Related Experiment Videos
Multiple factors contribute to the pathogenesis of hypertension in Cushing's syndrome
Insights
High blood pressure in Cushing's syndrome is linked to increased sensitivity to vasoactive substances and altered renin-angiotensin system activity. Depressor systems were suppressed, contributing to elevated blood pressure in patients.
Area of Science:
- Endocrinology
- Nephrology
- Cardiovascular Medicine
Background:
- Cushing's syndrome is associated with significant hypertension.
- The precise mechanisms underlying this hypertension remain incompletely understood.
Purpose of the Study:
- To investigate the humoral factors and pharmacological responses contributing to hypertension in Cushing's syndrome.
- To elucidate the role of the renin-angiotensin system and other vasoactive substances.
Main Methods:
- Studied 12 patients with adrenal adenomas causing Cushing's syndrome.
- Measured humoral factors including plasma cortisol, aldosterone, renin-angiotensin system components, urinary kallikrein, and prostaglandin E2.
- Conducted pharmacological challenges with captopril, angiotensin II analog, norepinephrine, and angiotensin II infusions.
Main Results:
- Patients exhibited significantly elevated systolic (171 mmHg) and diastolic (109 mmHg) blood pressure.
- Plasma renin substrate was elevated; urinary kallikrein and prostaglandin E2 were decreased.
- Captopril lowered blood pressure, while angiotensin II analog infusion did not.
- Pressor responses to norepinephrine and angiotensin II were enhanced.
Conclusions:
- Hypertension in Cushing's syndrome results from heightened pressor responses to vasoactive substances.
- Suppression of endogenous depressor systems contributes to elevated blood pressure.
- Abnormalities in the renin-angiotensin system are implicated in the pathophysiology.
Abstract:
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.