In:
British Journal of Pharmacology, Wiley, Vol. 127, No. 1 ( 1999-05), p. 109-114
Abstract:
We examined effects of γ‐aminobutyric acid (GABA) on vasoconstriction and noradrenaline (NA) release induced by electrical renal nerve stimulation (RNS) in the isolated pump‐perfused rat kidney. RNS (1 and 2 Hz for 2.5 min each, 0.5‐ms duration, supramaximal voltage) increased renal perfusion pressure (PP) and renal NA efflux. GABA (3, 10 and 100 μ M ) attenuated the RNS‐induced increases in PP by 10–40% ( P 〈 0.01) and NA efflux by 10–30% ( P 〈 0.01). GABA did not affect exogenous NA (40 and 60 n M )‐induced increases in PP. The selective GABA B agonist baclofen (3, 10 and 100 μ M ) also attenuated the RNS‐induced increases in PP and NA efflux, whereas the RNS‐induced responses were relatively resistant to the selective GABA A agonist muscimol (3, 10 and 100 μ M ). The selective GABA B antagonist 2‐hydroxysaclofen (50 μ M ), but not the selective GABA A antagonist bicuculline (50 μ M ), abolished the inhibitory effects of GABA (10 μ M ) on the RNS‐induced responses. The selective α 2 ‐adrenoceptor antagonist rauwolscine (10 n M ) enhanced the RNS‐induced responses. GABA (3, 10 and 100 μ M ) potently attenuated the RNS‐induced increases in PP by 40–60% ( P 〈 0.01) and NA efflux by 20–50% ( P 〈 0.01) in the presence of rauwolscine. Prazosin (10 and 30 n M ) suppressed the RNS‐induced increases in PP by about 70–80%. Neither rauwolscine (10 n M ) nor GABA (10 μ M ) suppressed the residual prazosin‐resistant PP response. These results suggest that GABA suppresses sympathetic neurotransmitter release via presynaptic GABA B receptors, and thereby attenuates adrenergically induced vasoconstriction in the rat kidney. British Journal of Pharmacology (1999) 127 , 109–114; doi: 10.1038/sj.bjp.0702524
Type of Medium:
Online Resource
ISSN:
0007-1188
,
1476-5381
DOI:
10.1038/sj.bjp.0702524
Language:
English
Publisher:
Wiley
Publication Date:
1999
detail.hit.zdb_id:
2029728-2
SSG:
15,3
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