Atrial natriuretic peptide (ANP) is a peptide hormone that has potent natriuretic, diuretic, vasodilator, sympatholytic, and renin - and aldos-terone - suppressing activities and is involved in the regulation of volum...Atrial natriuretic peptide (ANP) is a peptide hormone that has potent natriuretic, diuretic, vasodilator, sympatholytic, and renin - and aldos-terone - suppressing activities and is involved in the regulation of volume and electrolyte balance and blood pressure. Further, ANP has also been shown to inhibit cellular growth, proliferation and induce apoptosis in a variety of cell lines, including vascular smooth muscle cells and cardiac myocytes. Recent studies have demonstrated that ANP is not only involved in blood pressure and volume homeostasis but also in the direct regulation of cardiac growth. We and other investigators have demonstrated the existence of natriuretic peptide receptors in the heart and cardiac cells, suggesting that ANP has direct actions on cardiac tissue. Several recent in vivo studies have suggested that statement of ANP is inversely related to cardiac growth/hypertrophy. Transgenic mice overexpressing ANP have lower heart weight and blood pressure than wild type mice. Conversely, we demonstrated that transgenic mice with homozygous disruption of the pro - ANP gene (Nppa) (ANP -/- mice) have no circulating or tissue ANP and exhibit significant cardiac hypertrophy and increased blood pressure. Further, transgenic mice lacking a functional natriuretic peptide receptor A (NPR-A) gene display elevated blood pressure and marked cardiac hypertrophy. The role of ANP in the development of cardiac hypertrophy in response to hemodynamic stress has not previously been studied. Our previous studies demonstrated that ANP - / -mice with hypoxia - induced pulmonary hypertension and high salt diet - induced systemic hypertension develop greater cardiac enlargement than their wild type controls under same experimental conditions, suggest-ing that cardiac enlargement in ANP -/- mice might, at least in part, be related to increased afterload. In a recent study, we used ANP -/- mice to further test the hypothesis that ANP plays an important role in protecting against the development of cardiac enlargement induced by volume overload stress. Adult (8-10 wk old) male ANP -/- and wild type ANP+/+ mice underwent an aorto - caval fistula (ACF) or sham surgery and were subjected to echocardiographic examination at 2 wks. Mean arterial pressure (MAP) and atrial, left ventricular (LV) and right ventricular (RV) mass were greater in sham - operated ANP-/-mice than in ANP+/+mice. MAP decreased following ACF to a similar extent in both genotypes. ACF induced significant concentric cardiac enlargement in both genotypes. Cardiac enlargement and lung weight increased to a greater extent in ANP - / - mice than in ANP+/ + mice, indicating that disrupted ANP statement worsens ACF- induced cardiac enlargement and pulmonary congestion. LV function (velocity of circumferential shortening [VCFr], circumferential stress, fraction shortening, fraction shortening, and e-jection time and fraction) assessed by echocardiography did not differ between sham - operated ANP + / + and ANP - / - mice and remained unchanged after ACF. These findings indicate that ANP deletion results in biventricular enlargement and an exaggerated response to the stress of volume overload. This support the hypothesis that ANP has direct antihypertrophic and car-dioprotective actions in heart. Further study is needed to dissect the contributions of increased afterload from those of removing the antihypertrophic effects of ANP to basal and stress induced cardiac enlargement in this animal model.展开更多
Objective: To observe the therapeutic effect of electroacupuncture (EA) on plasma angiotensin (Ang Ⅱ), aldosterone (ALD) and atrial natriuretic polypeptide (ANP) contents in experimental cerebral infarction rabbits f...Objective: To observe the therapeutic effect of electroacupuncture (EA) on plasma angiotensin (Ang Ⅱ), aldosterone (ALD) and atrial natriuretic polypeptide (ANP) contents in experimental cerebral infarction rabbits for analyzing the underlying mechanism of acupuncture in ameliorating blood supply of the brain tissue. Methods: A total of 80 rabbits were randomized into control (n = 8), pseudo-operation (n = 24), model (n = 24) and EA (n = 24) groups. Cerebral infarction model was established by infusion of self-thrombus into the carotid artery. EA (1 mA, 2 Hz) was applied to 'Baihui'(百会 GV 20) and 'Shuigou'(水沟 GV 26) for 30 min, once every 12 hours. Plasma Ang Ⅱ, ALD and ANP contents were detected with radioimmunoassay method. In the later 3 groups, blood samples were taken at 6 h, 24 h and 48 h after cerebral ischemia. Results: Compared with control and pseudo-operation groups, Ang Ⅱ and ALD contents of model group at 6 h, 24 h and 48 h after cerebral ischemia increased significantly while plasma ANP of the 3 time-courses of model group decreased considerably (P<0.01). In comparison with model group, results showed that Ang-Ⅱ and ALD contents of EA group decreased significantly whereas ANP level of EA group increased strikingly (P<0.01). Conclusion: Electroacupuncture has the effects of raising plasma ANP level and lowering plasma Ang-Ⅱ and ALD in cerebral infarction rabbits.展开更多
