Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We evaluated the effects of angiotensin-(1-7) (Ang-(1-7)) on post-ischemic function in isolated hearts from adult male Wistar rats perfused according to the Langendorff technique. Local ischemia was induced by coronary ligation for 15 min. After ischemia, hearts were reperfused for 30 min. Addition of angiotensin II (Ang II) (0.20 nM, N = 10) or Ang-(1-7) (0.22 nM, N = 10) to the Krebs-Ringer perfusion solution (KRS) before the occlusion did not modify diastolic or systolic tension, heart rate or coronary flow (basal values for Ang-(1-7)-treated hearts: 0.72 +/- 0.08 g, 10.50 +/- 0.66 g, 216 +/- 9 bpm, 5.78 +/- 0.60 ml/min, respectively). During the period of occlusion, the coronary flow, heart rate and systolic tension decreased (values for Ang-(1-7)-treated hearts: 2.83 +/- 0.24 ml/min, 186 +/- 7 bpm, 6.95 +/- 0.45 g, respectively). During reperfusion a further decrease in systolic tension was observed in control (4.95 +/- 0.60 g) and Ang II-treated hearts (4.35 +/- 0.62 g). However, in isolated hearts perfused with KRS containing Ang-(1-7) the further reduction of systolic tension during the reperfusion period was prevented (7.37 +/- 0.68 g). The effect of Ang-(1-7) on the systolic tension was blocked by the selective Ang-(1-7) antagonist A-779 (2 nM, N = 9), by the bradykinin B2 antagonist HOE 140 (100 nM, N = 10), and by indomethacin pretreatment (5 mg/kg, ip, N = 8). Pretreatment with L-NAME (30 mg/kg, ip, N = 8) did not change the effect of Ang-(1-7) on systolic tension (6.85 +/- 0.61 g). These results show that Ang-(1-7) at low concentration (0.22 nM) improves myocardial function (systolic tension) in ischemia/reperfusion through a receptor-mediated mechanism involving release of bradykinin and prostaglandins.
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PMID:Angiotensin-(1-7) improves the post-ischemic function in isolated perfused rat hearts. 1221 80

The role of nitric oxide (NO) on the vasorelaxant effect of atrial natriuretic peptide (ANP) on the basal tone of rabbit aortic rings conditioned to angiotensin II (Ang II) was studied. ANP aortic relaxation and nitrite release were measured in the presence and absence of endothelium and a NO-synthase inhibitor. Ang II at 10(-8) M triggered a contractile response, conditioning the vessel to a vasorelaxant effect of ANP (10(-8) M). This effect was significantly enhanced by endothelium removal, NG-nitro-L-arginine methyl ester (L-NAME, 10(-4) M), and methylene blue (10(-5) M). ANP decrease of basal tone in Ang-II-sensitized aortic rings was improved when a higher concentration of Ang II was used (l0(-6) M). Basal and Ang-II-stimulated nitrite release were measured in stretched (S) and nonstretched (NS) aortic rings. Nitrite release was significantly increased in S rings (p < 0.001). L-NAME (10(-4) M) partially inhibited nitrite release in both basal and Ang-II-stimulated S aortic rings. In NS aortic rings, the NO inhibitor did not inhibit basal nitrite release but blunted the Ang-II-stimulated nitrite level. A significant negative correlation between nitrite release and the ANP vasorelaxant effect on basal tone was dependent on the Ang-II-sensitizing dose. The present results demonstrate that ANP relaxant effects on aortic basal tone are related to NO levels, which are regulated by S- and Ang-II-concentration-dependent NO generation and quenching.
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PMID:Role of nitric oxide on the vasorelaxant effect of atrial natriuretic peptide on rabbit aorta basal tone. 1245 70

