Neuronal aldosterone elicits a distinct genomic response in pain signaling molecules contributing to inflammatory pain.

ABSTRACT:

Background

Recently, mineralocorticoid receptors (MR) were identified in peripheral nociceptive neurons, and their acute antagonism was responsible for immediate and short-lasting (non-genomic) antinociceptive effects. The same neurons were shown to produce the endogenous ligand aldosterone by the enzyme aldosterone synthase.

Methods

Here, we investigate whether endogenous aldosterone contributes to inflammation-induced hyperalgesia via the distinct genomic regulation of specific pain signaling molecules in an animal model of Freund's complete adjuvant (FCA)-induced hindpaw inflammation.

Results

Chronic intrathecal application of MR antagonist canrenoate-K (over 4 days) attenuated nociceptive behavior in rats with FCA hindpaw inflammation suggesting a tonic activation

SUBMITTER: Shaqura M 

PROVIDER: S-EPMC7291517 | biostudies-literature | 2020 Jun

REPOSITORIES: biostudies-literature