scholarly journals Resveratrol Attenuates Ovariectomy-Induced Hypertension and Bone Loss in Stroke-Prone Spontaneously Hypertensive Rats.

2000 ◽  
Vol 46 (2) ◽  
pp. 78-83 ◽  
Author(s):  
Kenichi MIZUTANI ◽  
Katsumi IKEDA ◽  
Yasuhiro KAWAI ◽  
Yukio YAMORI
Keyword(s):  
Bone Loss ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension

scholarly journals Metformin Attenuates Salt-Induced Hypertension in Spontaneously Hypertensive Rats

Hypertension ◽  
1999 ◽  
Vol 33 (5) ◽  
pp. 1135-1140 ◽  
Author(s):  
Martin S. Muntzel ◽  
Ibrahima Hamidou ◽  
Shean Barrett
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension

scholarly journals Mast cells contribute to alveolar bone loss in Spontaneously Hypertensive Rats with periodontal disease regulating cytokines production

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0247372
Author(s):  
Victor Gustavo Balera Brito ◽  
Mariana Sousa Patrocinio ◽  
Maria Carolina Linjardi Sousa ◽  
Ayná Emanuelli Alves Barreto ◽  
Sabrina Cruz Tfaile Frasnelli ◽  
...  
Keyword(s):  
Mast Cells ◽  
Bone Loss ◽  
Periodontal Disease ◽  
Spontaneously Hypertensive Rats ◽  
Alveolar Bone ◽  
Inflammatory Responses ◽  
Alveolar Bone Loss ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Inflammatory Status

Mast cells (MCs) play a pivotal role in inflammatory responses and had been studied in inflammatory bone disorders, however, their role in alveolar bone loss induced by periodontal disease (PD) is not yet fully understood. We, therefore, aimed to evaluate the effects of MCs depletion in the PD-induced alveolar bone loss in Wistar (W) and Spontaneously Hypertensive Rats (SHRs). PD was induced by ligating the lower first molars with silk thread one day after the MCs depletion, by the pre-treatment with compound 48/80 for 4 days. After 15 days of PD induction, the hemi-mandibles were surgically collected for qRT-PCR, histological analyses, immunostaining, and ELISA. Systolic blood pressure (SBP) was verified by tail plethysmography to confirm the hypertensive status, and SHR presented SBP >150 mmHg, and previous MC depletion alone or associated with PD did not alter this parameter. SHRs showed a more severe alveolar bone loss compared to W, and MC depletion significantly inhibited this response in both strains, with a more significant response in SHRs. MCs were less abundant in 48/80+PD groups, thus validating the previous MCs depletion in our model. PD increased the number of MC in the gingival tissue of SHR. Cytokine production (TNF-α, IL-6, IL-1β, and CXCL3) was constitutively higher in SHR and increased further after PD, which was also significantly reduced in the MCs-depleted animals. PD led to an increased expression of Opn, Rankl, Rank, Vtn, Itga5, Itgb5, Trap, and Ctsk in the mandible of W and SHRs, which was reversed in MCs-depleted animals. These results suggest that MCs significantly contributes to the PD-induced alveolar bone resorption, especially in the SHR, which is associated with a more severe PD progression compared to Wistar, partly explained by these cells contribution to the inflammatory status and mediator production, stimulating osteoclast-related response markers, which were reduced after MC depletion in our experimental model.

Vascular Sodium—Potassium Pump Activity in Various Models of Experimental Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 179s-181s ◽  
Author(s):  
M. B. Pamnani ◽  
D. L. Clough ◽  
S. J. Huot ◽  
F. J. Haddy
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Cell Membrane Permeability ◽  
Experimental Hypertension ◽  
Hypertensive Rats ◽  
Primary Defect ◽  
Sodium Potassium ◽  
Spontaneously Hypertensive ◽  
Induced Hypertension ◽  
Pump Activity ◽  
Sodium Potassium Pump

1. Ouabain-sensitive 86Rb uptake was used to assess sodium-potassium pump activity in vascular smooth muscle of animals with various types of experimental hypertension. 2. The findings suggest that pump activity is suppressed in the non-genetic low renin, presumably volume-expanded forms of hypertension. 3. By contrast, pump suppression does not appear to be involved in spontaneously hypertensive rats or in salt-induced hypertension in Dahl's salt-sensitive rats. In these genetic models the primary defect may be increased cell membrane permeability.

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