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- W1991654564 abstract "In rodent models and humans, sympathetic dysfunction in immune organs occurs concomitantly with immune senescence. Our previous studies in Brown Norway (BN rats) a commonly used aging model, indicate splenic sympathetic nerve activity (SNA) is elevated. This is accompanied by sympathetic nerve loss, and uncoupling of beta-adrenergic receptors (beta-AR) to cAMP in splenocytes. We tested the hypothesis that increased SNA in the aging spleen contributes to sympathetic dysfunction in BN rats. Male BN rats (15-month-old, M) received 0, 0.5 or 1.5 μg/kg/day rilmenidine intraperitoneally for 90 days to chronically lower splenic SNA. Untreated 3 M and 18 M BN rats controlled for aging and stress effects. We evaluated splenic norepinephrine (NE) turnover and plasma and splenic catecholamines levels using HPLC and a NE synthesis blocker. Splenic sympathetic innervation was assessed with histofluorescence. Beta-AR density and beta-AR-stimulated cAMP production were determined by binding assays and ELISA, respectively. Splenic NE concentration or total content did not differ between rilmenidine, 3 M or 18 M control groups. However, rilmenidine dose-dependently reduced splenic NE turnover and circulating NE and modestly reversed splenic sympathetic neuropathy. Rilmenidine also increased beta-AR density in splenocytes, without affecting affinity, but had no effect on the age-related impairment of beta-AR-stimulated cAMP production. Thus, lowering SNA in the aging BN rat spleen does not prevent sympathetic neuropathy or restore beta-AR signaling via cAMP in splenic lymphocytes." @default.
- W1991654564 created "2016-06-24" @default.
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- W1991654564 date "2014-09-01" @default.
- W1991654564 modified "2023-09-27" @default.
- W1991654564 title "149. Lowering splenic sympathetic activity by chronic rilmenidine treatment fails to restore sympathetic neurotransmission in spleens from aging brown norway rats" @default.
- W1991654564 doi "https://doi.org/10.1016/j.bbi.2014.06.169" @default.
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