Figure 3.

(A,B) Effects of the selective α₂-adrenoceptor antagonist rauwolscine (A) and the selective α₁-adrenoceptor antagonist prazosin (B) on renal nerve stimulation (RNS)-induced endogenous noradrenaline (NA) release in isolated kidneys of SHAM-operated (SHAM) and subtotal nephrectomized (SNx) wild-type (WT) mice. There were four stimulation periods in experiments with rauwolscine (S₀–S₃) and five stimulation periods in experiments with prazosin (S₀–S₄). Each stimulation period was performed at 5 Hz for 3 s, 1 ms width, 40 mA. Rauwolscine was applied in increasing concentrations of 0.01, 0.1 and 1 µM to the perfusion solution to S₁–S₃ and prazosin in increasing concentrations of 0.01, 0.1, 1 and 10 µM to S₁–S₄. Noradrenaline release was measured and expressed as a percentage of control S₀ (S_n as % of S₀) (A, B). In (A') and (B') the same data are given but expressed in pg·g⁻¹ kidney wet weight for SHAM and SNx mice. Data given are mean and vertical lines show SEM. The increase in NA release after α₂-adrenoceptor blockade by rauwolscine was significantly reduced in SNx-WT, compared with SHAM-WT mice (A; *P < 0.05 indicates a significant difference). The increase in NA release after α₁-adrenoceptor blockade was similar in kidneys of SHAM and SNx-WT mice (B). Graphs indicating absolute NA release demonstrate the higher level of stimulation-induced transmitter release in SNx compared with SHAM animals (A',B'). Rauwolscine and prazosin lead to a concentration-dependent increase in NA release in SHAM and SNx animals (A',B') (§P < 0.05 indicates significant differences compared with S₀, §P within SHAM group and §'P within SNx group).