Wyniki wyszukiwania

1

Effects of angiotensin derivatives [Lang] - filled liposomes on isolated rat aorta

100%

Costuleanu M., Costuleanu N., Foia L., Slatineanu S. M., Costuleanu A., Petrescu G.

Cellular and Molecular Biology Letters

|

1999

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tom 04

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nr 2

2

ACE inhibitor and AT1 antagonist stimulate duodenal HCO3 secretion mediated by a common pathway - involvement of PG, NO and bradykinin

100%

Aihara E., Kagawa S., Hayashi M., Takeuchi K.

Journal of Physiology and Pharmacology

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2005

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tom 56

|

nr 3

Recent study demonstrated that duodenal HCO3- secretion is affected by modulation of the renin-angiotensin system. We examined the effects of enalapril (angiotensin-converting enzyme (ACE) inhibitor) or losartan (angiotensin AT1 receptor antagonist) on duodenal HCO3- secretion in rats and investigated the mechanisms involved in the renin-angiotensin system-related HCO3- response. A proximal duodenal loop was perfused with saline, and HCO3- secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. Enalapril increased the HCO3- secretion in a dose-dependent manner, with a decrease in arterial blood pressure (MBP), and these effects were significantly attenuated by pretreatment with indomethacin, L-NAME and FR172357 (a selective bradykinin B2 receptor antagonist). Although losartan alone did not affect the HCO3- secretion, despite reducing MBP, the agent dose-dependently increased the HCO3- secretion in the presence of angiotensin II, and this response was totally antagonized by prior administration of FR172357, indomethacin and L-NAME. Bradykinin also dose-dependently increased the HCO3- secretion with no change in MBP, though transient, and again the effects were blocked by indomethacin, L-NAME and FR172357. Both prostaglandin (PG) E2 and the nitric oxide (NO) donor NOR-3 also increased the HCO3- secretion, the latter effect being inhibited by indomethacin. These results suggest that both an ACE inhibitor and AT1 antagonist (in the presence of angiotensin II) increase duodenal HCO3- secretion via a common pathway, involving bradykinin, NO and PGs. It is also assumed that bradykinin releases NO locally, which in turns stimulates HCO3- secretion mediated by PGs.

3

Comparison between the effects of lisinopril and losartan on the cough reflex in anesthetized and awake rabbits

84%

Mutolo D., Cinelli E., Bongianni F., Evangelista S., Pantaleo T.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 2

4

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Neuroendocrine factors in salt appetite

84%

Stellar E., Epstein A. N.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 4

We dedicate this paper to Curt P. Richter, father of the study of salt appetite, who died recently at the age of 94. Richter first demonstrated that the adrenalectomized rat’s voracious appetite for salt kept it alive (1936) and showed the same in humans (1940). Our first paper in 1955 demonstrated that salt appetite was an innate response to salt depletion. Since then, we have pursued the notion that the neuroendocrine consequences of sodium depletion create a brain state that raises salt appetite. In Epstein’s laboratory, it was shown that angiotensin and aldosterone, the hormones of salt retention in the periphery, act synergistically in the brain to produce salt appetite in the rat. Block either hormone and the appetite is reduced by half; block both and the appetite is eliminated despite severe bodily need. With repeated depletions or treatments of the brain with angiotensin and aldosterone, salt ingestion increases, reaching an asymptote by the third depletion. Need-free intake of NaCI also increaes, especially in female rats which ingest more NaCI than male rats. In Stellar’s laboratory, running speed to salt solutions in a runway is used as a measure of salt appetite. When the appetite is raised with large doses of DOCA, a mimic of aldosterone, rats run rapidly for a taste of strong salt solutions as high as 24% (almost 4 molar). Using ingestion as a measure, the role of the atrial natriuretic peptide (ANP), an antagonist of angiotensin’s physiological effect, was investigated as a modulator of salt appetite. When angiotensin is involved is producing salt appetite, following sodium depletion by a diuretic combined with a low-salt diet, ANP reduced salt intake by 40%. When salt appetite was raised by DOCA, however, ANP either had no effect or reduced salt ingestion by only 10%. The subfornical organ, the lateral preoptic area, and the central and medial nuclei of the amygdala are being investigated as major components of the limbic circuit underlying salt appetite produced by the actions of angiotensin, aldosterone and ANP in the brain.

