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Basal and saline-stimulated plasma atrial natriuretic hormone in Cushing's syndrome
J A McKnight1, D R McCance, G Roberts
1Sir George E. Clark Metabolic Unit, Royal Victoria Hospital, Belfast, Northern Ireland.
Insights
Hypertension in Cushing's syndrome may involve elevated atrial natriuretic hormone (ANH). Patients showed higher ANH levels and increased sodium excretion during salt loading, suggesting ANH
Area of Science:
- Endocrinology
- Cardiovascular Physiology
- Nephrology
Background:
- Hypertension is a common complication of Cushing's syndrome, but its underlying mechanisms are not fully understood.
- Atrial natriuretic hormone (ANH) plays a role in regulating blood pressure and sodium balance.
Purpose of the Study:
- To investigate the role of plasma atrial natriuretic hormone (ANH) in the pathogenesis of hypertension in patients with Cushing's syndrome.
- To compare ANH levels and responses to saline loading between patients with Cushing's syndrome and healthy controls.
Main Methods:
- Studied basal and saline-stimulated plasma ANH levels in 10 patients with Cushing's syndrome and 10 age- and sex-matched controls.
- Measured plasma renin activity, serum aldosterone, blood pressure, and urinary sodium excretion.
- Administered a saline infusion and collected blood samples hourly.
Main Results:
- Patients with Cushing's syndrome had higher mean blood pressure compared to controls.
- Saline loading resulted in significantly higher plasma ANH levels in Cushing's syndrome patients.
- Urinary sodium excretion was also higher in Cushing's patients during saline infusion.
Conclusions:
- Elevated atrial natriuretic hormone (ANH) may contribute to hypertension in Cushing's syndrome.
- The exaggerated natriuresis observed in Cushing's syndrome during salt loading could be mediated by ANH.
Abstract:
The pathogenesis of hypertension associated with Cushing's syndrome is incompletely understood. We have studied basal and saline-stimulated levels of plasma atrial natriuretic hormone in 10 subjects with active Cushing's syndrome (8 F: 2 M), aged 43 +/- 4 years (mean +/- SEM). Ten age- and sex-matched normal control subjects were also studied. Subjects fasted from 22.00 h, rose at 07.45 h, and remained ambulant until 09.45 h when blood was taken for plasma ANH, plasma renin activity and serum aldosterone. Subjects then rested supine until 10.00 h when blood was again taken, and blood pressure recorded. Then, while subjects remained supine, 21 of 0.9% NaCl were infused between 10.00 and 14.00 h. Blood was taken hourly. Basal plasma ANH was 8.0 +/- 0.9 pmol/l in Cushing's subjects and 6.9 +/- 2.5 pmol/l in controls. Levels increased in response to saline in both groups, and became significantly higher in the group of patients with Cushing's syndrome (14.00 h level 21.3 +/- 3.9 vs 10.4 +/- 1.9 pmol/l; p less than 0.05). Serum aldosterone and plasma renin activity were not different between groups. Mean blood pressure was higher in patients (114 +/- 4 vs 91 +/- 7 mmHg; p less than 0.05). Urinary sodium excretion was not different between groups before saline, but during the four hours of saline was higher in Cushing's subjects (133 +/- 12 vs 67 +/- 11 mmols; N = 6; p less than 0.05). Our results suggest that during salt loading the exaggerated natriuresis seen in the Cushing's group may have been caused by ANH.