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Plasma catecholamines and alpha 1-adrenoceptor function in hemodialysis-associated hypotension
1Department of Internal Medicine, Justus-Liebig University, Giessen, Germany.
Renal Failure
|January 1, 1990
Summary
This study found no evidence of alpha 1-adrenoceptor dysfunction in hemodialysis-induced hypotension. Plasma catecholamine levels, particularly dopamine, showed alterations in hypotensive patients, but did not explain the condition.
Area of Science:
- Nephrology
- Pharmacology
- Cardiovascular Physiology
Background:
- Hemodialysis-induced hypotension (HIH) is a common complication.
- The role of alpha 1-adrenoceptor function and plasma catecholamines in HIH is not fully understood.
Purpose of the Study:
- To investigate alpha 1-adrenoceptor function and plasma catecholamine levels in hemodialysis patients with and without HIH.
- To determine if postsynaptic alpha-adrenoceptor dysfunction contributes to HIH.
Main Methods:
- Assessed blood pressure responses and mydriasis to phenylephrine (alpha 1-agonist) and miosis to carbachol (muscarinic agonist) in patients with and without HIH.
- Measured plasma catecholamine levels (noradrenaline, dopamine) before and during hemodialysis.
- Compared responses between normotensive and hypotensive groups.
Main Results:
- No significant differences in blood pressure response or mydriasis to phenylephrine between groups.
- Hypotensive patients showed increased susceptibility to carbachol-induced miosis.
- Phenylephrine's blood pressure effect was attenuated after 120 min of hemodialysis in normotensive patients.
- Plasma noradrenaline levels were similar; plasma dopamine was elevated in hypotensive patients.
Conclusions:
- Postsynaptic alpha-adrenoceptor dysfunction is unlikely to be the primary cause of HIH.
- Elevated plasma dopamine in hypotensive patients warrants further investigation.
- Altered muscarinic receptor sensitivity may play a role in HIH.