scholarly journals Enhanced phospholipase C activity in the vascular wall of spontaneously hypertensive rats.

Hypertension ◽  
1988 ◽  
Vol 11 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Y Uehara ◽  
M Ishii ◽  
T Ishimitsu ◽  
T Sugimoto
Keyword(s):  
Phospholipase C ◽  
Spontaneously Hypertensive Rats ◽  
Vascular Wall ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Identification of Aortic Proteins Involved in Arterial Stiffness in Spontaneously Hypertensive Rats Treated With Perindopril:A Proteomic Approach

2021 ◽  
Vol 12 ◽  
Author(s):  
Danyelle S. Miotto ◽  
Aline Dionizio ◽  
André M. Jacomini ◽  
Anderson S. Zago ◽  
Marília Afonso Rabelo Buzalaf ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Spontaneously Hypertensive Rats ◽  
Wistar Rats ◽  
Molecular Mechanisms ◽  
Rho Kinase ◽  
Vascular Wall ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Cytoskeleton Organization ◽  
Proteomic Approach

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.

Vasopressin receptors and inositol trisphosphate production in blood vessels of spontaneously hypertensive rats

1989 ◽  
Vol 67 (3) ◽  
pp. 232-239 ◽  
Author(s):  
Richard Larivière ◽  
Johanne Baribeau ◽  
Jean St-Louis ◽  
Ernesto L. Schiffrin
Keyword(s):  
Blood Pressure ◽  
Phospholipase C ◽  
Binding Sites ◽  
Spontaneously Hypertensive Rats ◽  
Pressor Response ◽  
Inositol Trisphosphate ◽  
Normal Density ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Phosphoinositide Breakdown

To understand the regulation of vasopressin (AVP) receptors in spontaneous hypertension, we investigated the pressor response of AVP in the perfused mesenteric vasculature, AVP binding sites in the membrane preparation of the same vascular bed, and the production of inositol trisphosphate (InsP3) stimulated by AVP in the aorta of spontaneously hypertensive rats (SHR), Wistar–Kyoto rats (WKY), and Wistar rats (WR) at different ages (4–16 weeks). Plasma AVP concentrations were similar in SHR, WKY, and WR at all ages. The density of AVP vascular binding sites was significantly higher in WKY than in SHR and WR at 12 weeks. Receptor affinity was similar in all strains. The pressor response of the mesenteric vasculature to AVP was similar in the three strains of rats at 4 weeks (prehypertensive stage) and increased progressively in SHR compared with WKY and WR at 8 and 12 weeks of age by 43 and 35%, respectively, and by more than 80% at 16 weeks of age (established hypertensive stage). There was no difference in vascular sensitivity to AVP. A significantly increased pressor response to a supramaximal dose of norepinephrine was also found at 16 weeks in SHR, but not in younger rats. InsP3 production in the aorta in response to AVP was increased in SHR at 8, 12, and 16 weeks, compared with WKY and WR. These results suggest that the vascular response to AVP is increased in SHR, in spite of decreased or normal density of binding sites compared with WKY or WR. The increased responsiveness to AVP in SHR may be mediated in part by the enhanced activity of AVP receptor-coupled phospholipase C, resulting in increased membrane phosphoinositide breakdown and inositol trisphosphate production, which may play a role in the elevation of blood pressure in SHR.Key words: vascular reactivity, vasopressin binding sites, phosphoinositide breakdown, phospholipase C, high blood pressure.

scholarly journals Attenuation of renomedullary phospholipase C isozyme, PLC-δ1, in spontaneously hypertensive rats

IUBMB Life ◽  
1997 ◽  
Vol 43 (4) ◽  
pp. 741-747
Author(s):  
Kweon-Haeng Lee ◽  
Young-Jin Cho ◽  
Seok Ho Cha ◽  
Hitoshi Endou
Keyword(s):  
Phospholipase C ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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