頁籤選單縮合
題 名 | Role of Cyclic GMP-Inhibited Phosphodiesterase (PDE3) in Furosemide-Stimulated Renin Secretion=在Furosemide刺激下Cyclic GMP抑制劑的第三類Phosphodiesterase(PDE)對腎素分泌的功能 |
---|---|
作 者 | 邱永仁; | 書刊名 | 臺灣腎臟醫學會雜誌 |
卷 期 | 14:3 2000.09[民89.09] |
頁 次 | 頁91-96+131 |
分類號 | 418.22 |
關鍵詞 | 第三類phosphodiesterase; 腎素分泌; Furosemide; Renin secretion; Phosphodiesterase Ⅲ; Phosphodiesterase inhibitor; Milrinone; Trequinsin; Rabbit; |
語 文 | 英文(English) |
中文摘要 | 本實驗研究是提供證明cyclic GMP抑制的第三類phosphodiesterase(PDE3)在靜止情況下參與腎素分泌的調節,由於β-腎上腺性激素的刺激來引起腎素分泌的上升,以及一氧化氮合成的阻斷來造成腎素分泌的抑制。這個實驗研究的目的是用來測定PDE3也參與緻密班(macula densa)腎素分泌的控制作用。這個實驗的完成是由於測定PDE3抑制劑(Trequinsin及milrinone)對furosemide在腎素的反應上,至少有部分是由於緻密班的居間調節作用。注射furosemide(2mg/kg靜脈注射)入6隻清醒的白兔,會引起下列反應:增加血清腎素活動(PRA)由3.8 ± 0.6到3.8 ± 0.9 ng/ml/2h(P<0.01),也會增加平均動脈壓(mean arterial pressure)由70 ± 3到78 ± 5 mmhg,以心跳由201 ± 8到236 ± 12 bpm(P<0.01)。注射Trequinsin(1.0 µg/kg/min)會增加血清腎素活動(plasma rennin activity)由3.8 ± 0.7到8.8 ± 1.9 ng/ml/2h(P<0.01),以及心跳由221 ± 3到274 ± 14bpm(P<0.01),但不會改變平均動脈壓(mean arterial pressure)(由68 ± 2到65 ± 2 mmhg)。在Trequisin存在時,furosemide會增加血清腎素活動(plasma rennin activity)由9.2 ± 6到50.7 ±10.5 ng/ml/2h(P<0.01),此反應表示比單獨使用Trequisin時有意義地增加(P<0.01)。幾乎有相等的結果在另一組7隻白兔,由milrinone(10 µg/kg/min)來做實驗。這兩組實驗結果顯示,PDE3的抑制會擴大對furosemide的腎素反應,並且可以預測PDE3參與緻密對腎素分泌的控制作用。 |
英文摘要 | Studies in this laboratory have provided evidence that the cyclic GMP-inhibited phosphodiesterase (PDE3) participates in the regulation of rennin secretion under resting conditions, the increase in rennin secretion produced by beta-adrenergic stimulation, and the inhibition of rennin secretion resulting from blockade of nitric oxide synthesis. The sim of the present investigation was to determine if PDE3 also participates in macula densa control of rennin secretion. This was accomplished by testing the effect of the PDE3 inhibitors trequinsin and milrinone on the rennin response to furosemide which is mediated, at least in part, by the macula densa. Injection of furosemide (2 mg/kg i.v.) in six conscious rabbits increased plasma rennin activity from 3.8 ± 0.6 to 8.3 ±0.9 ng/ml/2h (P<0.01) in association with increases in mean arterial pressure from 70 ± 3 to 78 ± 5 mmHg and heart rate from 210 ± 8 to 236 ± 12bpm (P<0.01). Infusion of trequinsin (1.0µg/kg/min) increased plasma rennin activity from 3.8 ± 0.7 to 8.8 ± 1.9ng/ml/2h (P<0.01) and heart rate from 221 ± 3 to 274 ±14 bpm (P<0.01), but did not change mean arterial pressure (68 ± 2 to 65 ± 2mmHg). In the presence of trequinsin, furosemide increased plasma rennin activity from 9.2 ± 6 to 50.7 ± 10.5 ng/ml/2h (P<0.01), a response significantly greater (P<0.01) than that produced by trequinsin alone. Almost identical results were obtained in another seven rabbits when milrinone (10 µg/kg/min) was infused instead of trequinsin. These results demonstrate that inhibition of PDE3 amplifies the rennin response to furosemide, and suggest that PDE3 participates in the macula densa control of rennin secretion. |
本系統中英文摘要資訊取自各篇刊載內容。