Increased Noradrenaline Content of Hypothalamic Nuclei in Association with Worsening of Hypertension after High Sodium Intake in the Young Spontaneously Hypertensive Rat

1982 ◽  
Vol 63 (s8) ◽  
pp. 339s-342s ◽  
Author(s):  
S. R. Winternitz ◽  
J. M. Wyss ◽  
J. R. Meadows ◽  
S. Oparil

1. High sodium intake results in an exacerbation of hypertension accompanied by evidence of increased peripheral sympathetic activity in the young spontaneously hypertensive rat (SHR) of the Okamoto strain. 2. To examine the hypothesis that high sodium intake increases peripheral sympathetic activity via an influence on central noradrenergic pathways involved in cardiovascular regulation, the effect of dietary sodium intake on noradrenaline stores of individual hypothalamic nuclei was examined in young SHR. 3. After 2 weeks of high sodium intake, the noradrenaline content of the anterior and dorsomedial hypothalamic nuclei of SHR was increased when compared with SHR receiving normal sodium intake. Increases in the noradrenaline content of anterior hypothalamic nucleus persisted at 4 weeks. No changes were seen in other regions examined. 4. These observations lend support to the hypothesis that sodium and the sympathetic nervous system have synergistic effects in the pathogenesis of hypertension in the SHR.

2001 ◽  
Vol 19 (Supplement) ◽  
pp. 635-639 ◽  
Author(s):  
Yoshiyu Takeda ◽  
Takashi Yoneda ◽  
Masashi Demura ◽  
Kenji Furukawa ◽  
Isamu Miyamori ◽  
...  

1988 ◽  
Vol 29 (4) ◽  
pp. 562-562
Author(s):  
Hiroaki Tomori ◽  
Hiroshi Kawamura ◽  
Masahiro Maki ◽  
Hideaki Higashi ◽  
Kazuyoshi Tsukamoto ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Rosita Stanzione ◽  
Franca Bianchi ◽  
Maria Cotugno ◽  
Simona Marchitti ◽  
Maurizio Forte ◽  
...  

Based on preliminary evidence that highlights microRNA-122 as a contributing factor to stroke pathogenesis, we aimed at assessing its expression level, along with the presence of early signs of cerebrovascular disease, in the brain of stroke-prone spontaneously hypertensive rat (SHRSP), a suitable model of human disease that accelerates stroke occurrence under a high sodium/low potassium (Japanese-style) diet (JD). After one month of JD, before stroke occurrence, brain microRNA-122 level was significantly decreased in SHRSP as compared to the stroke-resistant SHR (SHRSR). At this time, levels of markers of oxidative stress and inflammation, as well as of endothelial integrity and function, apoptosis and necrosis were differently modulated in the brains of JD-fed SHRSP as compared to SHRSR, pointing to a significant activation of all deleterious mechanisms underlying subsequent stroke development in SHRSP. We also showed that miR-122 improved survival of rat endothelial cerebral cells upon stress stimuli (excess NaCl, hydrogen peroxide). Our data suggest that a decrease of brain microRNA-122 level is deleterious and can be considered as an early marker of stroke in the SHRSP. Understanding the mechanisms by which microRNA-122 protects vascular cells from stress stimuli may provide a useful approach to improve preventive and treatment strategies against stroke.


1986 ◽  
Vol 333 (2) ◽  
pp. 117-123 ◽  
Author(s):  
Angelo Parini ◽  
Laurent Diop ◽  
Dominique Laude ◽  
Drori Ben-Ishay ◽  
Jean-Pierre Dausse

1973 ◽  
Vol 45 (s1) ◽  
pp. 325s-329s ◽  
Author(s):  
R. M. Zusman ◽  
B. H. Forman ◽  
G. Schneider ◽  
B. V. Caldwell ◽  
L. Speroff ◽  
...  

1. In normal and hypertensive rats prostaglandin A (PGA) in plasma and kidney increased on low sodium intake and decreased on high sodium intake. 2. Plasma and renal concentrations of PGA were higher in spontaneously hypertensive rats than in normal Wistar rats in each dietary group.


1998 ◽  
Vol 274 (4) ◽  
pp. H1269-H1276 ◽  
Author(s):  
Bing S. Huang ◽  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen

Both brain ouabain-like activity (“ouabain”) and brain angiotensin II (ANG II) contribute to the sympathoexcitatory and pressor responses to high sodium intake in spontaneously hypertensive (SHR) and Dahl salt-sensitive (Dahl S) rats. To assess whether increases in cerebrospinal fluid (CSF) sodium can mimic this pattern of changes, Wistar rats were chronically infused with artificial CSF (aCSF) or sodium-rich aCSF (0.8 or 1.2 M sodium) intracerebroventricularly through osmotic minipumps for 14 days. Sodium-rich aCSF (0.8 M) was also infused intracerebroventricularly for 2 wk concomitantly with either antibody Fab fragments that bind ouabain and related steroids with high affinity, γ-globulins as control (200 μg/day for both), or the AT1blocker losartan (1 mg ⋅ kg−1 ⋅ day−1). Sodium-rich aCSF increased CSF sodium from 146 ± 2 to 152 ± 2 (0.8 M) and 160 ± 3 (1.2 M) mmol/l, and increased brain “ouabain” in the hypothalamus, pituitary, and pons. In conscious rats, sodium-rich aCSF increased baseline mean arterial pressure (MAP), enhanced MAP, heart rate (HR), and renal sympathetic nerve activity (RSNA) responses to intracerebroventricular α2-adrenoceptor agonist guanabenz and air stress, and desensitized arterial and cardiopulmonary baroreflex control of HR and RSNA. These effects were largely prevented by intracerebroventricular Fab fragments or losartan. Thus, in Wistar rats, both brain “ouabain” and the brain renin-angiotensin system contribute to sympathoexcitation, impairment of baroreflexes, and hypertension caused by chronically increased CSF sodium. The similar patterns of changes caused by CSF sodium in Wistar rats and by high sodium intake in SHR and Dahl S rats indicate that if high sodium intake increases central sodium, such changes may contribute to sympathoexcitation and hypertension.


Hypertension ◽  
2001 ◽  
Vol 38 (5) ◽  
pp. 1172-1176 ◽  
Author(s):  
Karima Et-taouil ◽  
Pierre Schiavi ◽  
Bernard I. Lévy ◽  
Gérard E. Plante

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