scholarly journals Sustained Normalization of High Blood Pressure in Spontaneously Hypertensive Rats by Implanted Hemin Pump

Hypertension ◽  
2006 ◽  
Vol 48 (4) ◽  
pp. 685-692 ◽  
Author(s):  
Rui Wang ◽  
Rany Shamloul ◽  
Xiaoxia Wang ◽  
Qinghe Meng ◽  
Lingyun Wu
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Abstract P241: Autophagic Flux is Diminished in Mesenteric Resistance Arteries of Spontaneously Hypertensive Rats

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Cameron G McCarthy ◽  
Camilla F Wenceslau ◽  
R. Clinton Webb
Keyword(s):  
Blood Pressure ◽  
High Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Cellular Aging ◽  
Experimental Hypertension ◽  
Autophagic Flux ◽  
Vascular Aging ◽  
Resistance Arteries ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Autophagy is the constitutively active catabolic process regulating protein quality control and energy homeostasis. However, dysregulation of this process can have detrimental effects on cellular function. In particular, insufficient autophagy has been proposed as a mechanism of cellular aging, as this leads to the accumulation of damaged macromolecules and organelles. Hypertension is a condition of vascular aging. In fact, many factors that contribute to the deterioration of vascular function as we age are exacerbated in clinical and experimental hypertension. Nonetheless, whether high blood pressure per se is the cause or effect of diminished autophagy remains to be clarified. We hypothesized that mesenteric resistance arteries (MRA) from spontaneously hypertensive rats (SHR) would have decreased autophagic flux as measured by conversion of microtubule-associated protein light chain 3 (LC3-I to LC3-II) compared to normotensive Wistar Kyoto rats (WKY). We observed that MRA from male 12-15 week old SHR have decreased basal expression both cytosolic LC3 (LC3-I) and phosphatidylethanolamine conjugated LC3 (LC3-II), and expression of these proteins are similarly decreased in SHR chronically treated with hydrochlorothiazide and reserpine (SHR+HCTZ/Res) [Arbitrary units (AU), LC3-1: WKY: 1.4±0.1, SHR: 1.1±0.1*, and SHR+HCTZ/Res: 0.7±0.1*; LC3-II: WKY: 1.4±0.1, SHR: 1.1±0.1*, and SHR+HCTZ/Res: 0.7±0.1*, *p<0.05 vs. WKY]. To understand autophagic flux, some MRA were incubated with lysosomal inhibitor chloroquine (CQ; 30 μM) for 2 hours. CQ incubation significantly increased LC3-II expression to a similar magnitude in WKY, SHR, and SHR+HCTZ/Res MRA (all *p<0.05 vs. basal). However, the percent increase in LC3-II expression after CQ incubation was significantly less in SHR compared to WKY, and SHR+HCTZ/Res was not different from either WKY or SHR (% increase from basal LC3-II, WKY: 546±187, SHR: 156±38*, and SHR+HCTZ/Res: 273±106, *p<0.05 vs. WKY). Overall, these data suggest that SHR have impaired autophagosome-lysosomal fusion, and this is not solely attributable to high blood pressure. Therefore, reconstituting autophagic activity could be a novel prophylactic or therapeutic measure against vascular aging in hypertension.

Central Neurohormonal Mechanisms in Spontaneously Hypertensive Rats Compared with Human Essential Hypertension

1974 ◽  
Vol 48 (s2) ◽  
pp. 205s-214s ◽  
Author(s):  
B. Folkow
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
High Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Common Type ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Genetic Elements

Consideration of the results obtained in studies of spontaneously hypertensive rats indicates that these animals can serve as useful models for perhaps the most common type of essential hypertension of man. Other variants of essential hypertension probably occur where the relative balance between the genetic elements predisposing to high blood pressure may be somewhat different.

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