Agnieszka Cudnoch-Jedrzejewska

Medical University of Warsaw, Warszawa, Masovian Voivodeship, Poland

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Publications (14)30.77 Total impact

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    ABSTRACT: Abstract The role of central oxytocin in the regulation of cardiovascular parameters under resting conditions and during acute stress was investigated in male normotensive Wistar-Kyoto (WKY; n=40) and spontaneously hypertensive (SHR; n=28) rats. In Experiment 1 mean arterial blood pressure (MABP) and heart rate (HR) were recorded in WKY and SHR rats at rest and after an air jet stressor during intracerebroventricular (ICV) infusions of vehicle, oxytocin or oxytocin receptor (OTR) antagonist. In Experiment 2 the effects of vehicle, oxytocin and OTR antagonist were determined in WKY rats after prior administration of a V1a vasopressin receptor (V1aR) antagonist. Resting MABP and HR were not affected by any of the ICV infusions either in WKY or in SHR rats. In control experiments (vehicle), the pressor response to stress was significantly higher in SHR. Oxytocin enhanced the pressor response to stress in the WKY rats but reduced it in SHR. During V1aR blockade, oxytocin infusion entirely abolished the pressor response to stress in WKY rats. Combined blockade of V1aR and OTR elicited a significantly greater MABP response to stress than infusion of V1a antagonist and vehicle. This study reveals significant differences in the regulation of blood pressure in WKY and SHR rats during alarming stress. Specifically, the augmentation of the pressor response to stress by exogenous oxytocin in WKY rats is caused by its interaction with V1aR, and endogenous oxytocin regulates the magnitude of the pressor response to stress in WKY rats by simultaneous interaction with OTR and V1aR.
    Stress (Amsterdam, Netherlands) 12/2013; · 3.21 Impact Factor
  • Elwira Milik, Ewa Szczepanska-Sadowska, Agnieszka Cudnoch-Jedrzejewska, Jakub Dobruch
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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. · 2.03 Impact Factor
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    E Szczepanska-Sadowska, A Cudnoch-Jedrzejewska, M Ufnal, T Zera
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    ABSTRACT: In spite of significant progress in pharmacotherapy the incidence of newly diagnosed cases of cardiovascular diseases and cardiovascular morbidity is alarmingly high. Treatment of hypertension or heart failure still remains a serious challenge. Continuous attempts are made to identify the mechanisms that decide about susceptibility to pathogenic factors, and to determine effectiveness of a specific therapeutic approach. Coincidence of cardiovascular diseases with metabolic disorders and obesity has initiated intensive research for their common background. In the recent years increasing attention has been drawn to disproportionately greater number of depressive disorders and susceptibility to stress in patients with coronary artery disease. An opposite relationship, i.e. a greater number of sudden cardiovascular complications in patients with depression, has been also postulated. Progress in functional neuroanatomy and neurochemistry provided new information about the neural network responsible for regulation of cardiovascular functions, metabolism and emotionality in health and under pathological conditions. In this review we will focus on the role of neuromodulators and neurotransmitters engaged in regulation of the cardiovascular system, neuroendocrine and metabolic functions in health and in pathogenesis of cardiovascular diseases and obesity. Among them are classical neurotransmitters (epinephrine and norepinephrine, serotonin, GABA), classical (CRH, vasopressin, neuropeptide Y) and newly discovered (orexins, apelin, leptin IL-1beta, TNF-alpha, ghrelin) neuropeptides, gasotransmitters, eicozanoids, endocannabinoids, and some other compounds involved in regulation of neuroendocrine, sympatho-adrenal and parasympathetic nervous systems. Special attention is drawn to those factors which play a role in immunology and inflammatory processes. Interaction between various neurotransmitter/neuromodulatory systems which may be involved in integration of metabolic and cardiovascular functions is analyzed. The survey gives evidence for significant disturbances in release or action of the same mediators in hypertension heart failure, obesity, diabetes mellitus, metabolic syndrome, starvation, chronic stress, depression and other psychiatric disorders. With regard to the pathogenic background of the cardiovascular diseases especially valuable are the studies showing inappropriate function of angiotensin peptides, vasopressin, CRH, apelin, cytokines and orexins in chronic stress, cardiovascular and metabolic diseases. The studies surveyed in this review suggest that multiple brain mechanisms interact together sharing the same neural circuits responsible for adjustment of function of the cardiovascular system and metabolism to current needs.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 10/2010; 61(5):509-21. · 2.48 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. · 3.28 Impact Factor
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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. · 1.36 Impact Factor
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    ABSTRACT: The present study was designed to determine the role of central oxytocin (OXY) in regulation of the cardiovascular responses to the alarming stress. Three groups of male, normotensive Sprague Dawley rats, received intracerebroventricular (i.c.v.) infusion of one of the following: 1) vehicle, 2) OXY or 3) OXY antagonist (OXANT). Mean arterial blood pressure (MABP) and heart rate (HR) were recorded at rest, during and after application of the alarming stressor (air jet). Under resting conditions the i.c.v. infusions of vehicle, OXY or OXYANT did not influence the cardiovascular parameters. The alarming stressor evoked significant increases in MABP and HR that were significantly greater in the rats receiving i.c.v. infusion of oxytocin antagonist than in those receiving vehicle or OXY. The study provides evidence that stimulation of the brain oxytocin receptors by endogenous oxytocin plays significant role in inhibition of cardiovascular responses to stress.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 01/2009; 59 Suppl 8:123-7. · 2.48 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
