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Norepinephrine increases angiotensin II binding in rat brain synaptosomes.
1Department of Physiology, College of Medicine, University of Florida, Gainesville 32610.
Brain Research Bulletin
|March 1, 1992
Summary
Norepinephrine (NE) increases angiotensin II (AII) binding sites in rat brain synaptosomes via alpha 1-adrenergic receptors and protein kinase C (PKC). This suggests NE modulates brain AII receptors, impacting central nervous system functions.
Area of Science:
- Neuroscience
- Pharmacology
- Molecular Biology
Background:
- Angiotensin II (AII) receptors are present in rat hypothalamus and brainstem synaptosomes.
- Norepinephrine (NE) is a key neurotransmitter in the central nervous system.
Purpose of the Study:
- To investigate the effect of norepinephrine on angiotensin II binding in rat brain synaptosomes.
- To elucidate the receptor subtypes and signaling pathways involved in NE-mediated regulation of AII receptors.
Main Methods:
- Preparation of synaptosomes from rat hypothalamus and brainstem.
- Measurement of [125I]-angiotensin II specific binding after norepinephrine treatment.
- Use of alpha 1-adrenergic receptor antagonists (prazosin) and agonists.
- Assessment of protein kinase C (PKC) involvement using PKC activators (TPA) and inhibitors (H-7).
Main Results:
- Norepinephrine (NE) treatment increased the number of [125I]-AII binding sites in a concentration-dependent manner.
- The effect of NE was antagonized by prazosin, indicating alpha 1-adrenergic receptor involvement.
- PKC activation mimicked NE's effect, and PKC inhibition blocked it, suggesting a role for PKC signaling.
Conclusions:
- Norepinephrine modulates brain angiotensin II receptors through alpha 1-adrenergic receptors and protein kinase C.
- These findings support a role for catecholamines in regulating central angiotensin II receptor activity.
- The study provides evidence for NE's influence on AII receptor regulation in the brain.