Wyniki wyszukiwania

1

Angiotensin-(1-7): an active member of the renin-angiotensin system

100%

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

Journal of Physiology and Pharmacology

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2002

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tom 53

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nr 4,1

Angiotensin-(1-7) [Ang-(1-7)] is an active member of renin-angiotensin system (RAS). It counterbalances vasoconstriction, mitogenic, arrhythmogenic and prothrombotic actions of Ang II. Inducing natiuresis and diuresis opposes also the water and sodium retention produced by Ang II. Till now the specific receptor side for Ang-(1-7) has been not cloned, but the current data strongly suggest that an interaction (cross- talk) between angiotensin receptors may play a role in the effects of Ang-(1-7).

2

Cerebroprotective effect of angiotensin IV in experimental ischemic stroke in the rat mediated by AT4 receptors

88%

Faure S., Chapot R., Tallet D., Javellaud J., Achard J. M., Oudart N.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 3

Recent studies have reported potential roles of angiotensins in an adaptative physiological mechanism of protection against cerebral ischemia-induced neurological damages. In the present study, we examined the protective role of angiotensin IV (AngIV) in a rat model of embolic stroke induced by intracarotid injection of calibrated microspheres (50 µm). Internal carotid infusions of increasing doses of AngIV (0.01, 0.1 and 1 nmol/0.1 mL saline) dose dependently decreased mortality, neurological deficit and cerebral infarct size at 24 hours. With the highest dose of AngIV, mortality was reduced from 55 % in saline infused controls to 10 % (p=0.003), neurological deficit was reduced from 3.8 ± 0.3 to 1.4 ± 0.3 , (p<0.0001) and cerebral infarct size at 24 hours was decreased from 432 ± 26 mm3 to 185 ± 19, (p=0.0001). The AT4 antagonist divalinal-AngIV (10-9 mol/0.1 mL), or pretreatment with L-NAME (10-7 mol/0.1 mL), both completely abolished the protective effect of AngIV (1 nmol). The AT2 antagonist PD123319 (10-7 mol/0.1 mL) partially prevented the protective effect of AngIV on the neurological score. Sequential cerebral arteriographies revealed that AngIV induced a redistribution of blood flow to the ischemic areas within minutes. These results suggest that pharmacological doses of AngIV are protective against acute cerebral ischemia by triggering an AT4-mediated, NO-dependent intracerebral hemodynamic mechanism.

3

Involvement of the cholinergic system in the central histamine-induced reversal of critical haemorrhagic hypotension in rats

75%

Yalcin M., Savci V., Jochem J.

Journal of Physiology and Pharmacology

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2009

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tom 60

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nr 2

133-137

Histamine, acting centrally as a neurotransmitter, evokes a reversal of haemorrhagic shock in rats due to the activation of the sympathetic and the renin-angiotensin systems as well as the release of arginine vasopressin and proopiomelanocortin-derived peptides. In the present study, we demonstrate influences of cholinergic receptor antagonists on the central histamine-induced resuscitating action. Experiments were carried out in male anaesthetised Wistar rats subjected to a haemorrhagic hypotension of 20-25 mmHg, resulting in the death of all control animals within 30 min. Histamine (100 nmol) administered intracerebroventricularly (icv) at 5 min of critical hypotension produced a long-lasting pressor effect with increases in heart rate and peripheral blood flows, and a 100% survival at 2 h. Mean arterial pressure and blood flow changes were almost completely blocked by nicotinic receptor antagonist mecamylamine (246.3 nmol; icv) and partially inhibited by muscarinic receptor blocker atropine sulphate (14.8 nmol; icv). Cholinergic receptor antagonists given alone in the control saline-treated groups did not affect cardiovascular parameters in the post-bleeding period. In conclusion, there are interactions between the histaminergic and cholinergic systems, with an involvement of both nicotinic and muscarinic receptors, in the central cardiovascular regulation in haemorrhagic hypotension in rats.

4

Latest aspects of aldosterone actions on the heart muscle

75%

Kritis A. A., Gouta C. P., Liaretidou E. I., Kallaras K. I.

Journal of Physiology and Pharmacology

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2016

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tom 67

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nr 1

5

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

75%

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

Journal of Physiology and Pharmacology

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2005

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tom 56

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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.