5

Angiotensin 1-7 formation in breast tissue is attenuated in breast cancer - a study on the metabolism of angiotensinogen in breast cancer cell lines

84%

Bujak-Gizycka B., Madej J., Bystrowska B., Toton-Zuranska J., Kus K., Kolton-Wroz M., Jawien J., Olszanecki R.

Journal of Physiology and Pharmacology

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2019

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tom 70

|

nr 4

6

Angiotensin metabolism in rat stomach wall: prevalence of angiotensin-(1-7) formation

84%

Olszanecki R., Madej J., Suski M., Gebska A., Bujak-Gizycka B., Korbut R.

Journal of Physiology and Pharmacology

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2009

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tom 60

|

nr 1

191-196

Our view of renin-angiotensin system (RAS) has changed over the past two decades: new metabolites and pathways have been described; also the importance of local renin-angiotensin systems became more clearly understood. However, there is relatively scarce information about formation and action of angiotensin peptides in gastrointestinal tract, especially in the stomach. Here, using LC-ESI-MS method we assessed the metabolism of Ang I in organ bath of rat stomach wall. Additionally we compared the expression of mRNA of angiotensin converting enzymes (ACE, ACE2) and neprilysin (NEP) in the stomach, aorta and renal artery in rats. Despite, similar levels of expression of ACE and ACE2 mRNA in stomach wall, aorta and renal artery, the absolute amounts of main Ang I metabolites produced by stomach wall (in ng/mg of dry tissue) were much lower than that produced by aorta and renal artery. Also, the pattern of angiotensin I metabolites was different: opposite to aorta and renal artery, incubation of Ang I with stomach wall fragments resulted in predominant formation of Ang-(1-7) and relatively lower production of Ang II. In stomach wall both, perindoprilat and tiorphan decreased production of Ang II, but did not influence generation of Ang-(1-7). In conclusion, we identified Ang-(1-7) as the main product of Ang I conversion in rat stomach wall. The biological role of prevalence of Ang-(1-7) formation in stomach require further investigation.

7

Angiotensin II - derived peptides devoid of phenylalanine in position 8 have full psychotropic activity of the parent hormone

84%

Holy Z., Braszko J., Kupryszewski G., Witczuk B., Wisniewski K.

Journal of Physiology and Pharmacology

|

1992

|

tom 43

|

nr 2

In this work we compared in rats the influence of heptapeptide 1-7-angiotensin II, hexapeptide 2-7-angiotensin II, pentapeptide 3-7-angiotensin II and angiotensin II on motility, stereotypy, learning of conditioned avoidance responses and recall of passive avoidance behaviour allowing to avoid aversive stimulation. The 4 peptides administered 15 min before the experiment, tended to increase the number of crossings, rearings and bar approaches in open field, significantly accelerated acquisition of conditioned avoidance responses and improved recall of the passive avoidance. All the peptides applied immediately before the experiment intensified stereotypy evoked by apomorphine in the dose 1 mg/kg and amphetamine in the dose 6.5 mg/kg given intraperitoneally. These results show full psychotropic activity of the examined fragments of angiotensin II, comparable with the activity of the parent octapeptide. Our previous hypothesis that the Val-Tyr-Ile-His-Pro fragment of angiotensin II is responsible for the psychotropic activity evoked by angiotensins in rats is thus confirmed.

8

Short term 13-cis-retinoic acid treatment at therapeutic doses elevates expression of leptin, GLUT4, PPARgamma and aP2 in rat adipose tissue

67%

Krskova-Tybitanclova K., Macejova D., Brtko J., Baculikova M., Krizanova O., Zorad S.