Angiotensin II (Ang II) may be a key molecule in the development of atherosclerosis. Because the incidence of coronary atherosclerosis in premenopausal women is lower than that observed in men or postmenopausal women, we have investigated the effect of estrogens on Ang II-induced leukocyte recruitment in vivo using intravital microscopy in the rat mesenteric microcirculation. Superfusion for 60 minutes with Ang II induced a significant increase in leukocyte rolling flux, adhesion, and emigration. Administration of 17-beta-estradiol (17-beta-E) after 30 minutes of Ang II superfusion produced a reduction of these leukocyte responses by 55.1%, 72.7%, and 70.9%, respectively, an additional 30 minutes later. The effect observed with 17-beta-E was receptor-mediated and specific. 17-beta-E superfusion did not modify either L-NAME or indomethacin-induced leukocyte responses. Inhibitory responses caused by 17-beta-E were not altered by either 7-nitroindazole or actinomycin D cosuperfusion. Stimulation of endothelial cells with 17-beta-E caused a rapid and dose-dependent release of prostacyclin. Finally, tamoxifen or ICI 182,780 administration provoked a significant increase in leukocyte-endothelial cell interactions 90 minutes later, which were significantly attenuated by systemic preadministration with an Ang II AT(1) receptor antagonist. Tamoxifen-induced leukocyte responses were also reduced by systemic pretreatment with an anti-P-selectin mAb and an anti-CD18 mAb. Hence, the antiatherogenic effects of estrogens may be mediated by inhibition of Ang II-induced leukocyte recruitment through endothelial NO and prostacyclin release. Furthermore, scarcity of estrogens resulted in decreased levels of vasodilators and the exposure of the endothelium to the deleterious action of Ang II, which may explain the higher incidence of coronary atherosclerosis in men and postmenopausal women.
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PMID:Estrogens inhibit angiotensin II-induced leukocyte-endothelial cell interactions in vivo via rapid endothelial nitric oxide synthase and cyclooxygenase activation. 1248 Aug 15

Angiotensin II is synthesized locally in various tissues; however, the role of interstitial angiotensin II in the regulation of regional metabolism and tissue perfusion is not clear. We characterized the effect of interstially applied angiotensin II in skeletal muscle and subcutaneous adipose tissue of young, normal-weight, healthy subjects by using the microdialysis technique. Furthermore, we tested the hypothesis that the effect of interstitial angiotensin II is modulated by nitric oxide. Tissues were perfused with 0.01, 0.1, and 1 micro mol/L angiotensin II in the presence of the L- or D-isomer of N(G)-nitro-arginine-methyl ester (L- or D-NAME), the effective and noneffective isomer, respectively, for blocking nitric oxide synthase. Dialysate ethanol, glycerol, glucose, lactate, and pyruvate concentrations were measured to assess changes in blood flow (ethanol dilution technique), lipolysis, and glycolysis, respectively. Baseline blood flow and dialysate concentrations of the metabolites were similar with L- and D-NAME in both tissues. Blood flow and dialysate glucose and lactate did not change significantly in both tissues during perfusion with angiotensin II. Dialysate glycerol dose-dependently increased in adipose tissue (P<0.0438) but decreased in muscle (P<0.007). In muscle, dialysate pyruvate increased (P<0.0002), whereas lactate/pyruvate ratio decreased (P<0.001), both dose-dependently. All effects were similar with L- and D-NAME and could be reversed by nitroprusside. We conclude that in contrast to the profound hemodynamic effect of intravascular angiotensin II, interstitial angiotensin II has a minimal acute effect on blood flow in both tissues. However, interstitial angiotensin II modulates lipid and carbohydrate metabolism in a tissue specific fashion. Thus, the physiology of interstitial angiotensin II cannot be predicted from intravascular studies.
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PMID:Tissue-specific response to interstitial angiotensin II in humans. 1251 27