6

The post-haemorrhagic vasopressin release into the blood

75%

Lipinska S., Forys S., Lipinska J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,1

The aim of the present study was to compare the influence of the renin-angiotensin and sympathetic system in the process of post-haemorrhagic vasopressin release. A dialysis of the venous blood from the sella turcica region was performed in male rats under anaesthesia. The animals were divided into eight experimental groups: 1) control; 2) bleeding; 3) 20 days after superior cervical ganglionectomy; 4) 20 days after superior cervical ganglionectomy and bleeding; 5) injection of captopril; 6) injection of captopril and bleeding; 7) 20 days after superior cervical ganglionectomy and injection of captopril; 8) 20 days after superior cervical ganglionectomy, injection of captopril and bleeding. The content of vasopressin in dialysates was determined by radioimmunoassay. In control rats the release of vasopressin into dialysates was constant during 180 min of the experiment. Bleeding, as well as, superior cervical ganglionectomy caused an increase in vasopressin release. Captopril did not change vasopressin release in comparison to control group. Furthermore, vasopressin release after both, bleeding and sympathetic denervation performed simultaneously was significantly abolished. We conclude that renin-angiotensin, as well as, sympathetic nervous system are involved in the increased post-haemorrhagic vasopressin release.

7

Oxytocin release after bleeding in rat: the role of sympathetic and renin-angiotensin system

75%

Lipinska S., Zebrowska-Badalla A., Lipinska J.

Journal of Physiology and Pharmacology

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2006

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tom 57

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nr 4

The aim of this experiment was to compare the role of renin-angiotensin and sympathetic nervous system in post-haemorrhagic mechanism of oxytocin release. Oxytocin content in venous dialysates was determined by radioimmunoassay. In control rats the release of oxytocin into dialysates did not change during whole experiment. The injection of captopril induced 2-fold higher oxytocin release, but caused no change in oxytocin release after bleeding. Superior cervical ganglionectomy (SCGx) 20 days before, caused 5-fold higher increase in oxytocin release than in control group. Injection of captopril in rats after SCGx, did not decrease the high level of oxytocin in dialysate. However, bleeding increased oxytocin release and 1 hour after bleeding the highest - 14-fold increase, took place. In the contrary to 14-fold increase in oxytocin release in animals with superior cervical ganglia (SCG), bleeding after SCGx caused only 2-fold higher oxytocin release. When SCGx, bleeding and injection of captopril were done simultaneously, oxytocin release remained on the control concentration level. We assumed that blockade of renin angiotensin system and sympathetic dennervation prevent the increase in oxytocin release after bleeding. On basis of our present experiments, it can be assumed that, in posthaemorrhagic oxytocin release into the blood, sympathetic innervation derived from SCGx, as well as, renin-angiotensin system are involved.

8

Involvement of the renin-angiotensin system in endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats

75%

Jochem J.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,1

The study was undertaken to examine the involvement of the renin-angiotensin system in the reversal by endogenous central histamine of critical haemorrhagic hypotension in anaesthetised Wistar rats. Histamine N-methyltransferase inhibitor metoprine (20 µg) administered intracerebroventricularly at 5 min of critical hypotension 20-25 mmHg produced increases in histamine concentrations as measured 20 min after treatment in the hypothalamus (581.33 ± 63.23 vs. 488.26 ± 56.34 ng/g of wet tissue; P < 0.01) and medulla oblongata (53.42 ± 14.65 vs. 34.68 ± 13.52 ng/g of wet tissue; P < 0.05). That was accompanied by 34.7% higher plasma angiotensin II concentration in comparison to the control group. Metoprine produced dose-dependent (5-20 µg) rises in mean arterial pressure (MAP) and heart rate, which were significantly higher than those in normotensive animals. The resuscitating action of metoprine (20 µg) was associated with rises in renal, mesenteric and hindquarters blood flows, and a 100% survival at 2 h after treatment, while in the saline-treated group, all the animals died within 30 min. Angiotensin type 1 (AT1) receptor antagonist ZD 7155 (0.5 mg/kg; iv) decreased regional vascular resistance and inhibited metoprine-induced increase in MAP, whereas AT2 receptor blocker PD 123319 (10 mg/kg; iv) had no effect. Angiotensin-converting enzyme inhibitor captopril (30 mg/kg; iv) reduced the increase in plasma angiotensin II level and the haemodynamic effects of metoprine. Neither capropril, nor angiotensin receptor antagonists influence the survival at 2 h after treatment. In conclusion, the renin-angiotensin system is involved in central histamine-induced resuscitating action in rats.