Journal of Physiology and Pharmacology

|

2008

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tom 59

|

nr 4

731-743

Temporary defects in the plasma lipid and glucose homeostasis are frequent complication accompanying chronic treatment with 13-cis-retinoic acid (13cRA). White adipose tissue acts as an endocrine organ producing a variety of hormones (adipocytokines) including leptin, adiponectin, tumor-necrosis factor alpha (TNF) and angiotensin II (Ang II), which influence lipid metabolism, systemic insulin sensitivity and inflammation. To study the effect of a short-term 13cRA administration on metabolism of epididymal fat tissue, we treated Wistar rats with five identical therapeutic doses of 13cRA (0.8 mg/kg b.w.) by gavage during a period of 10 days. Expression of adiponectin, leptin, TNF and selected proteins such as adipocyte fatty acid binding protein (aP2), insulin-dependent glucose transporter GLUT4, peroxisome proliferator-activated receptor gamma (PPAR) and retinoid X receptors (RXRs) was investigated using RT-PCR. Short-term treatment with therapeutic doses of 13cRA caused significant increase of the aP2, PPAR and moderately RXR gene expression. Similarly, the relative amount of mRNA for leptin and GLUT4 was increased, while the TNF transcript was decreased after treatment with 13cRA. The gene expression and plasma concentration of adiponectin were without any significant changes. Since local adipose renin-angiotensin system (RAS) has been presumed to be involved in the regulation of fat tissue metabolism, we also investigated the gene expression of RAS components in epididymal fat depot. Our data has shown that 13cRA elevated Ang II receptor type 1 (AT1 receptor) - at both, mRNA and protein level. Thus, our results demonstrate that short-term 13cRA treatment is inducing alterations in fat tissue metabolism in relation to stimulated adipogenesis.

9

Myrtus communis improves cognitive impairment in renovascular hypertensive rats

67%

Cevikelli-Yakut Z.-A., Ertas B., Sen A., Koyuncuoglu T., Yegen B. C., Sener G.

Journal of Physiology and Pharmacology

|

2020

|

tom 71

|

nr 5

10

Angiotensinogen and angiotensin-converting enzyme mRNA decrease and AT1 receptor mRNA and protein increase in epididymal fat tissue accompany age-induced elevation of adiposity and reductions in expression of GLUT4 and peroxisome proliferator-activated receptor (PPARgamma)

67%

Krskova K., Filipcik P., Zilka N., Olszanecki R., Korbut R., Gajdosechova L., Zorad S.

Journal of Physiology and Pharmacology

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2011

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tom 62

|

nr 4

11

Spironolactone, but not enalapril, potentiates hypoxia-inducible factor-1alpha and Ets-1 expression in newborn rat kidney

67%

Yim H. E., Kim J. H., Yoo K. H., Bae I. S., Jang G. Y., Hong Y. S., Lee J. W.

Journal of Physiology and Pharmacology

|

2010

|

tom 61

|

nr 1

73-81

Hypoxia is regarded as an important physiological factor that controls nephrogenesis. We investigated whether the renin-angiotensin-aldosterone system (RAAS) affects hypoxia-related target genes in developing kidneys. Newborn rat pups were treated with enalapril (30 mg/kg/d) or spironolactone (200 mg/kg/d) for 7 days. Tissue hypoxia was assessed by the uptake of a hypoxyprobe-1, pimonidazole (200 mg/kg), and the expression of hypoxia-responsive genes. In the enalapril group, hypoxia-inducible factor (HIF)-1, HIF-2, and Ets-1 protein expression were not changed, compared to the control group. In the spironolactone group, HIF-1 and Ets-1 protein expression were significantly increased by immunoblots and immunohistochemistry, whereas HIF-2 protein expression was not changed, compared to the control group. In the enalapril group, the immunoactivity of pimonidazole was not significantly different from that of the controls. However, in the spironolactone group, pimonidazole staining demonstrated that the cortex and medulla underwent severe hypoxia. In summary, our data showed that aldosterone inhibition in the developing kidney augmented the hypoxic responses, and up-regulated the expression of key mediators of hypoxia including HIF-1 and Ets-1. Angiotensin II inhibition did not affect hypoxia-related alterations in the developing kidney. The components of RAAS may differentially modulate renal hypoxia and its related target genes in the developing rat kidney.

12

Bradykinin in ischemia-reperfusion injury of the rat lung

67%

Nowak K., Weih S., Post S., Gebhard M. M., Hohenberger P.

