Role of locally formed angiotensin II and bradykinin in the reduction of myocardial infarct size in dogs

Noda, Kohei; Sasaguri, Manabu; Ideishi, Munehito; Ikeda, Masaharu; Arakawa, Kikuo

doi:10.1093/cvr/27.2.334

Cited by 122 publications

(45 citation statements)

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“…26 Increases in Ang II levels from the anterior interventricular vein during ischemia were suppressed by the serine protease inhibitors nafamostat and chymostatin and were unaffected by captopril. In addition, we have previously shown that chronic mitral regurgitation in the dog results in an increase in cardiac mast cells, which correlates positively with the increase in cardiac chymase activity.…”

Section: Discussionmentioning

confidence: 97%

Evidence for Angiotensin-Converting Enzyme– and Chymase-Mediated Angiotensin II Formation in the Interstitial Fluid Space of the Dog Heart In Vivo

et al. 1999

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Background-We have previously demonstrated that angiotensin II (Ang II) levels in the interstitial fluid (ISF) space of the heart are higher than in the blood plasma and do not change after systemic infusion of Ang I. In this study, we assess the enzymatic mechanisms (chymase versus ACE) by which Ang II is generated in the ISF space of the dog heart in vivo. Methods and Results-Cardiac microdialysis probes were implanted in the left ventricular (LV) myocardium (3 to 4 probes per dog) of 12 anesthetized open-chest normal dogs. ISF Ang I and II levels were measured at baseline and during ISF infusion of Ang I (15 mol/L, nϭ12), Ang Iϩthe ACE inhibitor captopril (cap) (2.5 mmol/L, nϭ4), Ang Iϩthe chymase inhibitor chymostatin (chy) (1 mmol/L, nϭ4), and Ang Iϩcapϩchy (nϭ4). ISF infusion of Ang I increased ISF Ang II levels 100-fold (PϽ0.01), whereas aortic and coronary sinus plasma Ang I and II levels were unaffected and were 100-fold lower than ISF levels. Compared with ISF infusion of Ang I alone, Ang Iϩcap (nϭ4) produced a greater reduction in ISF Ang II levels than did Ang Iϩchy (nϭ4) (71% versus 43%, PϽ0.01), whereas Ang Iϩcapϩchy produced a 100% decrease in ISF Ang II levels. Conclusions-This study demonstrates for the first time a very high capacity for conversion of Ang I to Ang II mediated by both ACE and chymase in the ISF space of the dog heart in vivo. (Circulation. 1999;99:2583-2589.)

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Section: Discussionmentioning

confidence: 97%

Evidence for Angiotensin-Converting Enzyme– and Chymase-Mediated Angiotensin II Formation in the Interstitial Fluid Space of the Dog Heart In Vivo

et al. 1999

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“…Twentythree patients were treated with streptokinase (1.5 million IU IV over 60 minutes) and 18 were treated with rTPA (8 with bolus of 10 mg IV, followed by 50 mg infused over 60 minutes and then 40 mg infused over 120 minutes; 10 patients were administered rTPA and heparin according to the accelerated infusion protocol indicated by the GUSTO study). C4a and C3a were measured by radioimmunoassay, soluble terminal complement components (SC5b-9) and anti-SK IgG antibodies were measured by ELISA.…”

mentioning

confidence: 99%

Activation of complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction. A comparison between streptokinase and recombinant tissue-type plasminogen activator.

et al. 1994

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Background We have previously shown that treatment with streptokinase induces abrupt complement activation and transient neutropenia in patients with acute myocardial infarction (AMI). The purpose of this study was to compare the effects of two different thrombolytic agents -streptokinase (SK) and recombinant tissue-type plasminogen activator (rTPA) -on activation of the complement and kinin systems in plasma of patients with AMI.Methods and Results Forty-one patients with AMI who were eligible for thrombolytic therapy were studied. Twentythree patients were treated with streptokinase (1.5 million IU IV over 60 minutes) and 18 were treated with rTPA (8 with

