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目的观察不同抗高血压药物对自发性高血压大鼠(SHR)痛阈的影响,探讨其与血管紧张素Ⅱ(AngⅡ)的关系。方法 12周龄雄性SHR 40只随机分为卡托普利[100 mg/(kg·d)]、氯沙坦[50 mg/(kg·d)]、普萘洛尔[40mg/(kg·d)]、非洛地平组[10mg/(kg·d)]和SHR对照组,并选取对应周龄雄性Wistar-Kyoto(WKY)大鼠作为正常血压对照组,每组8只,灌胃8周。采用无创尾袖法测量大鼠尾动脉收缩压。测量给药前、给药4和8周时大鼠的机械痛阈和热痛阈。应用酶联免疫吸附试验(ELISA)测定大鼠血浆及脊髓组织AngⅡ。结果卡托普利、氯沙坦、普萘洛尔、非洛地平治疗4和8周后,收缩压明显低于SHR对照组[4周:(178±9)、(168±10)、(177±11)、(172±7)比(201±10)mm Hg;8周:(177±9)、(166±10)、(176±7)、(172±8)比(200±11)mm Hg;均P<0.01]。SHR治疗前机械痛阈高于WKY,热痛阈低于WKY(P<0.01)。卡托普利组和氯沙坦组治疗4和8周末,机械痛阈和热痛阈较给药前明显升高(P<0.01);与SHR对照组比较,机械痛阈和热痛阈有不同程度升高(P<0.01或P<0.05)。卡托普利组和非洛地平组的血浆AngⅡ较SHR对照组减低(P<0.05),氯沙坦组血浆AngⅡ明显高于其他组(P<0.01);卡托普利组的脊髓AngⅡ较其他各组显著降低(P<0.05)。相关分析表明,痛阈改变与脊髓AngⅡ相关(P<0.01)。结论卡托普利和氯沙坦治疗高血压可增高SHR痛阈,其原因可能与脊髓水平AngⅡ下降或脊髓AngⅡ痛敏作用被阻滞有关。
Objective To observe the effect of different antihypertensives on the pain threshold in spontaneously hypertensive rats (SHR) and to explore its relationship with angiotensin Ⅱ (Ang Ⅱ). Methods Male SHR 40 at 12 weeks of age was randomly divided into captopril [100 mg / (kg · d)], losartan [50 mg / (kg · d)], propranolol [40 mg / (kg · (WKY) rats were selected as normal blood pressure control group, 8 rats in each group, and intragastric administration of 8 mg / (kg · d) of felodipine [10 mg / (kg · d)] and SHR control group week. The tail artery systolic pressure was measured by noninvasive tail cuff method. The mechanical and thermal pain thresholds of rats were measured before 4 and 8 weeks of administration. Ang Ⅱ was measured in plasma and spinal cord tissue of rats by enzyme linked immunosorbent assay (ELISA). Results After 4 and 8 weeks of treatment with captopril, losartan, propranolol and felodipine, the systolic pressure was significantly lower than that of the SHR control group [4 weeks: (178 ± 9), (168 ± 10), 177 ± 11, 172 ± 7, 201 ± 10 mm Hg; 8 weeks: (177 ± 9), (166 ± 10), (176 ± 7), (172 ± 8) ) mm Hg; all P <0.01]. The mechanical pain threshold before SHR was higher than WKY and the pain threshold was lower than WKY (P <0.01). In the captopril group and the losartan group for 4 and 8 weeks, the mechanical pain threshold and the thermal pain threshold were significantly higher than those before the administration (P <0.01). Compared with the SHR control group, the mechanical pain threshold and the thermal pain threshold were Varying degrees (P <0.01 or P <0.05). The plasma AngⅡ in captopril group and felodipine group was lower than that in SHR control group (P <0.05), and Ang Ⅱ in losartan group was significantly higher than that in other groups (P <0.01). The AngⅡ in captopril group was significantly lower than that in SHR control group The other groups were significantly lower (P <0.05). Correlation analysis showed that the change of pain threshold was correlated with spinal Ang Ⅱ (P <0.01). Conclusions Captopril and losartan can increase the pain threshold of SHR. Hypertension may be related to the decline of spinal cord AngⅡ or the pain of AngⅡ.