Journal of Physiology and Pharmacology. Supplement

|

2007

|

tom 58

|

nr 5

13

Role of neuropeptides in central control of cardiovascular responses to stress

67%

Szczepanska-Sadowska E.

Journal of Physiology and Pharmacology. Supplement

|

2008

|

tom 59

|

nr 8

14

Brain and cardiovascular diseases: common neurogenic background of cardiovascular, metabolic and inflammatory diseases

67%

Szczepanska-Sadowska E., Cudnoch-Jedrzejewska A., Ufnal M., Zera T.

Journal of Physiology and Pharmacology

|

2010

|

tom 61

|

nr 5

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-1ßeta, 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.

15

The increase in the cardiodepressant activity and vasopressin concentration in the sella turcica venous blood during vagal afferents stimulation or after angiotensin II infusion

67%

Goraca A., Orlowska-Majdak M., Traczyk W. Z.

Journal of Physiology and Pharmacology

|

1996

|

tom 47

|

nr 2

16

The role of endothelium in antithrombotic effect of the renin-angiotensin system blockade

67%

Buczko W., Matys T., Kucharewicz I., Chabielska E.

Journal of Physiology and Pharmacology

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1999

|

tom 50

|

nr 4

17

The history of inhibitors of angiotensin converting enzyme

67%

Vane J. R.

Journal of Physiology and Pharmacology

|

1999

|

tom 50

|

nr 4

18

The renal medullary thick ascending limb as a model for understanding lipid mediators in sepsis

67%

Escalante B. A., McGiff I. C., Ferreri N. R.

Journal of Physiology and Pharmacology

|

1997

|

tom 48

|

nr 4

19

Salt appetite: its neuroendocrine basis

67%

Stellar E.

Acta Neurobiologiae Experimentalis

|

1993

|

tom 53

|

nr 3

20

Vasopressin in vascular regulation and water homeostasis in the brain

51%

Kozniewska E., Romaniuk K.

Journal of Physiology and Pharmacology. Supplement

|

2008

|

tom 59

|

nr 8

Ograniczanie wyników

Effects of angiotensin derivatives [Lang] - filled liposomes on isolated rat aorta

ACE inhibitor and AT1 antagonist stimulate duodenal HCO3 secretion mediated by a common pathway - involvement of PG, NO and bradykinin

Comparison between the effects of lisinopril and losartan on the cough reflex in anesthetized and awake rabbits

Neuroendocrine factors in salt appetite

Angiotensin 1-7 formation in breast tissue is attenuated in breast cancer - a study on the metabolism of angiotensinogen in breast cancer cell lines

Angiotensin metabolism in rat stomach wall: prevalence of angiotensin-(1-7) formation

Angiotensin II - derived peptides devoid of phenylalanine in position 8 have full psychotropic activity of the parent hormone

Short term 13-cis-retinoic acid treatment at therapeutic doses elevates expression of leptin, GLUT4, PPARgamma and aP2 in rat adipose tissue

Myrtus communis improves cognitive impairment in renovascular hypertensive rats

Angiotensinogen and angiotensin-converting enzyme mRNA decrease and AT1 receptor mRNA and protein increase in epididymal fat tissue accompany age-induced elevation of adiposity and reductions in expression of GLUT4 and peroxisome proliferator-activated receptor (PPARgamma)

Spironolactone, but not enalapril, potentiates hypoxia-inducible factor-1alpha and Ets-1 expression in newborn rat kidney

Bradykinin in ischemia-reperfusion injury of the rat lung

Role of neuropeptides in central control of cardiovascular responses to stress

Brain and cardiovascular diseases: common neurogenic background of cardiovascular, metabolic and inflammatory diseases

The increase in the cardiodepressant activity and vasopressin concentration in the sella turcica venous blood during vagal afferents stimulation or after angiotensin II infusion

The role of endothelium in antithrombotic effect of the renin-angiotensin system blockade

The history of inhibitors of angiotensin converting enzyme

The renal medullary thick ascending limb as a model for understanding lipid mediators in sepsis

Salt appetite: its neuroendocrine basis

Vasopressin in vascular regulation and water homeostasis in the brain