Abstract
The role of prostaglandins in mediating angiotensin effects on autonomic neurotransmission was assessed. This was accomplished by examining the angiostensin-induced production of prostaglandins (PGE) and suppression of non-adrenergic (purinergic) neurotransmission in the presence and absence of cyclo-oxygenase inhibitors. The vas deferens of the rabbit was utilized for these studies because this preparation has a predominant non-adrenergic neurogenic component. Both angiotensins II and III enhanced PGE production and reduced non-adrenergic neurogenic contractions in a concentration-dependent manner from 1 to 1000 mM. Furthermore, indomethacin (2.8 μM) and eicosatetraynoic acid (10 μM) eliminated the inhibitory effect of the angiotensins on non-adrenergic neurotransmission. However, acetylsalicylic acid (10 μM) prevented the production of PGE in response to the angiotensins but failed to alter the suppression of non-adrenergic neurotransmission. The latter data are inconsistent with the hypothesis that PG's mediate angiotensin-induced depression of non-adrenergic neurotransmission. The mechanism by which indomethacin and eicosatetraynoic acid prevent angiotensin effects on non-adrenergic neurotransmission was not elucidated but previous reports suggest that these agents may act as angiotensin receptor antagonists. All of the cyclo-oxygenase inhibitors examined tended to potentiate angiotensin effects on adrenergic neurotransmission.
Original language | English (US) |
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Pages (from-to) | 215-228 |
Number of pages | 14 |
Journal | Prostaglandins |
Volume | 36 |
Issue number | 2 |
DOIs | |
State | Published - 1988 |
Externally published | Yes |