| Objective The present study was to investigate alteration in the sympathetic andparasympathetic components of the baroreflex control of HR in SHR and Wistar ratsfollowing ExT, and to determine the role of angiotensin II type1(AT1) receptor in thenucleus of the tractus solitarius (NTS) in mediating the improvemnet of baroreflexautonomic balance in SHR.Methods Male16-wk SHR and normotension Wistar rats were assigned randomlyinto sendentary (Sed) and exercise training (ExT) groups，and4groups was included:Wistar+Sed，Wistar+ExT，SHR+Sed，SHR+ExT，n=12each group. Rats were runon a treadmill at20-25m/min,60min/d,6days/wk for8weeks. At the end of ExT,the arterial baroreflex was assessed by intravenous injection of phenylephrine (PE8μg/kg) in both Sed and ExT rats under urethane and α-chlorose anesthesia. Baroreflexsensitivity (BRS) was calculated by change in HR in response to change in MAP.Baseline HR and BRS changes were recorded befored and after artropine (0.2mg/kg,iv) or metoprolol (2mg/kg, iv) for blocking parasympathetic and sympatheticactivities. After microinjection of angiotensin II (AngII)100pmol and AT1receptorantagonist losartan200pmol into baroreflex center NTS, the BRS were reassessed inthe autonomic blocked state. The protein expression of AT1receptor in the NTS wasdetermined by Western blot.Results1. Before ExT, BP did not differ between in the SHR+Sed and SHR+ExT groups （146±13.2mmHg vs.149±12.2mmHg）, which was higher than those ofcorresponding Wistar rats（112±13.2mmHg vs.108±11.8mmHg）（P <0.01）.Eight-wk ExT normalized blood pressure in the SHR group. BP reduced24mmHg inSHR+ExT compared with SHR+Sed（133±11.9mmHg vs.157±10.4mmHg，P <0.01），but HR was not different between SHR and Wistar. After ExT, HR decreased54bpm in SHR+ExT compared with SHR+Sed（334.5±24bpm vs.388.3±27bpm,P <0.01）. ExT did not decrease BP in Wistar rats,but reduced HR in the Wistargroup (327.5±13bpm vs.362.8±20bpm, P <0.05）.2．Compared with SHR+Sed group, ExT significantly improved the BRS in SHR（1.1±0.13bpm/mmHg vs.2.0±0.28bpm/mmHg，P<0.01）. ExT tended to enhance theBRS of Wistar rats（2.4±0.33bpm/mmHg vs.2.1±0.34bpm/mmHg）, but did notreach statistical significance.3. Atropine significantly increased baseline HR, but reduced the BRS among4groups.After treatment with atropine, the BRS in the SHR+Sed group was still lower thanthose in Wistar+Sed and SHR+ExT group. On the other hand, metoprolol significantlydecreased baseline HR and the BRS among4groups. Metoprolol also abolisheddifference in the BRS between SHR+Sed and Wistar+Sed as well as SHR+ExT rats.4. Following atropine, microinjection of AngII into the NTS further decreased theBRS in both SHR+Sed and SHR+ExT groups and abolished the difference in this twogroups. Pretreatment with losartan abolished the effects of AngII on the BRS in twoSHR groups. In addition, on the base of metoprolol treatment, NTS Ang II almostabolished baroreflex-mediating bradycardia. The BRS was very lower and notdifferent between SHR+Sed and SHR+ExT groups.5. Compared with Wistar+Sed rats, the protein expression of AT1receptor in the NTSwas upregulated in the SHR+Sed rats (0.89±0.23vs.1.73±0.26, P <0.05). ExTsignificantly downregulated AT1receptor expression in the NTS of SHR (0.92±0.45),but did not change AT1receptor expression in the Wistar rats (0.71±0.1).Conclusion1、 ExT-evoked an improvement of baroreflex function in SHR is involved inenhanced cardiac sympathoinhibition, mediating by AT1receptor in the NTS. 2、 Downregulation of AT1receptor expression in the NTS contributes to animprovement of baroreflex function in SHR following ExT. |
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