Role of Heme Oxygenase in Modulating Endothelial Function in Mesenteric Small Resistance Arteries of Spontaneously Hypertensive Rats

Porteri, Enzo; Rodella, Luigi Fabrizio; Rezzani, Rita; Rizzoni, Damiano; Paiardi, Silvia; Ciuceis, Carolina De; Boari, Gianluca E.M.; Foglio, Eleonora; Rizzardi, Nicola; Platto, Caterina; Rosei, Enrico Agabiti

doi:10.3109/10641960902927978

Cited by 9 publications

(6 citation statements)

References 33 publications

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“…In a basic experiment, the SHR model exhibited an obvious decrease in HO-1 expression levels compared with WKY [18], indicative of HO-1 system dysfunction in hypertension. Upregulating the activity and expression of HO-1 could inhibit the process of hypertension [17,19], which coincides with our results. The associated mechanisms involve restoration of endothelial function [17], inhibition of VSMC proliferation [20], suppression of kidney oxidative and inflammatory injury [21], amelioration of vascular regulative factors [22,23] and direct relaxation of blood vessels by CO [23].…”

Section: Resultssupporting

confidence: 91%

Effects of Heme Oxygenase-1 Upregulation on Blood Pressure and Cardiac Function in an Animal Model of Hypertensive Myocardial Infarction

Chen

Liu

et al. 2013

IJMS

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In this study, we evaluate the effect of HO-1 upregulation on blood pressure and cardiac function in the new model of infarct spontaneous hypertensive rats (ISHR). Male spontaneous hypertensive rats (SHR) at 13 weeks (n = 40) and age-matched male Wistar (WT) rats (n = 20) were divided into six groups: WT (sham + normal saline (NS)), WT (sham + Co(III) Protoporphyrin IX Chloride (CoPP)), SHR (myocardial infarction (MI) + NS), SHR (MI + CoPP), SHR (MI + CoPP + Tin Mesoporphyrin IX Dichloride (SnMP)), SHR (sham + NS); CoPP 4.5 mg/kg, SnMP 15 mg/kg, for six weeks, one/week, i.p., n = 10/group. At the sixth week, echocardiography (UCG) and hemodynamics were performed. Then, blood samples and heart tissue were collected. Copp treatment in the SHR (MI + CoPP) group lowered blood pressure, decreased infarcted area, restored cardiac function (left ventricular ejection fraction (LVEF), left ventricular fraction shortening (LVFS), +dp/dtmax, (−dp/dtmax)/left ventricular systolic pressure (LVSP)), inhibited cardiac hypertrophy and ventricular enlargement (downregulating left ventricular end-systolic diameter (LVEDD), left ventricular end-systolic diameter (LVESD) and heart weight/body weight (HW/BW)), lowered serum CRP, IL-6 and Glu levels and increased serum TB, NO and PGI2 levels. Western blot and immunohistochemistry showed that HO-1 expression was elevated in the SHR (MI + CoPP) group, while co-administration with SnMP suppressed the benefit functions mentioned above. In conclusion, HO-1 upregulation can lower blood pressure and improve post-infarct cardiac function in the ISHR model. These functions may be involved in the inhibition of inflammation and the ventricular remodeling process and in the amelioration of glucose metabolism and endothelial dysfunction.

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Section: Resultssupporting

confidence: 91%

Effects of Heme Oxygenase-1 Upregulation on Blood Pressure and Cardiac Function in an Animal Model of Hypertensive Myocardial Infarction

Chen

Liu

et al. 2013

IJMS

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“…For instance, the inoculation of PGPRs improved salinity stress tolerance in wheat through alleviating the activity of numerous antioxidant enzymes such as manganese-dependent superoxide dismutase (MnSOD), POD, CAT, GR, and APX (Bharti et al, 2013 ). The findings are in line with this study, where the excess Co significantly increased enzyme activity responsible for dismutation of O 2 , which were further increased by inoculation with archaea (Porteri et al, 2009 ). Furthermore, our results revealed that the activities of Grx, Trx, and peroxiredoxins, families of thiol oxidoreductases, were also increased, but again, they were higher in archaea combined with Co treatment.…”

