Changes of Functional and Biochemical Blood Parameters in Wistar Rats and in Spontaneously Hypertensive Rats of the SHR Line during Short-Term and Long Tredmill Running

2005 ◽  
Vol 41 (2) ◽  
pp. 162-168
Author(s):  
M. N. Maslova ◽  
A. L. Khama-Murad ◽  
A. M. Kazennov ◽  
L. P. Kislyakova ◽  
T. V. Tavrovskaya ◽  
...  
2021 ◽  
Vol 22 (3) ◽  
pp. 1382
Author(s):  
Jelena Nesovic Ostojic ◽  
Milan Ivanov ◽  
Nevena Mihailovic-Stanojevic ◽  
Danijela Karanovic ◽  
Sanjin Kovacevic ◽  
...  

Renal ischemia and reperfusion (I/R) injury is the most common cause of acute kidney injury (AKI). Pathogenesis of postischemic AKI involves hemodynamic changes, oxidative stress, inflammation process, calcium ion overloading, apoptosis and necrosis. Up to date, therapeutic approaches to treat AKI are extremely limited. Thus, the aim of this study was to evaluate the effects of hyperbaric oxygen (HBO) preconditioning on citoprotective enzyme, heme oxygenase-1 (HO-1), pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins expression, in postischemic AKI induced in normotensive Wistar and spontaneously hypertensive rats (SHR). The animals were randomly divided into six experimental groups: SHAM-operated Wistar rats (W-SHAM), Wistar rats with induced postischemic AKI (W-AKI) and Wistar group with HBO preconditioning before AKI induction (W-AKI + HBO). On the other hand, SHR rats were also divided into same three groups: SHR-SHAM, SHR-AKI and SHR-AKI + HBO. We demonstrated that HBO preconditioning upregulated HO-1 and anti-apoptotic Bcl-2 protein expression, in both Wistar and SH rats. In addition, HBO preconditioning improved glomerular filtration rate, supporting by significant increase in creatinine, urea and phosphate clearances in both rat strains. Considering our results, we can also say that even in hypertensive conditions, we can expect protective effects of HBO preconditioning in experimental model of AKI.


2009 ◽  
Vol 110 (1) ◽  
pp. 224-234 ◽  
Author(s):  
Mehdi S. Hazari ◽  
Najwa Haykal-Coates ◽  
Darrell W. Winsett ◽  
Daniel L. Costa ◽  
Aimen K. Farraj

2021 ◽  
Vol 12 ◽  
Author(s):  
Danyelle S. Miotto ◽  
Aline Dionizio ◽  
André M. Jacomini ◽  
Anderson S. Zago ◽  
Marília Afonso Rabelo Buzalaf ◽  
...  

Arterial stiffness, frequently associated with hypertension, is associated with disorganization of the vascular wall and has been recognized as an independent predictor of all-cause mortality. The identification of the molecular mechanisms involved in aortic stiffness would be an emerging target for hypertension therapeutic intervention. This study evaluated the effects of perindopril on pulse wave velocity (PWV) and on the differentially expressed proteins in aorta of spontaneously hypertensive rats (SHR), using a proteomic approach. SHR and Wistar rats were treated with perindopril (SHRP) or water (SHRc and Wistar rats) for 8 weeks. At the end, SHRC presented higher systolic blood pressure (SBP, +70%) and PWV (+31%) compared with Wistar rats. SHRP had higher values of nitrite concentration and lower PWV compared with SHRC. From 21 upregulated proteins in the aortic wall from SHRC, most of them were involved with the actin cytoskeleton organization, like Tropomyosin and Cofilin-1. After perindopril treatment, there was an upregulation of the GDP dissociation inhibitors (GDIs), which normally inhibits the RhoA/Rho-kinase/cofilin-1 pathway and may contribute to decreased arterial stiffening. In conclusion, the results of the present study revealed that treatment with perindopril reduced SBP and PWV in SHR. In addition, the proteomic analysis in aorta suggested, for the first time, that the RhoA/Rho-kinase/Cofilin-1 pathway may be inhibited by perindopril-induced upregulation of GDIs or increases in NO bioavailability in SHR. Therefore, we may propose that activation of GDIs or inhibition of RhoA/Rho-kinase pathway could be a possible strategy to treat arterial stiffness.


