scholarly journals Insulin nonattenuation of vasoactive agent-induced responses in mesangial cells from spontaneously hypertensive rats

1995 ◽  
Vol 47 (3) ◽  
pp. 891-898 ◽  
Author(s):  
Yoji Inishi ◽  
Toshihiro Okuda ◽  
Toshio Arakawa ◽  
Chikako Yasuda ◽  
Mamiko Ohara ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Mesangial Cells ◽  
Induced Responses ◽  
Hypertensive Rats ◽  
Vasoactive Agent ◽  
Spontaneously Hypertensive

Characterization of signaling pathways of Angiotensin I‐Converting Enzyme in mesangial cells of spontaneously hypertensive rats (SHR)

2011 ◽  
Vol 25 (S1) ◽  
Author(s):  
Rosana Inácio Reis ◽  
Lucas Tabajara Parreiras‐e‐Silva ◽  
Christiane Becari ◽  
Maria Claudina Andrade ◽  
Maria Cristina Oliveira Salgado ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Spontaneously Hypertensive Rats ◽  
Mesangial Cells ◽  
Converting Enzyme ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive ◽  
Angiotensin I Converting Enzyme

scholarly journals Higher Bumetanide Sensitive Na-K-Cl Cotransport in Cultured Mesangial Cells from Spontaneously Hypertensive Rats (SHR)

1991 ◽  
Vol 32 (4) ◽  
pp. 558-558
Author(s):  
Satoru Kuriyama ◽  
Koji Nakamura ◽  
Yoshihiko Kaguchi ◽  
Takao Hashimoto ◽  
Osamu Sakai
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Mesangial Cells ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Modification of mesangial cell function by chloride is attenuated in spontaneously hypertensive rats

1994 ◽  
Vol 266 (4) ◽  
pp. F586-F591 ◽  
Author(s):  
T. Okuda ◽  
Y. Inishi ◽  
T. Arakawa ◽  
M. Ohara ◽  
K. Kurokawa
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Cell Function ◽  
Mesangial Cell ◽  
Mesangial Cells ◽  
Pge2 Production ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Cell Contraction ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

The effects of extracellular Cl- concentration ([Cl-]o) on cultured mesangial cells from spontaneously hypertensive rats (SHR) were examined. Angiotensin II (ANG II)- and vasopressin (VP)-induced cell contraction and Ca2+ transients of SHR mesangial cells were unaffected when the cells were preincubated with 10 mM [Cl-]o, while obvious suppression of the responses to these agents was observed in Wistar-Kyoto (WKY) mesangial cells. Enhanced prostaglandin E2 (PGE2) production was elicited by a decrease in [Cl-]o in WKY mesangial cells. In contrast, PGE2 synthesis by SHR mesangial cells was not enhanced by low [Cl-]o. However, ANG II-stimulated PGE2 production and the attenuation of ANG II-induced cell contraction and Ca2+ transients by the addition of exogenous PGE2 were present equally in both WKY and SHR mesangial cells. Based on these findings, we conclude that the absence of modification of mesangial cell function by [Cl-]o in SHR is due to the inability of low [Cl-]o to enhance PGE2 production. Insensitivity of SHR mesangial cells to changes in [Cl-]o might underlie the dysregulation of renal function in SHR.

Calcium reactivity and antagonism in portal veins from spontaneously hypertensive and normotensive rats

1984 ◽  
Vol 62 (1) ◽  
pp. 146-150 ◽  
Author(s):  
A. L. Harris ◽  
V. C. Swamy ◽  
D. J. Triggle
Keyword(s):  
Inhibitory Activity ◽  
Spontaneously Hypertensive Rats ◽  
Age Groups ◽  
Induced Responses ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Activity Frequency ◽  
Blood Pressures ◽  
Portal Veins ◽  
Wistar Kyoto

Reactivities of portal veins from spontaneously hypertensive rats (SHR) and normotensive controls (Wistar Kyoto, WKY) at 5–7 and 15–17 weeks of age were compared. Systolic blood pressures were not different at 5–7 weeks but those of SHR were significantly elevated (177 ± 4 mmHg) (1 mmHg = 133.322 Pa) at 15–17 weeks. Spontaneous activity, frequency, and tension were greater in SHR for both age groups. Young SHR were more sensitive to K+ at 5–7 weeks but less sensitive at 15–17 weeks than age-matched WKY rats. Sensitivity to Ca2+ in a K+-depolarizing medium was higher in SHR than in WKY for both age groups. Maximum tension responses to K+ or Ca2+ were greater in SHR. The Ca2+ channel antagonists nifedipine, nitrendipine, and nisoldipine were potent inhibitors of both noradrenaline- and K+-induced responses but did not show differences in inhibitory activity between WKY and SHR.

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