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目的 探讨多巴胺D2 受体 (DAD2 R)在遗传性高血压中的调节机制。方法 通过免疫印迹分析 ,血浆Na+ K+ ATP酶活性、儿茶酚胺、血浆ET水平测定 ,观察多巴胺D2 受体基因敲除对血压的影响 ,多巴胺D2 受体与其他血管加压系统的相互作用。结果 多巴胺D2 受体基因敲除鼠的纯合子 (D2 - / - )、杂合子 (D2 +/ - )鼠的收缩压为 12 8± 2 (mmHg)、12 9± 4 (mmHg)和舒张压 97± 2 (mmHg)、98± 3(mmHg) ,高于野生型 (D2 +/ +)鼠 10 4± 2 (mmHg) ,77± 1(mmHg)。肾上腺素B受体阻滞剂对D2 - / -鼠的降压作用较D2 +/ +鼠强 ,D2 - / -鼠的尿液中肾上腺素排泄率高于D2 +/ +鼠 ,肾上腺切除后 ,D2 - / -鼠的血压下降幅度也远远大于D2 +/ +鼠。ETB受体拮抗剂BQ788降低D2 - /-鼠的血压 ,对D2 +/ +鼠的血压无影响。ETB1受体拮抗剂RES 70 1 1升高D2 - / -鼠的血压 ,对D2+/ +鼠的血压无影响。ET 1和ETB激动剂sarafatoxinS6c升高D2 +/ +鼠血压强于D2 - / -鼠。D2- / -鼠血浆ET水平与D2 +/ +相似 ,但D2 - / -鼠中ETB受体的表达强于D2 +/ +鼠。ETA和加压素V1受体拮抗剂对D2 +/ +和D2 - / -鼠血压无影响。ATI受体拮抗剂losartan对D2 - / -和D2 +/ +鼠的降压作用相同。D2 - / -鼠基础尿钠排泄量较D2 +/ +鼠高 ,而且D2 - / -鼠N
Objective To investigate the regulatory mechanism of dopamine D2 receptor (DAD2R) in hereditary hypertension. Methods The levels of plasma Na + K + ATPase activity, catecholamines and plasma ET levels were determined by immunoblotting. The effects of knockdown of dopamine D2 receptor on blood pressure and dopamine D2 receptor interaction with other vasopressors were observed. Results The systolic blood pressure of homozygous (D2 - / -) and heterozygote (D2 + / -) mice with dopamine D2 receptor knockout mice were 12 8 ± 2 (mmHg), 12 9 ± 4 97 ± 2 (mmHg), 98 ± 3 (mmHg), higher than the wild-type (D2 + / +) mice 10 4 ± 2 (mmHg), 77 ± 1 (mmHg). Adrenergic receptor blockers showed a stronger antihypertensive effect than that of D2 + / + mice on D2 - / - mice and a higher excretion rate of adrenaline on D2 - / - mice than D2 + / + mice. After adrenalectomy , D2 - / - mice blood pressure drop is also much greater than the D2 + / + mice. The ETB receptor antagonist BQ788 decreased the blood pressure of D2 - / - mice and had no effect on the blood pressure of D2 + / + mice. The ETB1 receptor antagonist RES 70 1 1 increased the blood pressure of D2 - / - mice and had no effect on the blood pressure of D2 + / + mice. ET 1 and ETB agonist sarafatoxinS6c elevated D2 + / + mice blood pressure more strongly than D2 - / - mice. Plasma ET levels in D2- / - mice were similar to those in D2 + / + but ETB receptors were more strongly expressed in D2 - / - mice than in D2 + / + mice. ETA and vasopressin V1 receptor antagonists had no effect on D2 + / + and D2 - / - mice blood pressure. The losartan, an ATI receptor antagonist, has the same hypotensive effects on D2 - / - and D2 + / + mice. D2 - / - mouse basal urinary sodium excretion was higher than D2 + / + mice, and D2 - / - mice N