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The contribution of bradykinin potentiation to both ACE inhibitor and angiotensin AT1-receptor subtype blockade was assessed by cotreatment of rats with a bradykinin B2-receptor antagonist. MI was produced by coronary artery ligation in adult male Wistar rats. Quinapril and losartan reduced left ventricular end-diastolic pressure and global left ventricular diastolic wall stress only in rats with large MI.
Pressure volume curves showed a rightward shift in proportion to MI size that was not prevented by quinapril or losartan treatment. Only the ACE inhibitor reduced left ventricular weight and this effect was prevented by cotreatment with the bradykinin antagonist.
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Baseline and peak cardiac index and stroke volume index, as determined using an electromagnetic flowmeter before and after an acute intravenous volume load, were restored by quinapril, whereas losartan had no effects. Treatments starting 30 min after coronary artery ligation, with either quinapril or losartan, reduced preload only in rats with large MI. Despite this unloading of the heart, structural dilatation was not prevented by this early treatment.
Only quinapril improved cardiac performance and reduced left ventricular weight and this effect was abolished by cotreatment with Hoe, suggesting an angiotensin II blockade-independent, but bradykinin potentiation-dependent, mechanism. Time for primary review 34 days. Left ventricular dilatation appears to play a key role in the development of heart failure [1, 2, 4—6] and for prognosis  in patients after a large infarct.
The potential for progressive ventricular dilatation exists from the time of coronary occlusion and infarction [4, 5, 8—13]. It might be important, therefore, to start ACE inhibitor therapy as soon as possible after myocardial infarction MI [1, 14—16]. However, it could also block early compensatory mechanisms, including early compensatory left ventricular dilatation .
Treatment with captopril 2 h, two days or three weeks after acute MI has beneficial effects in the rat MI model [1, 2, 17]. In contrast, the acute application of ACE inhibitors along with thrombolytic therapy showed some survival benefits as early as five—six weeks after the infarct [19, 20].
Thus, the long-term effects of early started treatment with ACE inhibitors post infarct are not well understood. AII receptor-independent effects have also been suggested [21—23]. Specific AII receptor antagonists have only recently become available . Most recently, Schieffer et al. Moreover, it is suggested that multiple actions relevant to cardiovascular control of ACE inhibitors were related in part to bradykinin potentiation, and cotreatment with a bradykinin receptor antagonist abolished all ACE inhibitor-induced effects on cardiac function in stroke-prone spontaneously hypertensive rats .
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Finally, the important role of myocardial infarct size has not been analyzed for the effect of early treatment with ACE inhibitors or AII receptor antagonists. It remains unclear so far why ACE inhibitors reduced left ventricular volume only in animals with large infarcts .
Therefore, we studied the chronic effects on hemodynamics, left ventricular volume and wall stress of ACE inhibition by quinapril or blockade of AII receptor by losartan. The contribution of bradykinin potentiation to both ACE inhibitor- and AII blocker actions was also assessed by cotreatment of rats with the bradykinin B2-receptor antagonist, Hoe All drugs were initiated 30 min after coronary artery ligation.
This article has been cited by other articles in PMC. Abstract The pattern of DNA methylation at cytosine bases in the genome is tightly linked to gene expression, and DNA methylation abnormalities are often observed in diseases. TET genes, and especially TET2, are frequently mutated in various cancers, but how the TET proteins contribute to prevent the onset and maintenance of these malignancies is largely unknown. Here, we highlight recent advances in understanding the physiological function of the TET proteins and their role in regulating DNA methylation and transcription.
In addition, we discuss some of the key outstanding questions in the field. Does deposition of 5-hydroxymethylcytosine 5hmC inhibit the maintenance of DNA methylation in vivo? What is the link between TET2 inactivation, transcriptional changes, and premalignant and malignant hematopoiesis? Are fully transformed tumor cells dependent on the initial TET mutation? Do the biological functions of the TET proteins depend on their catalytic function?
The vertebrate genome is bundled into a highly organized chromatin structure fundamental for precise gene regulation and maintenance of genome integrity.