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ABSTRACT: Vasopressin V1a receptors (V1aR) were found in the cerebellum but their functional role has not been determined. As V1aR are engaged in the central regulation of the cardiovascular system and anxiogenic behavior and their role increases in the heart failure and stress, we decided to find out whether expression of V1aR is altered after myocardial infarction and chronic stressing. RT-PCR and Western blot analysis were performed to determine V1aR mRNA and protein expression in the cerebellum of four groups of rats (control sham-operated, infarcted, chronically stressed and infarcted chronically stressed). The myocardial infarct was produced by left coronary artery ligation, and chronic stressing by exposing the rat for four weeks to different types of mild stressors. The rats were sacrificed four weeks after the myocardial surgery or sham operation. Expressions of V1aR mRNA and protein were significantly lower in the infarcted and infarcted chronically stressed rats than in the sham-operated controls and chronically stressed not infarcted rats. No significant differences were found between the sham-operated controls and chronically stressed rats and between the infarcted rats and infarcted rats exposed to chronic stressing. It is concluded that V1aR mRNA and protein expressions are significantly down-regulated in the rats with the post-infarct heart failure but they are not affected by mild chronic stressing.
Neuroscience Letters 07/2011; 499(2):119-23. · 2.11 Impact Factor
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ABSTRACT: The present study was designed to determine the role of central vasopressin 1 receptors (V(1)R) in the regulation of cardiovascular parameters in chronically stressed infarcted rats and sham-operated rats under resting conditions and during exposure to acute alarming stress. The experiments were performed on four groups of conscious sham-operated and four groups of infarcted rats subjected to intraventricular infusion of either vehicle or a V(1)R antagonist (V(1)RANT). Two groups of infarcted and two groups of sham-operated rats were subjected to mild chronic stressing. Mean arterial blood pressure (MABP) and heart rate (HR) were determined under resting conditions and after exposure to acute stress (air jet). During vehicle infusion, MABP and HR increases in response to acute stress in the infarcted rats not subjected to chronic stress, and in the infarcted and sham-operated chronically stressed rats, were significantly greater than in the sham-operated rats not exposed to chronic stress. However, MABP and HR responses to acute stress in the chronically stressed infarcted rats and chronically stressed sham-operated rats did not differ. V(1)RANT abolished differences in cardiovascular responses to acute stress between the experimental groups. Resting cardiovascular parameters were not affected by any of the experimental treatments. It is concluded that chronic stressing enhances the pressor and tachycardic responses to acute stress in the sham-operated rats but does not further intensify these responses in infarcted rats.The results provide evidence that central V(1)Rs are involved in potentiation of cardiovascular responses to acute stress in chronically stressed rats, infarcted rats, and chronically stressed infarcted rats.
AJP Regulatory Integrative and Comparative Physiology 03/2010; 298(3):R672-80. · 3.34 Impact Factor
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ABSTRACT: Stress is one of the factors provoking cardiovascular complications. The purpose of the study was to explore the role of vasopressin (VP) in central control of arterial blood pressure and heart rate under resting conditions and during stimulation by an alarming stress (air jet stress) in myocardial infarct-induced cardiac failure. Six groups of male Sprague Dawley (SD) rats were subjected either to sham surgery (sham rats) or to ligation of a left coronary artery (infarcted rats). After 5 weeks both infarcted and sham rats were subjected either to intracerebroventricular infusion of artificial cerebrospinal fluid (aCSF) (sham aCSF and infarcted aCSF), [Arg8]-VP (sham VP and infarcted VP) or VP V1a receptor antagonist (d(CH2)5[Tyr(Me)2Ala-]VP, sham V1ANT and infarcted V1ANT). Air jet stress elicited significantly greater increases in mean arterial blood pressure (MABP) and heart rate in the infarcted aCSF than in the sham aCSF rats. Intracerebroventricular infusion of V1ANT significantly reduced resting MABP and MABP and heart rate increases in response to stress in the infarcted but not in the sham rats. Intracerebroventricular infusion of VP elicited a significant increase in resting MABP in the infarcted VP but not in the sham VP rats. The results provide evidence for enhanced engagement of the brain V1 VP receptors in regulation of resting MABP and in generation of exaggerated cardiovascular responses to air jet stress during the post-infarct state.
07/2009; 8(4):273-284.
