Enhanced Na+, K+-ATPase activity and endothelial modulation decrease phenylephrine-induced contraction in aorta from ouabain-treated normotensive and hypertensive rats

AbstractThe purpose of this study was to compare the effect of long-term ouabain treatment on the vascular reactivity and NaMale Wistar rats were treated with ouabain (~8.0 µg/day, subcutaneously) or vehicle for 5 and 20 weeks, and spontaneously hypertensive rats (SHRs) for 5 weeks. Vasoconstrictor response to phenylephrine (10The phenylephrine-induced contraction was reduced, whereas the relaxation to KCl was enhanced in the aorta of ouabain-treated Wistar rats and SHRs. In both strains, endothelial modulation of α-adrenergic response was enhanced, related to an increased NO and reduced COX-derived vasoconstrictor factor modulation. Aortas from 20-week ouabain-treated Wistar rats showed reduced COX-2 and enhanced eNOS protein expression. In SHRs, 5-week ouabain treatment reduced COX-2 and increased nNOS protein expression.The results suggest that long-term ouabain treatment reduces the α-adrenergic response of aorta from normotensive rats and SHRs, associated with an increase of NO synthesis, reduced COX-2-derived vasoconstrictor factors, and enhanced ouabain-sensitive Na

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Hyperbaric Oxygen Preconditioning Upregulates Heme OxyGenase-1 and Anti-Apoptotic Bcl-2 Protein Expression in Spontaneously Hypertensive Rats with Induced Postischemic Acute Kidney Injury

International Journal of Molecular Sciences ◽

10.3390/ijms22031382 ◽

2021 ◽

Vol 22 (3) ◽

pp. 1382

Author(s):

Jelena Nesovic Ostojic ◽

Milan Ivanov ◽

Nevena Mihailovic-Stanojevic ◽

Danijela Karanovic ◽

Sanjin Kovacevic ◽

...

Keyword(s):

Acute Kidney Injury ◽

Protein Expression ◽

Hyperbaric Oxygen ◽

Heme Oxygenase ◽

Spontaneously Hypertensive Rats ◽

Wistar Rats ◽

Kidney Injury ◽

Heme Oxygenase 1 ◽

Hypertensive Rats ◽

Spontaneously Hypertensive

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.

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D-003 DIFFERENT EFFECT OF LONG-TERM NEURONAL NO-SYNTHASE INHIBITION ON CARDIOVASCULAR SYSTEM OF SPONTANEOUSLY HYPERTENSIVE RATS AND WISTAR RATS

Journal of Hypertension ◽

10.1097/01.hjh.0000408001.49539.29 ◽

2011 ◽

Vol 29 ◽

pp. e8

Author(s):

Frantisek Kristek ◽

Ria Koprdova

Keyword(s):

Cardiovascular System ◽

Spontaneously Hypertensive Rats ◽

Wistar Rats ◽

No Synthase ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Neuronal No Synthase

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Long-Term Stimulation with Electroacupuncture at DU20 and ST36 Rescues Hippocampal Neuron through Attenuating Cerebral Blood Flow in Spontaneously Hypertensive Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2013/482947 ◽

2013 ◽

Vol 2013 ◽

pp. 1-10 ◽

Cited By ~ 9

Author(s):

Gui-Hua Tian ◽

Kai Sun ◽

Ping Huang ◽

Chang-Man Zhou ◽

Hai-Jiang Yao ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Spontaneously Hypertensive Rats ◽

Wistar Rats ◽

Shr Rats ◽

Hypertensive Rats ◽

Sham Control ◽

Spontaneously Hypertensive ◽

Ca1 Region

This study was designed to investigate the effect of long-term electroacupuncture at Baihui (DU20) and Zusanli (ST36) on cerebral microvessels and neurons in CA1 region of hippocampus in spontaneously hypertensive rats (SHR). A total of 45 male Wistar rats and 45 SHR were randomly grouped, with or without electroacupuncture (EA) at DU20 and ST36, once every other day for a period of 8 weeks. The mean arterial pressure (MAP) was measured once every 2 weeks. Cerebral blood flow (CBF) and the number of open microvessels in hippocampal CA1 region were detected by Laser Doppler and immunohistochemistry, respectively. Nissl staining and Western blotting were performed, respectively, to determine hippocampus morphology and proteins that were implicated in the concerning signaling pathways. The results showed that the MAP in SHR increased linearly over the observation period and was significantly reduced following electroacupuncture as compared with sham control SHR rats, while no difference was observed in Wistar rats between EA and sham control. The CBF, learning and memory capacity, and capillary rarefaction of SHR were improved by EA. The upregulation of angiotensin II type I receptor (AT1R), endothelin receptor (ETAR), and endothelin-1 (ET-1) in SHR rats was attenuated by electroacupuncture, suggesting an implication of AT1R, ETAR, and ET-1 pathway in the effect of EA.

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Toll-like receptor 4 contributes to blood pressure regulation and vascular contraction in spontaneously hypertensive rats

Clinical Science ◽

10.1042/cs20110523 ◽

2012 ◽

Vol 122 (11) ◽

pp. 535-543 ◽

Cited By ~ 118

Author(s):

Gisele F. Bomfim ◽

Rosangela A. Dos Santos ◽

Maria Aparecida Oliveira ◽

Fernanda R. Giachini ◽

Eliana H. Akamine ◽

...

