scholarly journals Alterations in the plasma membrane properties of the myocardium of spontaneously hypertensive rats.

Hypertension ◽  
1986 ◽  
Vol 8 (7) ◽  
pp. 583-591 ◽  
Author(s):  
R V Sharma ◽  
C A Butters ◽  
R C Bhalla
Keyword(s):  
Plasma Membrane ◽  
Spontaneously Hypertensive Rats ◽  
Membrane Properties ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

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.

Calcium Transport in Synaptosomes and Subcellular Membrane Fractions of Brain Tissue in Spontaneously Hypertensive Rats

1983 ◽  
Vol 65 (2) ◽  
pp. 127-135 ◽  
Author(s):  
G. M. Kravtsov ◽  
S. N. Orlov ◽  
N. I. Pokudin ◽  
Yu. V. Postnov
Keyword(s):  
Plasma Membrane ◽  
Brain Tissue ◽  
Spontaneously Hypertensive Rats ◽  
Calcium Influx ◽  
Spontaneous Hypertension ◽  
Hypertensive Rats ◽  
Exchange Method ◽  
Spontaneously Hypertensive ◽  
Subcellular Membrane ◽  
Inhibitor Analysis

1. The uptake of Na+ and Ca2+ by synaptosomes and uptake of Ca2+ by the mitochondria and microsomes of brain tissue of rats with spontaneous hypertension (SH rats) and normotensive Kyoto-Wistar rats (WKY rats) were studied with an isotope-exchange method. 2. By means of inhibitor analysis it has been shown that calcium influx into the synaptosomes during depolarization of their plasma membrane takes place only through the potential-dependent channels in both groups of animals. 3. Basal Ca2+ uptake by the synaptosomes of hypertensive rats was increased, apparently by partial depolarization of the synaptosome membrane caused by the increased membrane permeability to Na+ (basal Na+ uptake by synaptosomes was found to be increased in hypertensive rats). 4. Ca2+ uptake by mitochondria of hypertensive rats was increased, and the Ca2+ uptake by microsomes was decreased in these rats compared with controls. 5. The increment of the maximal Ca2+ transport rate in microsomes after the addition of calmodulin was decreased in spontaneously hypertensive rats compared with normotensive animals. Thus alterations in the interaction of calmodulin with the Ca2+-transporting systems of the plasma membrane are an important part of the widespread membrane defect observed in spontaneous hypertension. 6. The changes in the Ca2+-transporting and Ca2+-regulating systems of the synaptosomes of brain tissue in spontaneously hypertensive rats may be the basis for the increase of the intrasynaptosomal Ca2+ concentration and, in turn, for the alteration in the rate of neurotransmitter release.

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).

The Plasma Membrane Ca2+-ATPase in Spontaneously Hypertensive Rats

1997 ◽  
Vol 834 (1 Na/K-ATPase a) ◽  
pp. 673-675 ◽  
Author(s):  
BASIL D. ROUFOGALIS ◽  
SHI CHEN ◽  
ELEANOR P. W. KABLE ◽  
TUAN H. KUO ◽  
G. R. MONTEITH
Keyword(s):  
Plasma Membrane ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive
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