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ABSTRACT: Progress in the management of myocardial infarction has contributed to the increased population of patients with asymptomatic left ventricular dysfunction or congestive heart failure. These patients are at high risk of sudden cardiac death. Factors that worsen this prognosis include exacerbation of coronary artery disease and acute coronary syndrome. We aimed to define and compare risk factors of acute coronary syndrome and sudden cardiac death as well as the cumulative incidence of both in patients after myocardial infarction with asymptomatic left ventricular dysfunction or congestive heart failure during a 2-year follow-up period.
We enrolled 320 patients who survived the first 2 to 3 weeks after first ST-elevated myocardial infarction. Seventy-one patients who developed acute coronary syndrome and 38 who experienced sudden cardiac death were analyzed.
In patients with asymptomatic left ventricular dysfunction, the only independent predictor of sudden cardiac death was male sex. Diabetes was the only predictor for acute coronary syndrome. In patients with chronic heart failure, low heart-rate variability was the strongest independent predictor of sudden cardiac death. Increased mean 24-hour heart rate was the most powerful predictor of acute coronary syndrome. The cumulative incidence of acute coronary syndrome and sudden cardiac death was most strongly associated with a total cholesterol level >200 mg/dL and increased QT-interval dispersion.
Predictors of acute coronary syndrome and sudden cardiac death differ in patients after myocardial infarction with asymptomatic left ventricular dysfunction or chronic heart failure and are inconsistent at different stages of development of chronic heart failure.
Medical science monitor: international medical journal of experimental and clinical research 06/2009; 15(6):PH40-8. · 1.70 Impact Factor
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ABSTRACT: Presently a lot of studies focus on metabolic syndrome. There are new studies regarding the relationship between metabolic syndrome (MS) and changes in myocardial structure and function and subsequent development of heart failure. The aim of the study was to assess the myocardial structure and function, particularly diastolic function, and to evaluate the exercise capacity in patients with metabolic syndrome.
53 patients with MS (defined according to NCEP ATP III criteria) and 33 individuals in control group were enrolled into the study. Echocardiographic examination (with evaluation of morphologic parameters, ejection fraction and diastolic function) and ergospirometry (to objectively assess the exercise capacity) were performed in all patients.
In patients with MS hypertension (100%) and abdominal obesity (98%) were the most frequent. In the studied group significantly lower E/A ratio (describing left ventricle relaxation) was observed in comparison to control group (E/A 1.0 +/- 0.05 vs. 1.29 +/- 0.11; p < 0.05). Diastolic dysfunction assessed with the use of E/A worsened with the number of metabolic syndrome elements (1.07 vs. 0.96 vs. 0.87 for 3, 4 and 5 metabolic syndrome elements respectively). Lower peak oxygen uptake (VO2 peak) was observed in patients with MS in comparison to control group (24 +/- 0.75 vs. 27 +/- 1.52 ml/kg/min; p < 0.05). There was the tendency to higher VE-CO2 slope index in patients with MS in comparison to control group (27 +/- 0.45 vs. 25 +/- 0.7; p = 0.057). VE-CO2 slope increased with the increase of the number of MS elements (26 vs. 28 vs. 29 for 3, 4 and 5 metabolic syndrome elements). There was significant positive correlation between E/A ratio and VO2 peak (r = 0.27; p < 0.05) and significant negative correlation between E/A ratio and VE-CO2 slope (r = -0.37; p < 0.01).
In patients with metabolic syndrome the significant decrease of exercise capacity assessed by ergospirometry and lower values of E/A ratio (that describes left ventricle relaxation) in comparison to control group. It seems that there is casual relation between these parameters and one may conclude that patients with MS are at risk of development of left ventricle dysfunction and in consequence heart failure.
Polski merkuriusz lekarski: organ Polskiego Towarzystwa Lekarskiego 07/2008; 25(145):15-8.
