scholarly journals Increased Expression and Activity of Phospholipase C in Renal Arterioles of Young Spontaneously Hypertensive Rats

2007 ◽  
Vol 20 (1) ◽  
pp. 38-43 ◽  
Author(s):  
Z PENG ◽  
A DANG ◽  
W ARENDSHORST
Keyword(s):  
Phospholipase C ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Expression And Activity

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

scholarly journals Improvement of vascular insulin sensitivity by downregulation of GRK2 mediates exercise-induced alleviation of hypertension in spontaneously hypertensive rats

2013 ◽  
Vol 305 (8) ◽  
pp. H1111-H1119 ◽  
Author(s):  
Wenjuan Xing ◽  
Youyou Li ◽  
Haifeng Zhang ◽  
Chunjuan Mi ◽  
Zuoxu Hou ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Exercise Induced ◽  
Grk2 Expression ◽  
Expression And Activity

Exercise training lowers blood pressure and is a recommended nonpharmacological strategy and useful adjunctive therapy for hypertensive patients. Studies demonstrate that physical activity attenuates progression of hypertension. However, underlying mechanisms remain elusive. Vascular insulin resistance and endothelial dysfunction plays a critical role in the development of hypertension. The present study investigated whether long-term physical exercise starting during the prehypertensive period prevents the development of hypertension via improving vascular insulin sensitivity. Young (4 wk old) prehypertensive spontaneously hypertensive rats (SHRs) and their normotensive Wistar-Kyoto (WKY) control rats were subjected to a 10-wk free-of-loading swim training session (60 min/day, 5 days/wk). Blood pressure, mesenteric arteriolar vasorelaxation, G protein-coupled receptor kinase-2 (GRK2) expression and activity, and insulin-stimulated Akt/endothelial nitric oxide synthase (eNOS) activation were determined. SHRs had higher systolic blood pressure, systemic insulin resistance, and impaired vasodilator actions of insulin in resistance vessels when compared with WKY rats. Systolic blood pressure in SHRs postexercise was significantly lower than that in sedentary rats. Vascular insulin sensitivity in mesenteric arteries was improved after exercise training as evidenced by an increased vasodilator response to insulin. In addition, exercise downregulated vascular GRK2 expression and activity, which further increased insulin-stimulated vascular Akt/eNOS activation in exercised SHRs. Specific small interfering RNA knockdown of GRK2 in endothelium mimicked the effect of exercise-enhanced vascular insulin sensitivity. Likewise, upregulation of GRK2 by Chariot-mediated delivery opposed exercise-induced vascular insulin sensitization. Taken together, our results suggest that long-term exercise beginning at the prehypertensive stage improves vascular insulin sensitivity via downregulation of vascular GRK2 that may help to limit the progression of hypertension.

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