9

Measurement of angiotensin metabolites in organ bath and cell culture experiments by liquid chromatography - electrospray ionization - mass epectrometry (LC-ESI-MS)

75%

Bujak-Gizycka B., Madej J., Wolkow P. P., Olszanecki R., Drabik L., Rutowski J., Korbut R.

Journal of Physiology and Pharmacology

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2007

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tom 58

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nr 3

The metabolism of renin-angiotensin system (RAS) is more complicated than previously expected and understanding the biological phenomena regulated by variety of angiotensin metabolites requires their precise and possibly comprehensive quantitation. Physiological concentrations of angiotensins (Ang) in biological fluids are low, therefore their accurate measurements require very sensitive and specific analytical methods. In this study we developed an accurate and reproducible method of quantitation of angiotensin metabolites through coupling of liquid chromatography and electrospray ionization - mass spectrometry (LC-ESI-MS). With this method main angiotensin metabolites (Ang I, II, III, IV, 1-9, 1-7, 1-5) can be reliably measured in organ bath of rat tissues (aorta, renal artery, periaortal adipose tissue) and in medium of cultured endothelial cells (EA.hy926), exposed to Ang I for 15 minutes, in the absence or in the presence of angiotensin converting enzyme inhibitor, perindoprilat. Presented LC-ESI-MS method proved to be a quick and reliable solution to comprehensive analysis of angiotensin metabolism in biological samples.

10

Proopiomelanocortin but not vasopressin or renin-angiotensin system induces resuscitative effects of central 5-HT1A activation in haemorrhagic shock in rats

63%

Sowa P., Adamczyk-Sowa M., Zwirska-Korczala K., Pierzchala K., Adamczyk D., Paluch Z., Misiolek M.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 5

11

AVE 0991 - angiotensin-(1-7) receptor agonist, inhibits atherogenesis in apoE - knockout mice

63%

Toton-Zuranska J., Gajda M., Pyka-Fosciak G., Kus K., Pawlowska M., Niepsuj A., Wolkow P., Olszanecki R., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 2

Recent evidence shows that the renin-angiotensin system is a crucial player in atherosclerotic processes. It was also proved that Ang II promotes atherogenesis. Angiotensin-(1-7) [Ang-(1-7)] opposites Ang II action. Therefore, we would like to find out whether Ang-(1-7) receptor agonist: AVE 0991, could ameliorate atherosclerosis progression in an experimental model of atherosclerosis: apolipoprotein E (apoE) - knockout mice. AVE 0991 inhibited atherogenesis, measured both by “en face” method (7.63±1.6% vs. 14.6±2.1%) and “cross-section” method (47 235±7 546 µm2 vs. 91 416±8 357 µm2). This is the first report showing the effect of AVE 0991 on atherogenesis in gene-targeted mice.

12

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

63%

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

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nr 4

13

Age-related changes in the local intestinal renin-angiotensin system in normotensive and spontaneously hypertensive rats

63%

Pasanen L., Launonen H., Siltari A., Korpela R., Vapaatalo H., Salmenkari H., Forsgard R. A.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 2

14

Effects of renin-angiotensin system inhibitors on fibrosis in patients with alcoholic chronic pancreatitis

63%

Madro A., Kurzepa J., Celinski K., Slomka M., Czechowska G., Kurzepa J., Kazmierak W., Buszewicz G., Ciesielka M., Madro R.

Journal of Physiology and Pharmacology

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2016

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tom 67

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nr 1

15

The influence of angiotensin-(1-7) peptidomimetic (AVE 0991) and nebivolol on angiotensin i metabolism in aorta of apoE-knockout mice

63%

Olszanecki R., Suski M., Gebska A., Toton-Zuranska J., Kus K., Madej J., Bujak-Gizycka B., Jawien J., Korbut R.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 3

16

Angiotensin-[1-9], the product of angiotensin I conversion in platelets, enhances arterial thrombosis in rats

63%

Kramkowski K., Mogielnicki A., Leszczynska A., Buczko W.