  • E Milik, E Szczepańska-Sadowska, W Maśliński, A Cudnoch-Jedrzejewska
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    ABSTRACT: Increasing evidence suggests that enhanced stimulation of the heart and kidney by mineralocorticoids plays significant role in development of the post-infarct cardiac failure. Because increased synthesis of mineralocorticoid receptors (MR) is one of the putative factors determining pathogenic effects of mineralocorticoids we decided to determine whether the myocardial infarct results in an enhanced expression of MR mRNA and MR protein. To this end male Sprague-Dawley rats were subjected either to ligation of the left coronary artery or to sham surgery. After four weeks expressions of MR mRNA and MR protein were evaluated in both groups of rats in the left (LV) and right (RV) ventricle walls, and in the renal cortex and renal medulla by means of semiquantitative PCR and Western blotting methods. Coronary ligation resulted in the myocardial infarction encompassing 30.2% +/- 1.9% (range 23-40%) of the left ventricle wall. In the infarcted rats expression of MR mRNA was significantly greater than in the sham-operated rats, both in the LV (P<0.02) and in the RV (P<0.005). In the left but not in the right ventricle increased MR mRNA expression was associated with significant increase in expression of MR protein (P<0.001). In the renal cortex and renal medulla MR mRNA and MR protein expression in the infarcted and the sham-operated rats did not differ. The study reveals that during the post-infarct state expression of MR mRNA is elevated in both cardiac ventricles while expression of MR mRNA protein is increased only in the left ventricle. The results suggest that the enhanced expression of mineralocorticoid receptors may contribute to enhanced effects of mineralocorticoids in the heart during the post-infarct state.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 12/2007; 58(4):745-55. · 2.48 Impact Factor
  • Agnieszka Cudnoch-Jedrzejewska, Jakub Dobruch, Liana Puchalska, Ewa Szczepańska-Sadowska
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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. · 2.06 Impact Factor
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    ABSTRACT: The myocardial infarct causes prolonged activation of the renin-angiotensin system and profoundly influences cardiac performance and renal excretory capabilities. The aim of the present study was to determine whether the myocardial infarct is also associated with an altered expression of AT1a receptors (AT1aR) mRNA in the heart and the kidney. To this end male Sprague-Dawley rats were subjected either to the left coronary artery ligation or to the sham surgery. Four weeks after the surgery the animals were sacrificed. In 11 infarcted and 10 sham-operated rats expression of AT1aR mRNA in the walls of the left and right ventricle of the heart, and in the renal cortex and renal medulla was determined by semiquantitative PCR method. In another group of 10 infarcted and 14 sham-operated rats the diameter of cardiomyocytes in the left and right cardiac ventricle was determined. The size of the infarct in the rats used for mRNA determination and for morphometric measurements was equal to 29.4 +/- 1.8% and to 31.0 +/- 1.2 % of the left ventricular wall, respectively. Expression of AT1aR mRNA was significantly greater in the left (P< 0.01) and right ventricle (P<0.03) of the heart in the infarcted than in the sham operated rats. AT1aR mRNA expression was also significantly greater (P<0.02) in the renal medulla of the infarcted rats than in the renal medulla of the sham operated rats whereas no significant difference was found in the renal cortex. The myocardial infarct was associated with a significant increase of diameter of cardiomyocytes of the left ventricle of the heart (P< 0.0001), however there was no significant correlation between changes in AT1aR mRNA expression and diameter of cardiomyocytes. The results provide evidence that the myocardial infarct results in significant and prolonged upregulation of AT1a receptors mRNA expression in the heart and in the medullary region of the kidney.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 10/2006; 57(3):375-88. · 2.48 Impact Factor
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    ABSTRACT: The purpose of the study was to determine effect of high sodium intake on fluid and electrolyte turnover and heart remodeling in the cardiac failure elicited by myocardial infarction (MI). The experiments were performed on four groups of Sprague Dawley rats maintained on food containing 0.45% NaCl and drinking either water (groups 1, 2) or 1% NaCl (groups 3, 4). Groups 1 and 3 were sham-operated while in groups 2 and 4 MI was produced by the coronary artery ligation. In each group food and fluid as well as sodium intake, urine (Vu), sodium (UNaV), potassium (UKV) and solutes (UosmV) excretion were determined before and four weeks after the surgery. Size of the infarct, left ventricle (LV) weight and diameter of LV and right ventricle (RV) myocytes were determined during post-mortem examination. Before the surgery groups 3 and 4 ingested significantly more fluid and sodium, had higher Vu, UNaV, UKV and UosmV than the respective groups 1 and 2. In groups 2 and 4 MI resulted in significant decrease in Vu, UNaV and UosmV in comparison to the pre-surgical level. In Group 4 MI resulted also in a significant decrease of food and sodium intake. The MI size did not differ in groups 2 and 4 while diameter of LV myocytes was significantly greater in groups 2 and 4 than in groups 1 and 3, and in group 4 than in group 2. The study reveals that prolonged high sodium consumption increases fluid and electrolyte turnover both in the sham and in the MI rats and that the MI causes decrease in food and sodium intake in rats on high but not on regular sodium intake. In addition high sodium diet promotes development of greater post-MI hypertrophy of the LV myocytes.
    Journal of physiology and pharmacology: an official journal of the Polish Physiological Society 01/2006; 56(4):599-610. · 2.48 Impact Factor
  • Jakub Dobruch, Agnieszka Cudnoch-Jedrzejewska, Ewa Szczepanska-Sadowska
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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. · 3.25 Impact Factor
  • Atherosclerosis Supplements - ATHEROSCLER SUPPL. 01/2006; 7(3):208-208.