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. 2022 Jan 20;119(1):316–331. doi: 10.1093/cvr/cvac008

Figure 2.

Figure 2

Prazosin injection (40 µL, 1 mmol/L) into the CB via the ICA attenuated the CB-evoked CSN discharge (n = 6), evoked sympatho-hyperreflexia and pressor response in SH rats (n = 10). (A) Typical tracing of CSN (raw and integrated waveforms) after chemoreflex stimulation with NaCN (0.4 µg/µL; 100 µL via aorta); on the right, the superimposition of control and prazosin responses after 4 min is shown. (B) A plot of the percentage change in the AUC relative to similar period of baseline. (C) Typical tracing of the tSNA (raw and integrated waveform) after chemoreflex stimulation. Other chemoreflex motor responses were not changed by prazosin. Group data for CB-evoked sympathoexcitation (D), bradycardia (E), tachypnoea (F), and pressor response (G) before and after prazosin. For CSN recordings, data were analysed using one-tail paired Student’s t-test, i.e. control vs. Prazosin 20 s and mixed-effects model from prazosin 20 s onwards, whereas for the CB-evoked motor responses, data were analysed using paired Student’s t-test or Wilcoxon test to compare control vs. Prazosin 4 min and mixed-effects model from prazosin 4 min; *P < 0.05 and **P < 0.01 vs. control. Note: the reduced number of data points in (B) reflects a missed injection for one time-point, whereas in (D–G), it reflects the loss of high-quality recordings in two preparations.