1 We examined eects of g-aminobutyric acid (GABA) on vasoconstriction and noradrenaline (NA) release induced by electrical renal nerve stimulation (RNS) in the isolated pump-perfused rat kidney. 2 RNS (1 and 2 Hz for 2.5 min each, 0.5-ms duration, supramaximal voltage) increased renal perfusion pressure (PP) and renal NA eux. GABA (3, 10 and 100 mM) attenuated the RNSinduced increases in PP by 10 ± 40% (P50.01) and NA eux by 10 ± 30% (P50.01). GABA did not aect exogenous NA (40 and 60 nM)-induced increases in PP. 3 The selective GABA B agonist baclofen (3, 10 and 100 mM) also attenuated the RNS-induced increases in PP and NA eux, whereas the RNS-induced responses were relatively resistant to the selective GABA A agonist muscimol (3, 10 and 100 mM). 4 The selective GABA B antagonist 2-hydroxysaclofen (50 mM), but not the selective GABA A antagonist bicuculline (50 mM), abolished the inhibitory eects of GABA (10 mM) on the RNSinduced responses. 5 The selective a 2 -adrenoceptor antagonist rauwolscine (10 nM) enhanced the RNS-induced responses. GABA (3, 10 and 100 mM) potently attenuated the RNS-induced increases in PP by 40 ± 60% (P50.01) and NA eux by 20 ± 50% (P50.01) in the presence of rauwolscine. 6 Prazosin (10 and 30 nM) suppressed the RNS-induced increases in PP by about 70 ± 80%. Neither rauwolscine (10 nM) nor GABA (10 mM) suppressed the residual prazosin-resistant PP response. 7 These results suggest that GABA suppresses sympathetic neurotransmitter release via presynaptic GABA B receptors, and thereby attenuates adrenergically induced vasoconstriction in the rat kidney.

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