Why the study?
How do catecholamines, renin, and aldosterone interrelate in response to physiological stimuli in patients with postural hypotension?
How do catecholamines, renin, and aldosterone interrelate in response to physiological stimuli in patients with postural hypotension?
The renin-angiotensin-aldosterone system can respond to physiological stimuli like salt restriction and tilting independently of sympathetic nervous system integrity in patients with postural hypotension.
May support RAAS responsiveness despite sympathetic failure in postural hypotension; leaves open generalizability beyond this single case.
The interrelation between catecholamines, renin and aldosterone has been studied in two patients with postural hypotension. Under basal conditions both patients presented subnormal values for urinary catecholamines and plasma renin activity. Urinary aldosterone was subnormal in one of the patients and normal in the other. Attempts to increase catecholamine production using insulin induced hypoglycaemia were ineffective in both patients. Tilting was performed in one of the patients but this did not change the urinary catecholamines whereas the plasma renin levels increased in relation to the degree of tilting in a manner known to occur in healthy subjects. In both patients the infusion of noradrenaline was accompanied by an increase in plasma renin activity. On a sodium deficient diet both patients conserved sodium at the renal level, although the response seemed delayed in one of them. During equilibration the urinary catecholamines did not increase whereas the plasma renin and urinary aldosterone values rose in both patients; again the response seemed delayed in one patient. Potassium chloride was administered orally to one of the patients and resulted in an increased urinary output of catecholamines and aldosterone. Our results indicate that baro- and/or osmoreceptor mechanisms can stimulate the production of renin and aldosterone adequately in response to salt restriction and tilting even in the presence of severe sympathetic insufficiency.
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Hedeland et al. (1969) studied this question.
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