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Pathogenetic aspects of hypertension in Cushing's syndrome
Insights
Hypertension in Cushing's syndrome may not stem from the renin-angiotensin-aldosterone system (RAAS). Other factors, such as catecholamines, likely play a larger role in blood pressure elevation in these patients.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
Background:
- Cushing's syndrome is characterized by excessive cortisol production.
- Hypertension is a common comorbidity in Cushing's syndrome.
- The role of the renin-angiotensin-aldosterone system (RAAS) in this hypertension is not fully understood.
Purpose of the Study:
- To investigate the abnormalities of the RAAS in patients with Cushing's syndrome.
- To assess the relationship between RAAS components and hypertension in this cohort.
Main Methods:
- Studied 12 patients with various causes of Cushing's syndrome.
- Measured plasma renin substrate, urinary-free cortisol, and circadian rhythms of plasma cortisol, aldosterone, and plasma renin activity.
Main Results:
- Elevated plasma renin substrate was observed in most patients.
- Plasma renin activity showed variable levels (elevated, normal, or lowered).
- Plasma aldosterone levels were in the lower normal range, with episodic secretion.
Conclusions:
- The RAAS may not be the primary driver of hypertension in Cushing's syndrome.
- Circulating catecholamines are suggested as a more significant factor in blood pressure elevation.
Abstract:
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.