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Beta-receptor responsiveness after desipramine treatment
R Pohl1, G N Pandey, V K Yeragani
1Wayne State University, Detroit, MI.
Psychopharmacology
|January 1, 1993
Summary
Tricyclic antidepressants like desipramine may reduce the body's response to beta-receptor agonists. This study found desipramine blunted blood pressure effects and altered heart rate responses to isoproterenol, suggesting reduced beta-1 receptor function.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Neuroscience
Background:
- Tricyclic antidepressants (TCAs) are widely used for depression.
- Their effects on the autonomic nervous system, particularly beta-adrenergic receptor function, require further elucidation.
- Desipramine, a secondary amine TCA, is known to inhibit norepinephrine reuptake.
Purpose of the Study:
- To investigate the impact of desipramine on the functional response to a beta-receptor agonist, isoproterenol, in humans.
- To assess changes in heart rate, blood pressure, and plasma cyclic adenosine monophosphate (cAMP) levels.
Main Methods:
- 14 healthy controls received 75 mg of desipramine daily.
- Responses to isoproterenol (bolus doses and infusions) were measured at different time points (3-8 days and 14-30 days).
- Plasma cAMP levels were measured in a subset of ten controls during isoproterenol infusions.
Main Results:
- Desipramine significantly increased the dose of isoproterenol required to elevate heart rate by 25 bpm at 14-30 days.
- Isoproterenol-induced increases in systolic blood pressure were blunted at both 3-8 and 14-30 days.
- Plasma cAMP levels in response to isoproterenol were not affected by desipramine treatment.
Conclusions:
- Desipramine treatment appears to decrease the functional response of beta-1 adrenergic receptors.
- The response of beta-2 adrenergic receptors to isoproterenol was not significantly affected.
- These findings suggest potential alterations in cardiovascular regulation with TCA use.