Abnormal Calcium Handling by Isolated Cardiac Plasma Membrane from Spontaneously Hypertensive Rats

1981 ◽  
Vol 61 (s7) ◽  
pp. 45s-48s ◽  
Author(s):  
Marie-Gabrielle Pernollet ◽  
Marie-Aude Devynck ◽  
P. Meyer
Keyword(s):  
Plasma Membrane ◽  
Calcium Binding ◽  
Spontaneously Hypertensive Rats ◽  
Membrane Vesicles ◽  
Calcium Handling ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Calcium Extrusion ◽  
Sarcolemmal Vesicles

1. Calcium handling by heart sarcolemmal vesicles from young spontaneously hypertensive rats (SHR) and normotensive Wistar—Kyoto (WKY) control rats were compared. 2. Calcium binding was significantly altered in SHR membranes at the physiological cytosolic Ca2+ concentrations which occur in resting and excited cells. 3. ATP-dependent calcium accumulation occurred at a higher rate in SHR than in WKY rat membrane vesicles. 4. Na+-dependent calcium extrusion of loaded vesicles was higher in SHR than in WKY rat membrane vesicles. 5. These alterations may play a significant role in the pathogenesis of hypertension.

Decreased Phosphorylation of Polyphosphoinositides in the Erythrocyte Membrane of Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 37s-39s ◽  
Author(s):  
P. Marche ◽  
S. Koutouzov ◽  
P. Meyer
Keyword(s):  
Erythrocyte Membrane ◽  
Calcium Binding ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Inositol Phospholipids ◽  
Wistar Kyoto

1. The distribution and metabolism of inositol phospholipids were studied in the erythrocyte membrane of spontaneously hypertensive and normotensive Wistar-Kyoto rats. The incorporation of 32P into these lipids was considered as an index of their turnover, and a reflection of their metabolism. 2. With [γ-32P]ATP as the source of label only the polyphosphoinositides (diphosphoinositide and triphosphoinositide) incorporated 32P. The levels of labelling were lower in hypertensive than in normotensive rats. Our data indicate that, in the hypertensive rats, the kinases responsible for the labelling of polyphosphoinositides exhibited decreased Vmax. for ATP. 3. These changes may be related to those described for calcium binding and transport in the erythrocyte of spontaneously hypertensive rats.

Increased transport of inorganic phosphate in renal brush borders of spontaneously hypertensive rats

1986 ◽  
Vol 250 (3) ◽  
pp. F470-F475 ◽  
Author(s):  
R. J. Bindels ◽  
J. A. Geertsen ◽  
C. H. Van Os
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Membrane Vesicles ◽  
Phosphate Transport ◽  
Serum Phosphate ◽  
Kidney Cortex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Renal Brush Border Membrane ◽  
Transport Of Inorganic Phosphate ◽  
Wistar Kyoto

Phosphate metabolism was studied in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) by measuring serum phosphate concentrations and 24-h urinary phosphate excretions in rats placed in metabolic cages from 6 to 23 wk of age. Serum phosphate concentrations in SHR were significantly lower than those in WKY at 6, 12, and 20 wk of age. In addition, 24-h urinary phosphate excretion was lower in SHR relative to WKY from 6 through 23 wk of age. The hypophosphaturia in SHR was accompanied with an increase in the maximal transport rate of Na+-dependent phosphate transport in renal brush border membrane vesicles (BBMV) isolated from kidney cortex at 6, 12, and 20 wk of age. The apparent affinity for phosphate did not differ significantly between WKY and SHR at all ages studied. A direct relationship between maximal Na+-dependent phosphate transport rates in BBMV and serum phosphate concentrations was observed in both strains. In SHR, phosphate homeostasis is disturbed from 6 wk of age on.

scholarly journals Mas receptor is translocated to the nucleus upon agonist stimulation in brainstem neurons from spontaneously hypertensive rats but not normotensive rats

2019 ◽  
Vol 116 (12) ◽  
pp. 1995-2008 ◽  
Author(s):  
Flavia M Cerniello ◽  
Mauro G Silva ◽  
Oscar A Carretero ◽  
Mariela M Gironacci
Keyword(s):  
Nitric Oxide ◽  
Arachidonic Acid ◽  
Plasma Membrane ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Coated Pits ◽  
Spontaneously Hypertensive ◽  
Mas Receptor ◽  
Early Endosomes ◽  
Wistar Kyoto