Keyword(s):

Blood Pressure ◽

Protein Expression ◽

Spontaneously Hypertensive Rats ◽

System Response ◽

Low Grade ◽

Resistance Arteries ◽

Hypertensive Rats ◽

Spontaneously Hypertensive ◽

Vascular Contractility ◽

Cox 2

Activation of TLRs (Toll-like receptors) induces gene expression of proteins involved in the immune system response. TLR4 has been implicated in the development and progression of CVDs (cardio-vascular diseases). Innate and adaptive immunity contribute to hypertension-associated end-organ damage, although the mechanism by which this occurs remains unclear. In the present study, we hypothesize that inhibition of TLR4 decreases BP (blood pressure) and improves vascular contractility in resistance arteries from SHR (spontaneously hypertensive rats). TLR4 protein expression in mesenteric resistance arteries was higher in 15-week-old SHR than in age-matched Wistar controls or in 5-week-old SHR. To decrease the activation of TLR4, 15-week-old SHR and Wistar rats were treated with anti-TLR4 (anti-TLR4 antibody) or non-specific IgG control antibody for 15 days (1 μg per day, intraperitoneal). Treatment with anti-TLR4 decreased MAP (mean arterial pressure) as well as TLR4 protein expression in mesenteric resistance arteries and IL-6 (interleukin 6) serum levels from SHR when compared with SHR treated with IgG. No changes in these parameters were found in treated Wistar control rats. Mesenteric resistance arteries from anti-TLR4-treated SHR exhibited decreased maximal contractile response to NA (noradrenaline) compared with IgG-treated SHR. Inhibition of COX (cyclo-oxygenase)-1 and COX-2, enzymes related to inflammatory pathways, decreased NA responses only in mesenteric resistance arteries of SHR treated with IgG. COX-2 expression and TXA2 (thromboxane A2) release were decreased in SHR treated with anti-TLR4 compared with IgG-treated SHR. Our results suggest that TLR4 activation contributes to increased BP, low-grade inflammation and plays a role in the augmented vascular contractility displayed by SHR.

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Antihypertensive Effect ofSyzygium cuminiin Spontaneously Hypertensive Rats

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2014/605452 ◽

2014 ◽

Vol 2014 ◽

pp. 1-7 ◽

Cited By ~ 8

Author(s):

Rachel Melo Ribeiro ◽

Vicente Férrer Pinheiro Neto ◽

Kllysmann Santos Ribeiro ◽

Denilson Amorim Vieira ◽

Iracelle Carvalho Abreu ◽

...

Keyword(s):

Blood Pressure ◽

Heart Rate ◽

Spontaneously Hypertensive Rats ◽

Wistar Rats ◽

Vascular Reactivity ◽

Antihypertensive Effect ◽

Maximum Effect ◽

Syzygium Cumini ◽

Hypertensive Rats ◽

Spontaneously Hypertensive

This study evaluated thein vivopotential antihypertensive effect of hydroalcoholic extract ofSyzygium cuminileaves (HESC) in normotensive Wistar rats and in spontaneously hypertensive rats (SHR), as well as itsin vitroeffect on the vascular reactivity of resistance arteries. The hypotensive effect caused by intravenous infusion of HESC (0.01–4.0 mg/kg) in anesthetized Wistar rats was dose-dependent and was partially inhibited by pretreatment with atropine sulfate. SHR received HESC (0.5 g/kg/day), orally, for 8 weeks and mean arterial pressure, heart rate, and vascular reactivity were evaluated. Daily oral administration of HESC resulted in a time-dependent blood pressure reduction in SHR, with a maximum reduction of 62%. In the endothelium-deprived superior mesenteric arteries rings the treatment with HESC reduced by 40% the maximum effect (Emax⁡) of contraction induced by NE. The contractile response to calcium and NE of endothelium-deprived mesenteric rings isolated from untreated SHR was reduced in a concentration-dependent manner by HESC (0.1, 0.25, and 0.5 mg/mL). This study demonstrated thatSyzygium cuminireduces the blood pressure and heart rate of SHR and that this antihypertensive effect is probably due to the inhibition of arterial tone and extracellular calcium influx.

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Insulin-induced endothelin release and vasoreactivity in hypertriglyceridemic and hypertensive rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.277.1.h399 ◽

1999 ◽

Vol 277 (1) ◽

pp. H399-H404 ◽

Cited By ~ 1

Author(s):

Pilar Nava ◽

Verónica Guarner ◽

Rosalinda Posadas ◽

Israel Pérez ◽

Guadalupe Baños

Keyword(s):

Drinking Water ◽

Receptor Antagonist ◽

Wistar Rats ◽

Receptor Blocker ◽

Hypertensive Rats ◽

Contractile Responses ◽

Femoral Arteries ◽

Male Wistar Rats

Insulin-elicited endothelin release in hypertriglyceridemic, hypertensive, hyperinsulinemic (HTG) rats was shown. Weanling male Wistar rats were given 30% sucrose in their drinking water for 20–24 wk. In vitro contractions of aorta and femoral arteries were elicited with 40 mM KCl. Endothelin release induced with KCl plus 50 μU/ml insulin resulted in increases in contractile responses: 41 ± 5.9 and 57 ± 6% for control and 65.5 ± 6 and 95 ± 9% for HTG aortas and femoral arteries, respectively. The endothelin ETB-receptor blocker BQ-788 decreased responses to KCl + insulin by 39 ± 8 and 53 ± 5% in control and 48 ± 13 and 79 ± 3.5% in HTG aortas and femoral arteries, respectively. The ETA-receptor antagonist PD-151242 inhibited these responses by 12 ± 10 and 1 ± 9% in control and by 51.5 ± 9 and 58.5 ± 1% in HTG aortas and femoral arteries, respectively. These results suggest that endothelin may contribute to the hypertension in this model.

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