Carretta R, Fabris B, Fischetti F, Muiesan S, Bardelli M, Melchior C, Cesanelli R, Pizzolitto A, Giraldi T, Greco P L
Istituto di Patologia Medica and Pharmacology, Trieste's University, Italy.
Am J Med. 1988 Jan 29;84(1B):31-5.
The effect of long-term treatment with indapamide in platelet alpha 2-adrenoceptors has been evaluated in 10 patients with essential hypertension, in a double-blind, cross-over study with placebo. After three months of therapy, indapamide significantly reduced mean blood pressure (from 137 +/- 12 to 116 +/- 6 mm Hg, p less than 0.001), whereas heart rate did not change (from 72 +/- 8 to 73 +/- 7 beats/minute). At the same time, platelet alpha 2-adrenoceptor number increased (from 168.2 +/- 48.4 to 256.8 +/- 14.5 fmol/mg protein, p less than 0.02), whereas the dissociation constant did not change (from 3.79 +/- 2.9 to 4.97 +/- 4.48). The plasma norepinephrine level was significantly reduced after long-term treatment with indapamide (from 275 +/- 118 to 210 +/- 56 pg/ml, p less than 0.02). These results bring about an inhibition of norepinephrine release from sympathetic nerve endings with a likely secondary increase of the number of platelet alpha 2-adrenoceptors.
在一项针对10名原发性高血压患者的双盲交叉安慰剂对照研究中，评估了吲达帕胺长期治疗对血小板α2 -肾上腺素能受体的影响。治疗三个月后，吲达帕胺显著降低了平均血压（从137±12降至116±6 mmHg，p＜0.001），而心率未改变（从72±8降至73±7次/分钟）。同时，血小板α2 -肾上腺素能受体数量增加（从168.2±48.4增至256.8±14.5 fmol/mg蛋白，p＜0.02），而解离常数未改变（从3.79±2.9变为4.97±4.48）。长期使用吲达帕胺治疗后，血浆去甲肾上腺素水平显著降低（从275±118降至210±56 pg/ml，p＜0.02）。这些结果导致去甲肾上腺素从交感神经末梢释放受到抑制，血小板α2 -肾上腺素能受体数量可能继发性增加。
