The effects of highly-potent atrial natriuretic peptide (HPANP) on circulating re nin-angiotensin-aldos-terone system (RAAS) and cardiac function were studied in an acute ischemic heart failure model. HPANP (6 μg/kg ...The effects of highly-potent atrial natriuretic peptide (HPANP) on circulating re nin-angiotensin-aldos-terone system (RAAS) and cardiac function were studied in an acute ischemic heart failure model. HPANP (6 μg/kg and 3 μg/kg) was infused intracoronarily. It was found that both doses of HPANP could cause significant decrease in plasma renin activity (PRA), angiotensin II (AII) and aldosterone (Ald). After the administraticn of HPANP, PRA, AII and Ald in the coronary sinus were decreased by 73. 2% (P<0.01), 68. o% (P<0.01) and 73. 6% (P<0.01), and the hormones in peripheral venous blood by 63. 3% (P<0.01), 53. 3% (P<0.01) and 64. 9% (P<0.01), respectively at the dose of 6 μg/kg. While PRA, AII and Ald in the coronary sinus and in peripheral venous blood decreased by 55. 9%, 55. 3%, 61. 9%, and 54. 0%, 42. 3%, 53, 3%, respectively at the 3μg/kg dose level. At the higher dose, HPANP increased left ventricular systolic pressure (LVSP, +13. 1%, P<0. 05), +dP/dtmax(+24.1 %, P<0.01), -dp/dtmax (+35.9%, P<0.01), and VCE(+28.9%, P<0.05). Mean arterial pressure and left ventricular end-diastolic pressure (LVEDP) were decreased (-15.0%, P<0.01, and 29. 6%, P<0.01, respectively). In contrast, the lower dose caused no significant changes of LVSP, +dp/dtmex,dp/dtmax and VCE(not including LVEDP, - 20. 5 %, P<0.05). Neither of the doses caused significant changes in heart rate and T value- Normal saline infusion has no effects on cardiac function and circulating RAAS- We conclude that in ischemic heart failure, intracoronary administration of HPANP can significantly suppress the activity of circulating RAAS, and improve cardiac function by reducing pre- and after-load of the heart, but has no direct myocardial effects.展开更多
Objective: To determine whether vasculature depends on circulatory or locally produced renin toinitiate its renin angiotensin-aldosterone system (RAAS), and to evaluate the effect of nephrectomy on vascular aldosteron...Objective: To determine whether vasculature depends on circulatory or locally produced renin toinitiate its renin angiotensin-aldosterone system (RAAS), and to evaluate the effect of nephrectomy on vascular aldosterone biosynthesis. Methods: The expression of vascular renin mRNA was observed by reversetranscription polyrnerase chain reaction (RT-PCR) 30 h after nephrectomy, and the production of aldosteroneand angiotensin Ⅱ in vessels measured by high performance liquid chromatography (HPLC) and radioimmunoassay (RIA). Results: Aorta was still able to express renin mRNA after nephrectorny when plasmarenin activity disappeared. There were no significant differences among the control group, the sham operationgroup and the nephrectomy group for both the levels of aldosterone and angiotensin Ⅱ (P >0. 05) althoughthe levels of both ACTH and potassium were significantly increased in the nephrectomy group as comparedwith the control group (P <0. 01 ). However, there were significant differences between the control groupand ACEI-perindopril group for both aldosterone and angiotensin Ⅱ (P <0. 05). Conclusion: The resultssuggest that there exists an independent RAAS in vasculature which is different from that of the heart whichdepends on plasma renin and the biosynthesis of vascular aldosterone is induced mainly by angiotensin Ⅱ.展开更多
文摘The effects of highly-potent atrial natriuretic peptide (HPANP) on circulating re nin-angiotensin-aldos-terone system (RAAS) and cardiac function were studied in an acute ischemic heart failure model. HPANP (6 μg/kg and 3 μg/kg) was infused intracoronarily. It was found that both doses of HPANP could cause significant decrease in plasma renin activity (PRA), angiotensin II (AII) and aldosterone (Ald). After the administraticn of HPANP, PRA, AII and Ald in the coronary sinus were decreased by 73. 2% (P<0.01), 68. o% (P<0.01) and 73. 6% (P<0.01), and the hormones in peripheral venous blood by 63. 3% (P<0.01), 53. 3% (P<0.01) and 64. 9% (P<0.01), respectively at the dose of 6 μg/kg. While PRA, AII and Ald in the coronary sinus and in peripheral venous blood decreased by 55. 9%, 55. 3%, 61. 9%, and 54. 0%, 42. 3%, 53, 3%, respectively at the 3μg/kg dose level. At the higher dose, HPANP increased left ventricular systolic pressure (LVSP, +13. 1%, P<0. 05), +dP/dtmax(+24.1 %, P<0.01), -dp/dtmax (+35.9%, P<0.01), and VCE(+28.9%, P<0.05). Mean arterial pressure and left ventricular end-diastolic pressure (LVEDP) were decreased (-15.0%, P<0.01, and 29. 6%, P<0.01, respectively). In contrast, the lower dose caused no significant changes of LVSP, +dp/dtmex,dp/dtmax and VCE(not including LVEDP, - 20. 5 %, P<0.05). Neither of the doses caused significant changes in heart rate and T value- Normal saline infusion has no effects on cardiac function and circulating RAAS- We conclude that in ischemic heart failure, intracoronary administration of HPANP can significantly suppress the activity of circulating RAAS, and improve cardiac function by reducing pre- and after-load of the heart, but has no direct myocardial effects.
文摘Objective: To determine whether vasculature depends on circulatory or locally produced renin toinitiate its renin angiotensin-aldosterone system (RAAS), and to evaluate the effect of nephrectomy on vascular aldosterone biosynthesis. Methods: The expression of vascular renin mRNA was observed by reversetranscription polyrnerase chain reaction (RT-PCR) 30 h after nephrectomy, and the production of aldosteroneand angiotensin Ⅱ in vessels measured by high performance liquid chromatography (HPLC) and radioimmunoassay (RIA). Results: Aorta was still able to express renin mRNA after nephrectorny when plasmarenin activity disappeared. There were no significant differences among the control group, the sham operationgroup and the nephrectomy group for both the levels of aldosterone and angiotensin Ⅱ (P >0. 05) althoughthe levels of both ACTH and potassium were significantly increased in the nephrectomy group as comparedwith the control group (P <0. 01 ). However, there were significant differences between the control groupand ACEI-perindopril group for both aldosterone and angiotensin Ⅱ (P <0. 05). Conclusion: The resultssuggest that there exists an independent RAAS in vasculature which is different from that of the heart whichdepends on plasma renin and the biosynthesis of vascular aldosterone is induced mainly by angiotensin Ⅱ.
