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Regional sources of free and sulfoconjugated catecholamines in hypertension
Insights
Hyperadrenergic essential hypertension involves significant adrenal release of free catecholamines, particularly epinephrine. Peripheral tissues extract free epinephrine, while dopamine surges likely stem from pulsatile adrenal release.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Hyperadrenergic essential hypertension (EH) is characterized by elevated sympathetic nervous system activity.
- Understanding the sources of catecholamines (CA) and their metabolites is crucial for managing this condition.
Purpose of the Study:
- To identify the origins of free catecholamines and their sulfates in patients with hyperadrenergic EH.
- To quantify arteriovenous differences across various organs to determine net release or uptake.
Main Methods:
- Radioenzymatic assays and sulfatase hydrolysis were used to measure free catecholamines and their sulfates.
- Arteriovenous differences were assessed across multiple organs and regions in 16 hyperadrenergic EH patients.
Main Results:
- Adrenal venous blood showed significantly higher concentrations of free epinephrine (E), norepinephrine (NE), and dopamine (DA) compared to arterial blood.
- Free E was extracted by peripheral tissues, and NE sulfate levels were elevated in the superior vena cava.
- No organ, except for the superior vena cava region regarding NE sulfate, demonstrated a net release of DA or NE sulfates.
Conclusions:
- The adrenal glands are the primary source of free E, NE, and DA in hyperadrenergic EH.
- Free E is taken up by peripheral tissues, and NE sulfate may be added in the superior vena cava region.
- Dopamine surges in hyperadrenergic EH are likely due to pulsatile adrenal release of free DA.
Abstract:
To elucidate the sources of free catecholamines (CA) and their sulfates in hyperadrenergic essential hypertensives (EH), their arteriovenous differences were determined radioenzymatically and by sulfatase hydrolysis (with correction for cross-contamination) across several organs and regions in 16 hyperadrenergic essential hypertensive patients. Comparison with arterial concentrations showed that: the adrenal venous outflow contains 240 times more free epinephrine (E), 55 times more free norepinephrine (NE), and 7 times more free dopamine (DA) concentrations, but E, NE, and DA sulfates are not different; free E concentrations are lower in the peripheral venous blood; NE sulfate concentrations are higher in the superior vena cava (p less than 0.05 for all differences noted). The data suggest the following conclusions for hyperadrenergic EH patients: with the exception of NE sulfate added into the superior vena cava region, no other organ or region can be associated with a net DA or NE sulfate release. The proportional adrenal vein concentrations of DA:NE:E are approximately 1:10:50, which are very close to those seen in other studies performed under different degrees of stress. Free E is extracted in peripheral tissues. The DA surges in hyperadrenergic EH patients probably result from the pulsatile, predominantly adrenal, release of free DA.