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 3

317-324

Angiotensin (Ang) (1-9) is the renin-angiotensin-system peptide found in the plasma of healthy volunteers and after angiotensin-converting-enzyme inhibitors therapy. In vitro experiments proved that Ang-(1-9) may be produced from Ang I. In our study, we tried to expand the poor data about the in vivo properties of Ang-(1-9). We revealed that Ang-(1-9) enhanced electrically stimulated arterial thrombosis in the carotid artery of Wistar rats. Losartan, a selective blocker of AT1 receptor for Ang II, abolished the prothrombotic activity of Ang-(1-9). This peptide increased plasma level of fibrinogen, augments fibrin generation, and similarly to Ang II, potentiated collagen induced platelet aggregation. Using HPLC, we found that after incubation of Ang-(1-9) with platelet homogenates or after intravenous administration this peptide is converted to Ang II. We concluded that Ang-(1-9) exerts an Ang II-like prothrombotic effect due to the conversion to Ang II in the circulatory system of rats and that platelets are involved in this process.

17

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

63%

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

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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.

18

Angiotensinogen metabolism in rat aorta: Robust formation of proangiotensin-12

63%

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

Journal of Physiology and Pharmacology

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2010

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tom 61

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nr 6

19

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Effects of alteration in fluid balance on angiotensinogen gene expression in the rat

63%

Doris P. A.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 2

20

Enhanced food and water intake in renin transgenic rats

63%

Szczepanska-Sadowska E., Paczwa P., Dobruch J.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 1

In short term experiments angiotensin II (Ang II) is a potent stimulant of thirst, however it is not known whether prolonged activation of the renin-angiotensin system is associated with chronic alteration of water or food intake. Renin transgenic rats TGRmRen(2)27 (TGR) exhibit significant elevation of AngII in the brain regions involved in regulation of body fluid balance. The purpose of the present study was to find out whether TGR rats manifest also different water (WI) and food (FI) intake and renal excretory functions in comparison to their parent Sprague Dawley (SD) strain. To this end 24h WI and FI as well as urine excretion (Vu) and urinary outputs of solutes (Cosm), sodium (UNaV) and potassium (UKV) were compared under baseline conditions in 16 TGR and 15 SD rats having free access to water and food. In 15 TGR and 17 SD rats effect of 24h dehydration on water intake was investigated. Under baseline conditions TGR rats consumed significantly greater amount of food and water than SD rats. Vu, UNaV and UKV were not significantly different in both strains. Cumulative water intakes in SD and TGR rats subjected to 24h dehydration did not differ. The results reveal that under baseline conditions TGR rats manifest greater food and water intakes than SD rats whereas stimulation of thirst by water deprivation is similar in both strains. The results suggest that the ingestive behavior may be chronically altered by upregulation of the renin-angiotensin system.

Ograniczanie wyników

Angiotensin-(1-7): an active member of the renin-angiotensin system

Cerebroprotective effect of angiotensin IV in experimental ischemic stroke in the rat mediated by AT4 receptors

Involvement of the cholinergic system in the central histamine-induced reversal of critical haemorrhagic hypotension in rats

Latest aspects of aldosterone actions on the heart muscle

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

The post-haemorrhagic vasopressin release into the blood

Oxytocin release after bleeding in rat: the role of sympathetic and renin-angiotensin system

Involvement of the renin-angiotensin system in endogenous central histamine-induced reversal of critical haemorrhagic hypotension in rats

Measurement of angiotensin metabolites in organ bath and cell culture experiments by liquid chromatography - electrospray ionization - mass epectrometry (LC-ESI-MS)

Proopiomelanocortin but not vasopressin or renin-angiotensin system induces resuscitative effects of central 5-HT1A activation in haemorrhagic shock in rats

AVE 0991 - angiotensin-(1-7) receptor agonist, inhibits atherogenesis in apoE - knockout mice

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

Age-related changes in the local intestinal renin-angiotensin system in normotensive and spontaneously hypertensive rats

Effects of renin-angiotensin system inhibitors on fibrosis in patients with alcoholic chronic pancreatitis

The influence of angiotensin-(1-7) peptidomimetic (AVE 0991) and nebivolol on angiotensin i metabolism in aorta of apoE-knockout mice

Angiotensin-[1-9], the product of angiotensin I conversion in platelets, enhances arterial thrombosis in rats

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

Angiotensinogen metabolism in rat aorta: Robust formation of proangiotensin-12

Effects of alteration in fluid balance on angiotensinogen gene expression in the rat

Enhanced food and water intake in renin transgenic rats