Fig. 1. Effects of intraduodenal injection of LJLa1 on RSNA, BP, and GVNA. Typical recordings of RSNA, BP, and GVNA (A) of rats injected intraduodenally with saline or LJLa1 (La1). The arrows indicate the time of injection. The horizontal bars represent 20 min, and the vertical scale bars to the right of the recordings represent neural discharge rates of 100 spikes/5 s or BP values of 100 mmHg. RSNA (B), MAP (C), and GVNA (D) after intraduodenal injection of saline or LJLa1 (La1) are expressed as means ± S.E.M. of the percentage of their values at 0 min. The numbers of animals used are shown in parentheses. The significance of the difference between values after saline and LJLa1 from 5 to 60 min were analyzed as a group by ANOVA (repeated measures). RSNA: saline vs. LJLa1 (1 × 10⁸ cfu), P < 0.0005 (F = 18.3); saline vs. LJLa1 (1 × 10⁹ cfu), P < 0.0005 (F = 39.4); LJLa1 (1 × 10⁸ cfu) vs. LJLa1 (1 × 10⁹ cfu), P < 0.005 (F = 9.04); MAP: saline vs. LJLa1 (1 × 10⁸ cfu), P < 0.0005 (F = 33.9); saline vs. LJLa1 (1 × 10⁹ cfu), P < 0.0005 (F = 53.1); LJLa1 (1 × 10⁸ cfu) vs. LJLa1 (1 × 10⁹ cfu), NS (0.05 < P < 0.1) (F = 2.02); GVNA: saline vs. LJLa1 (1 × 10⁸ cfu), P < 0.0005 (F = 40.3); saline vs. LJLa1 (1 × 10⁹ cfu), P < 0.0005 (F = 126); LJLa1 (1 × 10⁸ cfu) vs. LJLa1 (1 × 10⁹ cfu), P < 0.005 (F = 13.0).

Fig. 2. Effects of thioperamide on changes in RSNA, MAP, and GVNA after intraduodenal injection of LJLa1. RSNA (A), MAP (B), and GVNA (C) after intraduodenal injection of LJLa1 are expressed as means ± S.E.M. of percentage of their values at 0 min. An i.c.v. injection of aCSF or thioperamide (thiop) was given 30 min before intraduodenal injection of LJLa1. The significance of the difference between the values after saline and LJLa1 from 5 to 60 min were analyzed as a group by ANOVA (repeated measures). RSNA: aCSF–saline vs. aCSF–LJLa1, P < 0.0005 (F = 91.6); aCSF–LJLa1 vs. thioperamide–LJLa1, P < 0.0005 (F = 112); MAP: aCSF–saline vs. aCSF–LJLa1, P < 0.0005 (F = 49.0); aCSF–LJLa1 vs. thioperamide–LJLa1, P < 0.0005 (F = 33.9); GVNA: aCSF–saline vs. aCSF–LJLa1, P < 0.0005 (F = 103); aCSF–LJLa1 vs. thioperamide–LJLa1, P < 0.0005 (F = 47.5).

Fig. 3. Effects of bilateral lesions of the SCN on changes in RSNA, MAP, and GVNA after intraduodenal injection of LJLa. (A) Photomicrographs of representative coronal brain sections including the SCN from a sham-operated rat (SCN sham) and an SCN-lesioned rat (SCN lesion) stained with cresyl violet. SCN, suprachiasmatic nucleus; OC, optic chiasm. The length of the scale bar is 300 μm. RSNA (B), MAP (C), and GVNA (D) after intraduodenal injection of LJLa1 are expressed as means ± S.E.M. of percentages of their values at 0 min. Data from sham-operated (SCN-sham) and SCN-lesioned (SCN-lesion) rats are shown. The significance of the differences between the values after saline and LJLa1 from 5 to 60 min were analyzed as a group by ANOVA (repeated measures). RSNA: sham–LJLa1 vs. SCNL–LJLa1, P < 0.0005 (F = 224); MAP: sham–LJLa1 vs. SCNL–LJLa1, P < 0.0005 (F = 156); GVNA: sham–LJLa1 vs. SCNL–LJLa1, P < 0.0005 (F = 63.8).

Basal values of RSNA, MAP, and GVNA in experimental groups

RSNA, renal sympathetic nerve activity; MAP, mean arterial pressure; GVNA, gastric vagal nerve activity. Data are shown as means ± S.E.M. The Mann–Whitney U-test indicated no significant differences.