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目的:探讨高血压早期大鼠体内降钙素基因相关肽(CGRP)的变化,并观测两类降压药物,氯沙坦或哌唑嗪在降压过程中对CGRP的反应差异。方法:采用经典的两肾一夹型高血压大鼠(Goldblatt,2K1C)为研究模型,夹尾法测定大鼠清醒状态下血压,通过公式计算出平均动脉压;放射免疫法血浆内CGRP和血管紧张素II(Ang II)的含量。反转录聚合连反应(RT-PCR)测定脊髓背根神经节中CGRP mRNA的表达。结果:收缩压、平均动脉压在结扎肾动脉10 d后较对照组快速升高(P<0.01),给予氯沙坦或哌唑嗪治疗5 d后,血压明显降低(P<0.01);实验末,高血压未治疗组血浆中Ang II、CGRP浓度(P<0.01,P<0.01)和脊髓背根神经节中的CGRP mRNA的表达明显升高(P<0.05),高血压氯沙坦治疗组可进一步升高大鼠血浆中Ang II、CGRP浓度(P<0.01,P<0.01)和脊髓背根神经节中的CGRP mRNA的表达(P<0.05);但在高血压哌唑嗪治疗组大鼠血浆中Ang II变化不显著(P>0.05),但CGRP浓度和脊髓背根神经节中的CGRP mRNA的表达与未治疗组相比显著降低(P<0.05,P<0.01)。结论:在肾血管性高血压早期含CGRP感觉神经功能存在代偿性增高,氯沙坦或哌唑嗪的不同降压机制也可能与其影响体内CGRP合成和释放差异有关。
Objective: To investigate the changes of calcitonin gene-related peptide (CGRP) in the early stage of hypertension in rats and to observe the differences in the response to CGRP during the antihypertensive treatment of two types of antihypertensive drugs, losartan or prazosin. Methods: The classic two-kidney-clamp hypertensive rat (Goldblatt, 2K1C) was used as the experimental model. The blood pressure was measured by the clamp tail method in the awake state and the mean arterial pressure was calculated by the formula. The plasma CGRP and blood vessels Angiotensin II (Ang II) content. Reverse transcription polymerase chain reaction (RT-PCR) was used to determine the expression of CGRP mRNA in the dorsal root ganglion. Results: The systolic blood pressure and mean arterial pressure increased rapidly (P <0.01) 10 days after the ligation of the renal artery, and the blood pressure decreased significantly after the treatment with losartan or prazosin (P <0.01) (P <0.01, P <0.01), and the expression of CGRP mRNA in the dorsal root ganglion (P <0.05), and losartan in hypertensive patients (P <0.01, P <0.01) and CGRP mRNA expression in the dorsal root ganglion (P <0.05). However, in the hypertensive prazosin-treated group, the levels of Ang II and CGRP in the plasma were increased There were no significant changes in plasma Ang II in rats (P> 0.05). However, the CGRP concentration and the expression of CGRP mRNA in the dorsal root ganglion were significantly lower than those in the untreated group (P <0.05, P <0.01). CONCLUSIONS: There is compensatory increase in sensory nerve function of CGRP in the early stage of renovascular hypertension. Different hypotensive mechanism of losartan or prazosin may also be related to its effect on the synthesis and release of CGRP in vivo.