Systemic Hemodynamics and Cardiac Function in the Spontaneously Hypertensive Rat: Similarities with Essential Hypertension

1981 ◽  
pp. 53-71 ◽  
Author(s):  
E. D. Frohlich ◽  
M. A. Pfeffer ◽  
J. M. Pfeffer
Keyword(s):  
Essential Hypertension ◽  
Cardiac Function ◽  
Spontaneously Hypertensive Rat ◽  
Systemic Hemodynamics ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat

scholarly journals Endoplasmic reticulum stress inhibition blunts the development of essential hypertension in the spontaneously hypertensive rat

2019 ◽  
Vol 316 (5) ◽  
pp. H1214-H1223 ◽  
Author(s):  
Safaa Naiel ◽  
Rachel E. Carlisle ◽  
Chao Lu ◽  
Victor Tat ◽  
Jeffrey G. Dickhout
Keyword(s):  
Blood Pressure ◽  
Endoplasmic Reticulum ◽  
Essential Hypertension ◽  
Er Stress ◽  
Spontaneously Hypertensive Rat ◽  
Resistance Arteries ◽  
Spontaneously Hypertensive ◽  
Functional Changes ◽  
Hypertensive Rat ◽  
Hypertension Development

Essential hypertension is the leading cause of premature death worldwide. However, hypertension’s cause remains uncertain. endoplasmic reticulum (ER) stress has recently been associated with hypertension, but it is unclear whether ER stress causes hypertension. To clarify this question, we examined if ER stress occurs in blood vessels before the development of hypertension and if ER stress inhibition would prevent hypertension development. We used the spontaneously hypertensive rat (SHR) as a model of human essential hypertension and the Wistar-Kyoto (WKY) rat as its normotensive control. Resistance arteries collected from young rats determined that ER stress was present in SHR vessels before the onset of hypertension. To assess the effect of ER stress inhibition on hypertension development, another subset of rats were treated with 4-phenylbutyric acid (4-PBA; 1 g·kg−1·day−1) for 8 wk from 5 wk of age. Blood pressure was measured via radiotelemetry and compared with untreated SHR and WKY rats. Mesenteric resistance arteries were collected and assessed for structural and functional changes associated with hypertension. Systolic and diastolic blood pressures were significantly lower in the 4-PBA-treated SHR groups than in untreated SHRs. Additionally, 4-PBA significantly decreased the media-to-lumen ratio and ER stress marker expression, improved vasodilatory response, and reduced contractile responses in resistance arteries from SHRs. Overall, ER stress inhibition blunted the development of hypertension in the SHR. These data add evidence to the hypothesis that a component of hypertension in the SHR is caused by ER stress. NEW & NOTEWORTHY In this study, 4-phenylbutyric acid’s (4-PBA’s) molecular chaperone capability was used to inhibit endoplasmic reticulum (ER) stress in the small arteries of young spontaneously hypertensive rats (SHRs) and reduce their hypertension. These effects are likely mediated through 4-PBA's effects to reduce resistant artery contractility and increase nitric oxide-mediated endothelial vasodilation through a process preventing endothelial dysfunction. Overall, ER stress inhibition blunted the development of hypertension in this young SHR model. This suggests that a component of the increase in blood pressure found in SHRs is due to ER stress. However, it is important to note that inhibition of ER stress was not able to fully restore the blood pressure to normal, suggesting that a component of hypertension may not be due to ER stress. This study points to the inhibition of ER stress as an important new physiological pathway to lower blood pressure, where other known approaches may not achieve blood pressure-lowering targets.

Na-K-ATPase-inhibiting and glucose-6-phosphate dehydrogenase-stimulating activity of plasma and hypothalamus of the Okamoto spontaneously hypertensive rat

1986 ◽  
Vol 108 (1) ◽  
pp. 69-73 ◽  
Author(s):  
J. A. Millett ◽  
S. M. Holland ◽  
J. Alaghband-Zadeh ◽  
H. E. de Wardener
Keyword(s):  
Essential Hypertension ◽  
Salt Intake ◽  
Spontaneously Hypertensive Rat ◽  
Acetone Extract ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat ◽  
Cytochemical Bioassay ◽  
Normal Man ◽  
The Mean ◽  
Glucose 6 Phosphate Dehydrogenase

ABSTRACT The plasma of normal man and the rat, and an acetone extract of hypothalamus from the rat, have an ability to inhibit Na-K-ATPase which is related directly to salt intake. The ability of the plasma to inhibit Na-K-ATPase is raised in essential hypertension. The ability of plasma and of an acetone extract of hypothalamus from six spontaneously hypertensive (SHR) rats and six normotensive control (WKY) rats to inhibit Na-K-ATPase of fresh guinea-pig kidney was studied using cytochemical bioassay techniques. With a validated assay, which measures the capacity of biological samples to stimulate glucose-6-phosphate dehydrogenase (G6PD) as an index of their capacity to inhibit Na-K-ATPase, the mean G6PD-stimulating ability of the plasma from the SHR and the WKY rat was 772·3 ± 48·1 units/ml and 12·5 ± 2·6 units/ml respectively (P < 0·01) and of the hypothalamic extracts it was 2·2 ± 1·7 × 108 and 4·5 ± 1·8 × 104 units/hypothalamus (P < 0·01). With a semi-quantitative cytochemical assay, which measures Na-K-ATPase activity directly, plasma and an acetone extract of hypothalamus from the spontaneously hypertensive rat had much greater capacities to inhibit Na-K-ATPase than plasma and extract from the WKY rat. These raised levels of Na-K-ATPase inhibitory activity in the plasma of the SHR rat are similar to the highest values found in the plasma of patients with essential hypertension. The results suggest that the substance responsible for the increased capacity of the plasma to inhibit Na-K-ATPase may originate from the hypothalamus and that it may, in part, be involved in the mechanisms which induce the rise of arterial pressure in inherited forms of hypertension. J. Endocr. (1986) 108, 69–73

A Linkage Analysis of the Salt-sensitive Hypertensive Gene in the Stroke-prone Spontaneously Hypertensive Rat (SHRSP)

1996 ◽  
Vol 37 (4) ◽  
pp. 553-553
Author(s):  
Tomoji Mashimo ◽  
Yasuo Nara ◽  
Tomoko Tamada ◽  
Chiho Matsumoto ◽  
Katumi Ikeda ◽  
...  
Keyword(s):  
Linkage Analysis ◽  
Spontaneously Hypertensive Rat ◽  
Spontaneously Hypertensive ◽  
Hypertensive Rat
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