We have previously demonstrated that stimulation of the angiotensin (Ang) II type 2 receptor in vascular smooth muscle cells caused bradykinin production by activating kininogenase in transgenic mice. The aim of this study was to determine whether overexpression of AT2 receptors in cardiomyocytes attenuates Ang II-induced cardiomyocyte hypertrophy or interstitial fibrosis through a kinin/nitric oxide (NO)-dependent mechanism in mice. Ang II (1.4 mg/kg per day) or vehicle was subcutaneously infused into transgenic mice and wild-type mice for 14 days. The amount of cardiac AT2 receptor relative to AT1 receptor in transgenic mice was 22% to 37%. Ang II caused similar elevations in systolic blood pressure (by approximately 45 mm Hg) in transgenic mice and wild-type mice. Myocyte hypertrophy assessed by an increase in myocyte cross-sectional area, left ventricular mass, and atrial natriuretic peptide mRNA levels were similar in transgenic and wild-type mice. Ang II induced prominent perivascular fibrosis of the intramuscular coronary arteries, the extent of which was significantly less in transgenic mice than in wild-type mice. Inhibition of perivascular fibrosis in transgenic mice was abolished by cotreatment with HOE140, a bradykinin B2 receptor antagonist, or L-NAME, an inhibitor of NO synthase. Cardiac kininogenase activity was markedly increased (approximately 2.6-fold, P<0.001) after Ang II infusion in transgenic mice but not in wild-type mice. Immunohistochemistry indicated that both bradykinin B2 receptors and endothelial NO synthase were expressed in the vascular endothelium, whereas only B2 receptors were present in fibroblasts. These results suggest that stimulation of AT2 receptors present in cardiomyocytes attenuates perivascular fibrosis by a kinin/NO-dependent mechanism. However, the effect on the development of cardiomyocyte hypertrophy was not detected in this experimental setting.
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PMID:Cardiac angiotensin II type 2 receptor activates the kinin/NO system and inhibits fibrosis. 1251 37

We have evaluated the interaction between angiotensin II (Ang II) and the cholinergic transmission in anococcygeus smooth muscles isolated from rats treated (sympathectomised group) or not (vehicle group) with reserpine and alpha-methyl-p-tyrosine. For this, we contracted the tissues with Ang II in the presence and absence of atropine and hexamethonium. Ang II induced concentration-dependent contractions, which did not undergo temporal changes in tissues isolated from both groups of rats. In the vehicle group, Ang II induced more potent contractions than in the sympathectomised group. In the sympathectomised rat group, atropine inhibited the contractions induced by Ang II in a concentration-dependent fashion with no decrease in E(max). Additionally, hexamethonium inhibited the contraction induced by Ang II in a concentration-dependent fashion with a decrease in E(max). Association of atropine and hexamethonium produced Ang II-induced curves with rightward shifts from the control curve with a decrease in E(max). Incubation with N(G)-nitro-L-arginine methyl ester (L-NAME) reversed the effects of atropine and hexamethonium association. Conversely, in the vehicle group of rats, atropine and hexamethonium did not produce any significant effect. However, in the presence of yohimbine, atropine shifted the Ang II-induced curves to the right of the control curve with no E(max) decrease. Results suggest that there is a positive interaction between Ang II and cholinergic transmission in the rat anococcygeus smooth muscle mediated by angiotensin receptors located on pre-ganglionic cells.
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PMID:Inhibitory effects of atropine and hexamethonium on the angiotensin II-induced contractions of rat anococcygeus smooth muscles. 1259 59

We examined the effect of endogenous and exogenous nitric oxide (NO) on protein kinase C (PKC) activity induced by angiotensin II (Ang II) in cultured neonatal rat cardiomyocytes. The results are as follows. The activity of PKC was increased by Ang II (0.01-10 micromol/L) in a dose-dependent manner, but decreased by NO precursor L-arginine (L-Arg) (10 micromol/L-10 mmol/L) in a dose-dependent manner in cultured neonatal rat cardiomyocytes. Pretreatment with L-Arg (100 micromol/L) decreased significantly Ang II -activated PKC activity and PKC activity induced by phorbol 12-myristate 13-acetate (PMA) ( 10 micromol/L), a PKC activator. Pretreatment with N(G)-nitro-L-argingie methyl ester (L-NAME), a nitric oxide synthase (NOS) blocker, may inhibit significantly the role of L-Arg on Ang II - and PMA-activated PKC activity. The activity of PKC was also decreased by NO donor sodium nitroprusside (SNP) (10 micromol/L-1 mmol/L) in a dose-dependent manner in cultured neonatal rat cardiomyocytes. Pretreatment with SNP (10 micromol/L) decreased significantly Ang II - and PMA-activated PKC activity. These results indicate that PKC was controlled by both NO and Ang II. PKC may be a cross talk between Ang II and NO in cardiomyocytes. NO abolished the activity of PKC and impaired PKC downstream signaling transduction pathway cascades.
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PMID:[Influence of nitric oxide on the angiotensin II-activated protein kinase C activity in cultured neonatal rat cardiomycytes]. 1259 35