Section: Discussionsupporting

confidence: 91%

Selection of Newly Identified Growth-Promoting Archaea Haloferax Species With a Potential Action on Cobalt Resistance in Maize Plants

et al. 2022

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Soil contamination with cobalt (Co) negatively impacts plant growth and production. To combat Co toxicity, plant growth-promoting microorganisms for improving plant growth are effectively applied. To this end, unclassified haloarchaeal species strain NRS_31 (OL912833), belonging to Haloferax genus, was isolated, identified for the first time, and applied to mitigate the Co phytotoxic effects on maize plants. This study found that high Co levels in soil lead to Co accumulation in maize leaves. Co accumulation in the leaves inhibited maize growth and photosynthetic efficiency, inducing oxidative damage in the tissue. Interestingly, pre-inoculation with haloarchaeal species significantly reduced Co uptake and mitigated the Co toxicity. Induced photosynthesis improved sugar metabolism, allocating more carbon to defend against Co stress. Concomitantly, the biosynthetic key enzymes involved in sucrose (sucrose-P-synthase and invertases) and proline (pyrroline-5- carboxylate synthetase (P5CS), pyrroline-5-carboxylate reductase (P5CR)) biosynthesis significantly increased to maintain plant osmotic potential. In addition to their osmoregulation potential, soluble sugars and proline can contribute to maintaining ROS hemostasis. Maize leaves managed their oxidative homeostasis by increasing the production of antioxidant metabolites (such as phenolics and tocopherols) and increasing the activity of ROS-scavenging enzymes (such as POX, CAT, SOD, and enzymes involved in the AsA/GSH cycle). Inside the plant tissue, to overcome heavy Co toxicity, maize plants increased the synthesis of heavy metal-binding ligands (metallothionein, phytochelatins) and the metal detoxifying enzymes (glutathione S transferase). Overall, the improved ROS homeostasis, osmoregulation, and Co detoxification systems were the basis underlying Co oxidative stress, mitigating haloarchaeal treatment's impact.

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“…In the aortas and MRA of adult SHR, Ach-induced endothelium-dependent vasorelaxation was significantly milder versus in WKY rats. This indicates a partial impairment associated with the endothelium-dependent NO system in genetic hypertension, as previously suggested by other authors [23,24,25,26]. As expected, Ach failed to relax the aortas of LNHR, suggesting that chronic inhibition of NO synthesis results in the complete impairment of endothelium-dependent NO release, which is mainly responsible for Ach induced-vasodilatation in conductance vessels [27,28,29].…”

Section: Discussionsupporting

confidence: 61%

Changes in Adrenoceptors and G-Protein-Coupled Receptor Kinase 2 in <smlcap>L</smlcap>-NAME-Induced Hypertension Compared to Spontaneous Hypertension in Rats

Oliver

Flacco²,

Arce³

et al. 2014

J Vasc Res

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This work compares the expression of adrenoceptors (ARs) and G-protein-coupled receptor kinase (GRK) 2 (RT-PCR and immunoblotting) and functional responses in conductance (aorta) and resistance vessels (mesenteric resistance arteries; MRA) in two different models of rat hypertension: hypertension induced by chronic treatment with L-NAME (N^G-nitro-L-arginine methyl-ester) (L-NAME-treated rats; LNHR), and genetically induced hypertension (spontaneously hypertensive rats; SHR). Changes found in the aorta, but not in the MRA, were: (1) a loss of contractile capacity, more evidently in α₁-AR-mediated contraction, and an impairment of endothelium-dependent vasorelaxation, with both changes occurring independently of the hypertensive model; (2) a diminished sensitivity to α₁-AR-induced vasoconstriction along with increased β₂-AR-mediated vasodilation in LNHR, and (3) a lower expression of ARs and GRK2 in LNHR. The two latter changes are the opposite of those previously found in aortas of SHR. In the MRA of LNHR, a diminished sensitivity to isoprenaline, in parallel with a reduced expression of β₁-AR, was observed without changes in GRK2 expression. In the MRA of SHR, the increased GRK2 expression was not accompanied by significant changes in either β-AR expression or the vasorelaxant potency of isoprenaline. The present results highlight that changes in AR function differ not only between vessels but also between hypertensive models. Moreover, they suggest that changes in GRK2 expression could contribute to regulating β₂-AR function in conductance vessels but not β₁-AR function in resistance vessels.

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Role of Heme Oxygenase in Modulating Endothelial Function in Mesenteric Small Resistance Arteries of Spontaneously Hypertensive Rats

Cited by 9 publications

References 33 publications

Effects of Heme Oxygenase-1 Upregulation on Blood Pressure and Cardiac Function in an Animal Model of Hypertensive Myocardial Infarction

Effects of Heme Oxygenase-1 Upregulation on Blood Pressure and Cardiac Function in an Animal Model of Hypertensive Myocardial Infarction

Selection of Newly Identified Growth-Promoting Archaea Haloferax Species With a Potential Action on Cobalt Resistance in Maize Plants

Changes in Adrenoceptors and G-Protein-Coupled Receptor Kinase 2 in <smlcap>L</smlcap>-NAME-Induced Hypertension Compared to Spontaneous Hypertension in Rats

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