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“…In the present study, there was no evidence for AT1 receptor activation by endogenously formed angiotensin II during normoxic incubation, as demonstrated by unchanged noradrenaline release after antagonism of the AT1 receptor. This is well explained by a negligible formation of angiotensin II in the heart during normoxic conditions (Noda et al, 1993). In anoxia, however, the AT1 receptor was maximally stimulated by endogenous angiotensin II, as documented by an attenuation of noradrenaline release by losartan alone and the lack of effect of exogenous angiotensin II in anoxia.…”

Section: Facilitatory Receptorsmentioning

confidence: 79%

“…A reason for this finding could be a maximal activation of these receptors by endogenous transmitters during anoxia. In fact, a substantial increase of angiotensin II formation during ischaemia has been reported (Noda et al, 1993). The increase of local angiotensin II concentrations at the receptor site may lead to maximal activation of the presynaptic AT1 receptor by endogenous angiotensin II in anoxia.…”

Section: Facilitatory Receptorsmentioning

confidence: 99%

Differential presynaptic modulation of noradrenaline release in human atrial tissue in normoxia and anoxia

Münch¹,

Kurz²,

Urlbauer³

et al. 1996

British J Pharmacology

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1Presynaptic modulation of noradrenaline release in human atrial tissue specimens was investigated under normoxic and anoxic conditions. 2 Noradrenaline release was induced by electrical stimulation and release during experimental intervention (S2) was compared with release during a preceding control stimulation (S5). The results were expressed as the geometric means and 95% confidence intervals of the S2/Sj ratio. 3 The a2-adrenoceptor agonist, UK 14304 (0.1 ymol -') significantly inhibited noradrenaline release, resulting in a S2/S, ratio of 0.49 (0.40-0.59), and the a2-adrenoceptor antagonist, yohimbine(1 ymol I-') increased noradrenaline release (S2/S, 1.83 [1.43-2.35]) during normoxia. Both compounds were ineffective during anoxia.4 Adenosine (30 ymol -') inhibited noradrenaline release with a S2/S, ratio of 0.54 (0.42-0.66). The adenosine antagonist, 8-phenyltheophylline, alone had no effect during normoxia. During anoxia, neither adenosine nor 8-phenyltheophylline altered noradrenaline release.5 The /32-adrenoceptor agonist, terbutaline (1 ymol 1-1) increased (1.53 [1.14-2.01]) and the ,Badrenoceptor antagonist, pindolol (1 umol 1-') suppressed noradrenaline release (0.62 [0.49-0.79]) under normoxic conditions. During anoxia, pindolol significantly inhibited noradrenaline release with a S2/S, ratio of 0.66 (0.51-0.85), whereas terbutaline did not influence noradrenaline release. 6 Angiotensin 11 (0.1 Mmol 11) enhanced noradrenaline release resulting in a S2/S, ratio of 1.44 (1.34-1.54), while the angiotensin II antagonist, losartan (1 ymol 1-') had no effect on noradrenaline release during normoxia. Conversely, angiotensin II did not increase noradrenaline release and losartan significantly inhibited noradrenaline release to a S2/S, ratio of 0.60 (0.46-0.77) during anoxia. 7 In conclusion, human cardiac tissue possesses presynaptic inhibitory a2-adrenoceptors and adenosine receptors, as well as facilitatory fi2-adrenoceptors and angiotensin II receptors regulating noradrenaline release under normoxic conditions. During anoxia the responses to a2-adrenoceptors and adenosine receptor stimulation are lost, whereas facilitatory responses to f2-adrenoceptors and angiotensin II receptor stimulation are maintained and these receptors appear to be maximally stimulated. This differential presynaptic modulation in anoxia may contribute to enhanced sympathetic activity in ischaemia.

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Role of locally formed angiotensin II and bradykinin in the reduction of myocardial infarct size in dogs

Cited by 122 publications

References 0 publications

Evidence for Angiotensin-Converting Enzyme– and Chymase-Mediated Angiotensin II Formation in the Interstitial Fluid Space of the Dog Heart In Vivo

Evidence for Angiotensin-Converting Enzyme– and Chymase-Mediated Angiotensin II Formation in the Interstitial Fluid Space of the Dog Heart In Vivo

Activation of complement and kinin systems after thrombolytic therapy in patients with acute myocardial infarction. A comparison between streptokinase and recombinant tissue-type plasminogen activator.

Differential presynaptic modulation of noradrenaline release in human atrial tissue in normoxia and anoxia

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