2008 ◽  
pp. 137-139
Author(s):  
S Čačányiová ◽  
F Kristek ◽  
J Kuneš ◽  
J Zicha

We investigated the effect of pertussis toxin (PTX) on hypotensive response induced by acetylcholine (ACh) and bradykinin (BK) and on noradrenaline (NA)-induced pressor response in spontaneously hypertensive rats (SHR). Fifteenweek-old Wistar rats and age-matched SHR were used. Half of SHR received PTX (10 µg/kg/i.v.) and the experiments were performed 48 h later. After the anesthesia the right carotid artery was cannulated in order to record blood pressure (BP). The hypotensive response to ACh was enhanced in SHR compared to Wistar rats. After pretreatment of SHR with PTX the hypotensive response to ACh was reduced compared to untreated SHR and it was also diminished in comparison to Wistar rats. Similarly, the hypotensive response to BK was also decreased after PTX pretreatment. The pressor response to NA was increased in SHR compared to Wistar rats. NA-induced pressor response was considerably decreased after PTX pretreatment compared to untreated SHR. In conclusion, the enhancement of hypotensive and pressor responses in SHR was abolished after PTX pretreatment. Our results suggested that the activation of PTXsensitive inhibitory Gi proteins is involved in the regulation of integrated vasoactive responses in SHR and PTX pretreatment could be effectively used for modification of BP regulation in this type of experimental hypertension.


1981 ◽  
Vol 61 (s7) ◽  
pp. 41s-43s ◽  
Author(s):  
W. Zidek ◽  
H. Vetter ◽  
H. Zumkley ◽  
H. Losse

1. The intracellular concentrations of Na+, K+ and Ca2+ were measured in the erythrocytes of spontaneously hypertensive rats and normotensive Wistar rats. 2. The intracellular Na+ concentration in hypertensive rats was slightly elevated at 3.16 ± 0.25 compared with 2.85 ± 0.35 mmol/l (P ≈ 0.05) and intracellular Na+ activity was markedly increased in hypertensive rats. 3. Intracellular Ca2+ activity was 7519 ± 28 990 nmol/l of free water in hypertensive rats compared with 123 ± 98 in controls (P < 0.01). 4. The cytoplasm of hypertensive animals did not buffer Ca2+ as effectively as that of normal animals. 5. It is concluded that a decreased binding capacity of intracellular macromolecules for Na+ and Ca2+ may explain the disturbances of intracellular electrolyte composition in spontaneously hypertensive rats.


Folia Medica ◽  
2013 ◽  
Vol 55 (3-4) ◽  
pp. 63-69 ◽  
Author(s):  
Daniela M. Pechlivanova ◽  
Alexander G. Stoynev

ABSTRACT The renin-angiotensin system plays a crucial role in the regulation of cardiovascular function and maintenance of water-electrolyte balance. The two major receptor types of the system, AT1 and AT2, have different, often opposite effects on these functions. AIM: To elucidate the impact of long term treatment with selective angiotensin receptor antagonists and an agonist on water-salt balance in normotensive Wistar and spontaneously hypertensive rats (SHRs). MATERIALS AND METHODS: 12-week-old male Wistar rats and SHRs were individually housed in metabolic cages and 24-h food and water intake and urine and electrolyte excretion were measured. Urinary sodium (UNa), potassium (UK) and chlorine (UCl) were determined by a flame photometer. Losartan, a selective AT1 receptor antagonist, was administered in the Wistar rats and SHRs at a dose of 10 mg/kg/day subcutaneously (sc). Wistar rats were also given the AT2 receptor antagonist, PD123319, subcutaneously at a dose of 10 mg/kg/ day. CGP 42112A, an AT2 receptor agonist, was administered intracerebroventricularly in Wistar rats at a dose of 12 μg/rat/day. The drugs were infused continuously for 14 days through osmotic minipumps. RESULTS: Losartan selectively increased sodium excretion in both rat strains and decreased weight gain in SHRs. PD123319 increased potassium excretion and decreased weight gain in Wistar rats. CGP 42112A increased food and water intake, urine output and UNa+ and UK+ excretion and decreased weight gain in normotensive Wistar rats. CONCLUSIONS: Chronic treatment with selective angiotensin receptor ligands modifies water- salt balance in rats through changes both in renal excretory function and ingestive behaviors.


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