Abstract Aims  Activation of the angiotensin (Ang)-(1-7)/Mas receptor (R) axis protects from sympathetic overactivity. Endocytic trafficking is an essential process that regulates receptor (R) function and its ultimate cellular responses. We investigated whether the blunted responses to Ang-(1-7) in hypertensive rats are associated to an alteration in MasR trafficking. Methods and results  Brainstem neurons from Wistar-Kyoto (WKY) or spontaneously hypertensive rats (SHRs) were investigated for (i) Ang-(1-7) levels and binding and MasR expression, (ii) Ang-(1-7) responses (arachidonic acid and nitric oxide release and Akt and ERK1/2 phosphorylation), and (iii) MasR trafficking. Ang-(1-7) was determined by radioimmunoassay. MasR expression and functionality were evaluated by western blot and binding assays. MasR trafficking was evaluated by immunofluorescence. Ang-(1-7) treatment induced an increase in nitric oxide and arachidonic acid release and ERK1/2 and Akt phosphorylation in WKY neurons but did not have an effect in SHR neurons. Although SHR neurons showed greater MasR expression, Ang-(1-7)-elicited responses were substantially diminished presumably due to decreased Ang-(1-7) endogenous levels concomitant with impaired binding to its receptor. Through immunocolocalization studies, we evidenced that upon Ang-(1-7) stimulation MasRs were internalized through clathrin-coated pits and caveolae into early endosomes and slowly recycled back to the plasma membrane. However, the fraction of internalized MasRs into early endosomes was larger and the fraction of MasRs recycled back to the plasma membrane was smaller in SHR than in WKY neurons. Surprisingly, in SHR neurons but not in WKY neurons, Ang-(1-7) induced MasR translocation to the nucleus. Nuclear MasR expression and Ang-(1-7) levels were significantly greater in the nuclei of Ang-(1-7)-stimulated SHR neurons, indicating that the MasR is translocated with its ligand bound to it. Conclusion  MasRs display differential trafficking in brainstem neurons from SHRs, which may contribute to the impaired responses to Ang-(1-7).

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

scholarly journals Aging Additively Influences Insulin- and Insulin-Like Growth Factor-1-Mediated Endothelial Dysfunction and Antioxidant Deficiency in Spontaneously Hypertensive Rats

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 676
Author(s):  
Kunanya Masodsai ◽  
Yi-Yuan Lin ◽  
Sih-Yin Lin ◽  
Chia-Ting Su ◽  
Shin-Da Lee ◽  
...  
Keyword(s):  
Growth Factor ◽  
Endothelial Dysfunction ◽  
Spontaneously Hypertensive Rats ◽  
No Production ◽  
Organ Bath ◽  
Insulin Like Growth Factor ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Nos Inhibitors ◽  
Wistar Kyoto

This study aimed to investigate the aging-related endothelial dysfunction mediated by insulin and insulin-like growth factor-1 (IGF-1) and antioxidant deficiency in hypertension. Male spontaneously hypertensive rats (SHRs) and age-matched normotensive Wistar–Kyoto rats (WKYs) were randomly divided into 24-week-old (younger) and 48-week-old (older) groups, respectively. The endothelial function was evaluated by the insulin- and IGF-1-mediated vasorelaxation of aortic rings via the organ bath system. Serum levels of nitric oxide (NO), malondialdehyde (MDA), catalase, and total antioxidant capacity (TAC) were examined. The insulin- and IGF-1-mediated vasorelaxation was significantly impaired in both 24- and 48-week-old SHRs compared with age-matched WKYs and was significantly worse in the 48-week-old SHR than the 24-week-old SHR. After pretreatments of phosphoinositide 3-kinase (PI3K) or NO synthase (NOS) inhibitors, the insulin- and IGF-1-mediated vasorelaxation became similar among four groups. The serum level of MDA was significantly increased, while the NO, catalase, and TAC were significantly reduced in the 48-week-old SHR compared with the 24-week-old SHR. This study demonstrated that the process of aging additively affected insulin- and IGF-1-mediated endothelial dysfunction in SHRs, which could be partly attributed to the reduced NO production and antioxidant deficiency.

Effects of dietary Ca2+ on erythrocyte Na+-transport systems in spontaneously hypertensive rats

1991 ◽  
Vol 81 (1) ◽  
pp. 107-112 ◽  
Author(s):  
K. Fujito ◽  
M. Yokomatsu ◽  
N. Ishiguro ◽  
H. Numahata ◽  
Y. Tomino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Transport Systems ◽  
Hypertensive Rats ◽  
Na Transport ◽  
Spontaneously Hypertensive ◽  
Na Pump ◽  
Wistar Kyoto ◽  
Increased Activity ◽  
Regulation Of Blood Pressure

1. The purpose of this study was to determine the effect of dietary Ca2+ intake on blood pressure and erythrocyte Na+ transport in spontaneously hypertensive rats. 2. Spontaneously hypertensive rats and Wistar-Kyoto rats were fed diets with three different Ca2+ contents, 0.1% (low-Ca2+ diet), 0.6% (normal-Ca2+ diet) and 4.0% (high-Ca2+ diet), between 6 and 20 weeks of age. At 20 weeks of age, the levels of erythrocyte Na+ efflux, as well as Na+ and K+ contents in erythrocytes, were measured. 3. On the low-Ca2+ diet, spontaneously hypertensive rats showed an enhancement of hypertension. Conversely, on the high-Ca2+ diet, they showed an attenuation of the increase in blood pressure. Spontaneously hypertensive rats had a lower erythrocyte Na+ content and increased activity of the Na+ pump at higher levels of dietary Ca2+. Passive Na+ permeability and Na+-K+ co-transport were similar in spontaneously hypertensive rats on the low-, normal- and high-Ca2+ diets. There were no significant differences in blood pressure and in Na+ pump activity in WKY on the three different diets. 4. It is concluded that dietary Ca2+ might affect the regulation of blood pressure in spontaneously hypertensive rats by changing the activity of Na+ pump in the cell membrane.

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