Angiotensin II (Ang II) fails to constrict renal medullary vasculature, possibly due to the counteraction of local vasodilators, such as prostaglandins or nitric oxide (NO). The effects of exogenous Ang II on intrarenal circulation were determined in anaesthetised rats that were untreated or pretreated with indomethacin (Indo) or L-NAME. The total renal blood flow (RBF), representing cortical perfusion, and outer and inner medullary blood flow (OMBF and IMBF) were measured. In untreated rats, Ang II decreased RBF in a dose dependent manner. Intravenous administration of 30 ng kg-1 min-1 Ang II decreased RBF by 38 % and OMBF by 9 % (both significant); IMBF was unaffected. Indo (5 mg kg-1 I.V.) significantly and similarly decreased OMBF and IMBF without affecting RBF. Ang II decreased IMBF by 27 % in Indo-pretreated rats, but caused no change in rats without pretreatment. The decreases in OMBF and RBF were comparable with or without Indo pretreatment. Inhibition of NO synthesis with L-NAME (0.6 mg kg-1 I.V.) significantly decreased RBF, OMBF and IMBF. Ang II infusion into L-NAME-pretreated rats induced a further significant decrease in RBF and OMBF without changing IMBF. We conclude that within the inner medulla, but not the outer medulla or cortex, prostaglandins effectively counteract the vasopressor effect of circulating Ang II.
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PMID:Prostaglandins but not nitric oxide protect renal medullary perfusion in anaesthetised rats receiving angiotensin II. 1264 10

We have reported that the induction of diabetes in N(omega)-nitro-L-orginine methyl ester (L-NAME)-infused rats causes significant hypertension that is associated with increased plasma renin activity. This study tested the role of angiotensin II (Ang II) by clamping it chronically at baseline levels. The clamp consisted of an intravenous infusion of enalapril (10 mg/kg/d), which decreased mean arterial pressure (MAP) by approximately 20 mm Hg after 3 days, and adding chronic Ang II at 4 ng/kg/min, which restored MAP to normal. Chronic L-NAME infusion increased MAP to 127 +/- 1 and 132 +/- 2 mm Hg in normal and clamped rats, respectively, and induction of diabetes (streptozotocin) increased MAP progressively in normal rats to 161 +/- 8 mm Hg by day 12, whereas MAP in the clamped rats decreased progressively to 98 +/- 5 mm Hg by day 12. In non-L-NAME rats, MAP averaged 95 +/- 1 and 91 +/- 1 mm Hg for normal and clamped groups, respectively, before diabetes, and MAP was 10 to 13 mm Hg lower in the clamped versus normal rats midway through the diabetic period. This suggests that Ang II is important for maintaining blood pressure at the onset of diabetes, possibly to compensate for renal volume losses. Angiotensin II also is required for the hypertension caused by induction of diabetes in rats with chronic blockade of nitric oxide synthesis, but whether this is due to increased volume sensitivity in L-NAME-treated, vasoconstricted rats remains to be determined.
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PMID:Control of arterial pressure by angiotensin II and nitric oxide at the onset of diabetes. 1285 Mar 96

The present study was designed to examine the relaxant and anticonstrictive effects of berberine in the isolated thoracic aorta in rats. Intravenous injection of berberine lowered the mean arterial pressure (MAP) of anesthesized rats in a dose-dependent manner. The angiotensin-converting enzyme (ACE) activities were inhibited significantly by the addition of berberine in a dose-dependent manner of which the IC50 value of berberine for ACE was 42 micrograms/ml (125 microM). In the endothelium-intact rings, angiotensin I-induced contraction was markedly attenuated by prior exposure of aortic rings to berberine. Treatment of the intact aortic rings with berberine (10 micrograms/ml) increased the NOx and cGMP productions relative to the vehicle-treated group. Berberine induced a dose-dependent relaxation in phenylephrine-precontracted aortic rings, but NG-nitro-L-arginine methyl ester (L-NAME)-pretreated intact aortic rings or functional removal of the endothelium attenuated the berberine-induced relaxation without an effect on maximum response. These results suggest that berberine has a hypotensive effect, at least in part, via the inhibition of ACE and direct release of NO/cGMP in the vascular tissues.
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PMID:Effects of berberine on angiotensin-converting enzyme and NO/cGMP system in vessels. 1456 65


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