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ABSTRACT: The purpose of the present study was to elucidate if rats with myocardial infarction manifest altered responsiveness to central cardiovascular effects of low doses of angiotensin II (ANG II), and if ANG II and vasopressin (VP) cooperate in the central regulation of cardiovascular functions at rest and during stress. Conscious Sprague-Dawley rats with myocardial infarction induced by left coronary artery ligation, or sham-ligated (SL) controls were infused intracerebroventricularly with artificial cerebrospinal fluid (aCSF), ANG II, ANG II + VP or ANG II + V1a receptor antagonist (V1ANT) 4 weeks after cardiac surgery. In the infarcted but not in the SL rats, the resting mean arterial blood pressure (MABP) was significantly elevated by infusions of ANG II and ANG II + VP, while infusion of ANG II + V1ANT was not effective. During administration of aCSF, the pressor, and tachycardic responses to an air-jet stressor were significantly greater in the infarcted than in the SL rats. In the SL rats, the pressor responses to the stressor were significantly greater during infusions of ANG II, ANG II + VP and ANG II + V1ANT than during infusion of aCSF. The tachycardic response in the SL rats was enhanced only by the combined infusion of ANG II + VP. In the infarcted rats, the pressor and the tachycardic responses to the stressor were similar in all groups. It is concluded that: (1) under resting conditions the infarcted rats manifest sensitisation to the central pressor effect of ANG II and that this effect depends on concomitant stimulation of V1a VP receptors, (2) central ANG II may enhance the pressor response to an alarming stressor in the SL rats through an action which does not depend on the concomitant stimulation of V1a receptors, (3) the cooperative action of ANG II and VP is required for intensification of the tachycardic response to the alarming stressor in the SL rats and (4) exaggeration of the cardiovascular responses to the alarming stressor in the infarcted rats cannot be further augmented by an additional stimulation of central ANG II receptors or combined stimulation of ANG II and VP receptors.
Stress (Amsterdam, Netherlands) 02/2008; 11(4):290-301. · 3.21 Impact Factor
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ABSTRACT: Experimental objectives. Because myocardial infarct is associated with overactivation of brain angiotensin II (ANG II) and vasopressin (AVP) V1a receptors we decided to determine whether AT1 and V1a receptors-mediated effects of ANG II and AVP interact in central cardiovascular control during the post-infarct state. Four groups of infarcted and four groups of sham-operated conscious rats entered the study. Results. In the infarcted rats cerebroventricular infusion of AT1 (AT1ANT, losartan) and V1a antagonist {V1aANT,d(CH(2))(5)[Tyr(Me)(2)Ala-NH(2)(9)]VP} and combined infusion of both these compounds performed 4 weeks after induction of the infarct significantly and comparably reduced mean arterial blood pressure (MABP) in comparison to control experiments (artificial cerebrospinal fluid infusion). In the sham rats MABP was not affected by any of the infusions. In control experiments MABP and HR responses to an alarming air jet stress were significantly higher in the infarcted than in the sham rats. Both responses were normalized with the same effectiveness by administration of AT1ANT, V1aANT and AT1ANT+V1aANT. In the sham rats administration of these compounds did not affect MABP and HR responses to stress. CONCLUSION: The results provide evidence for interaction of AT1 and V1a receptors-mediated effects of ANG II and AVP in the central cardiovascular control during the post-infarct state.
Regulatory Peptides 09/2007; 142(3):86-94. · 2.11 Impact Factor
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ABSTRACT: Stress is one of the factors provoking cardiovascular complications. The purpose of the study was to explore the role of vasopressin (VP) in central control of arterial blood pressure and heart rate under resting conditions and during stimulation by an alarming stress (air jet stress) in myocardial infarct-induced cardiac failure. Six groups of male Sprague Dawley (SD) rats were subjected either to sham surgery (sham rats) or to ligation of a left coronary artery (infarcted rats). After 5 weeks both infarcted and sham rats were subjected either to intracerebroventricular infusion of artificial cerebrospinal fluid (aCSF) (sham aCSF and infarcted aCSF), [Arg8]-VP (sham VP and infarcted VP) or VP V1a receptor antagonist (d(CH2)5[Tyr(Me)2Ala-]VP, sham V1ANT and infarcted V1ANT). Air jet stress elicited significantly greater increases in mean arterial blood pressure (MABP) and heart rate in the infarcted aCSF than in the sham aCSF rats. Intracerebroventricular infusion of V1ANT significantly reduced resting MABP and MABP and heart rate increases in response to stress in the infarcted but not in the sham rats. Intracerebroventricular infusion of VP elicited a significant increase in resting MABP in the infarcted VP but not in the sham VP rats. The results provide evidence for enhanced engagement of the brain V1 VP receptors in regulation of resting MABP and in generation of exaggerated cardiovascular responses to air jet stress during the post-infarct state.
Stress 01/2006; 8(4):273-84. · 2.48 Impact Factor
