrome

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: Adrenal Cortex Hormones; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Aldosterone; Catecholamines; Cushing Syndrome; Diagnosis, Differential; Humans; Hyperaldosteronism; Hypertension; Pheochromocytoma; Renin; Saralasin

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

Topics: Adenoma; Adrenal Cortex Neoplasms; Adrenal Gland Diseases; Adrenocorticotropic Hormone; Cushing Syndrome; Female; Humans; Hydrocortisone; Hyperaldosteronism; Hyperplasia; Hypertension; Hypokalemia; Hypothalamo-Hypophyseal System; Methods; Middle Aged; Saralasin

To investigate the role of the renin angiotensin system in the pathogenesis of hypertension in Cushing's syndrome two patients with hypercorticism were infused with 20 mg saralasin (1-sar-8-ala-angiotensin II) over a period of 30 minutes under constant blood pressue control. In addition, one patient with primary aldosteronism, an established form of mineralocorticoid hypertension, served as control. Neither in the two patients with Cushing's syndrome nor in the patient with primary aldosteronism could a blood pressure lowering effect of saralasin be observed. In the two patients with hypercoritcism both renin activity and plasma aldosterone increased during saralasin infusion. The patient with primary aldosteronism only showed a weak increase in plasma aldosterone concentration.

Topics: Aldosterone; Angiotensin II; Blood Pressure; Cushing Syndrome; Female; Humans; Hyperaldosteronism; Hypertension; Renin; Saralasin

The angiotensin antagonist saralasin (1-sar-8-ala-angiotensin II) was given to 27 patients with different forms of secondary hypertension. The blood pressure fell in 6 of 7 patients with renal artery stenosis and in 4 of 10 patients with terminal renal failure on regular hemodialysis. No change or a rise in blood pressure was observed in 3 patients with Cushing's syndrome, 4 patients with primary aldosteronism, 3 patients with hypertension and a unilateral small kidney of other than renovascular origin, and 6 patients with terminal renal failure. It can be concluded from the results that angiotensin II is involved in the pathogenesis of renovascular hypertension and in some cases of hypertension accompanying chronic renal failure.

Topics: Angiotensin II; Cushing Syndrome; Humans; Hyperaldosteronism; Hypertension, Renal; Kidney Failure, Chronic; Renal Artery Obstruction; Saralasin

Specific antagonists of angiotensin II (AII) such as saralasin might theoretically be of great value in the recognition of angiotensinogenic hypertension. Evidence is presented to show the importance of overcoming any existing sodium overload and of administering saralasin first in small and then in larger amounts by infusion (or injection). When this was done in 600 hypertensive patients, 62 showed a fall in blood pressure of more than 10/8 mm Hg. Further tests in 50 of these subjects indicated that the fall in blood pressure was associated with high peripheral levels of plasma renin activity (PRA) and/or abnormal renal vein PRA ratios in 94%. The procedure rarely failed to detect even mild forms of angiotensinogenic hypertension. In 62 patients found to have angiotensinogenic hypertension, the responsible lesions included unilateral renal arterial stenosis with good contralateral renal function (29%), bilateral renal disease (21%), Cushing's syndrome (6%), small vessel disease or specific excess of renin production - without other detectable renal disease - (31%) and incompletely evaluated disorders (13%). Saralasin has been of great value in simply and reliably demonstrating the presence or absence of an angiotensinogenic component in a large group of hypertensive patients.

Topics: Adult; Angiotensin II; Animals; Blood Pressure; Cushing Syndrome; Drug Administration Schedule; Humans; Hypertension; Kidney; Male; Rats; Renal Artery Obstruction; Renal Veins; Renin; Saralasin; Sodium