文摘Atrial natriuretic peptide (ANP) is a peptide hormone that has potent natriuretic, diuretic, vasodilator, sympatholytic, and renin - and aldos-terone - suppressing activities and is involved in the regulation of volume and electrolyte balance and blood pressure. Further, ANP has also been shown to inhibit cellular growth, proliferation and induce apoptosis in a variety of cell lines, including vascular smooth muscle cells and cardiac myocytes. Recent studies have demonstrated that ANP is not only involved in blood pressure and volume homeostasis but also in the direct regulation of cardiac growth. We and other investigators have demonstrated the existence of natriuretic peptide receptors in the heart and cardiac cells, suggesting that ANP has direct actions on cardiac tissue. Several recent in vivo studies have suggested that statement of ANP is inversely related to cardiac growth/hypertrophy. Transgenic mice overexpressing ANP have lower heart weight and blood pressure than wild type mice. Conversely, we demonstrated that transgenic mice with homozygous disruption of the pro - ANP gene (Nppa) (ANP -/- mice) have no circulating or tissue ANP and exhibit significant cardiac hypertrophy and increased blood pressure. Further, transgenic mice lacking a functional natriuretic peptide receptor A (NPR-A) gene display elevated blood pressure and marked cardiac hypertrophy. The role of ANP in the development of cardiac hypertrophy in response to hemodynamic stress has not previously been studied. Our previous studies demonstrated that ANP - / -mice with hypoxia - induced pulmonary hypertension and high salt diet - induced systemic hypertension develop greater cardiac enlargement than their wild type controls under same experimental conditions, suggest-ing that cardiac enlargement in ANP -/- mice might, at least in part, be related to increased afterload. In a recent study, we used ANP -/- mice to further test the hypothesis that ANP plays an important role in protecting against the development of cardiac enlargement induced by volume overload stress. Adult (8-10 wk old) male ANP -/- and wild type ANP+/+ mice underwent an aorto - caval fistula (ACF) or sham surgery and were subjected to echocardiographic examination at 2 wks. Mean arterial pressure (MAP) and atrial, left ventricular (LV) and right ventricular (RV) mass were greater in sham - operated ANP-/-mice than in ANP+/+mice. MAP decreased following ACF to a similar extent in both genotypes. ACF induced significant concentric cardiac enlargement in both genotypes. Cardiac enlargement and lung weight increased to a greater extent in ANP - / - mice than in ANP+/ + mice, indicating that disrupted ANP statement worsens ACF- induced cardiac enlargement and pulmonary congestion. LV function (velocity of circumferential shortening [VCFr], circumferential stress, fraction shortening, fraction shortening, and e-jection time and fraction) assessed by echocardiography did not differ between sham - operated ANP + / + and ANP - / - mice and remained unchanged after ACF. These findings indicate that ANP deletion results in biventricular enlargement and an exaggerated response to the stress of volume overload. This support the hypothesis that ANP has direct antihypertrophic and car-dioprotective actions in heart. Further study is needed to dissect the contributions of increased afterload from those of removing the antihypertrophic effects of ANP to basal and stress induced cardiac enlargement in this animal model.
文摘Objective: To observe the therapeutic effect of electroacupuncture (EA) on plasma angiotensin (Ang Ⅱ), aldosterone (ALD) and atrial natriuretic polypeptide (ANP) contents in experimental cerebral infarction rabbits for analyzing the underlying mechanism of acupuncture in ameliorating blood supply of the brain tissue. Methods: A total of 80 rabbits were randomized into control (n = 8), pseudo-operation (n = 24), model (n = 24) and EA (n = 24) groups. Cerebral infarction model was established by infusion of self-thrombus into the carotid artery. EA (1 mA, 2 Hz) was applied to 'Baihui'(百会 GV 20) and 'Shuigou'(水沟 GV 26) for 30 min, once every 12 hours. Plasma Ang Ⅱ, ALD and ANP contents were detected with radioimmunoassay method. In the later 3 groups, blood samples were taken at 6 h, 24 h and 48 h after cerebral ischemia. Results: Compared with control and pseudo-operation groups, Ang Ⅱ and ALD contents of model group at 6 h, 24 h and 48 h after cerebral ischemia increased significantly while plasma ANP of the 3 time-courses of model group decreased considerably (P<0.01). In comparison with model group, results showed that Ang-Ⅱ and ALD contents of EA group decreased significantly whereas ANP level of EA group increased strikingly (P<0.01). Conclusion: Electroacupuncture has the effects of raising plasma ANP level and lowering plasma Ang-Ⅱ and ALD in cerebral infarction rabbits.
