Vascular Lesions in Hypertensive Rats under Salt Loading: Kidney Renin and Lysosomal Enzymes

1976 ◽  
Vol 51 (s3) ◽  
pp. 49s-51s
Author(s):  
N. Saito ◽  
S. Mukaino ◽  
K. Ogino ◽  
C. Kawai
Keyword(s):  
Enzyme Activities ◽  
Cathepsin D ◽  
Normal Diet ◽  
High Salt ◽  
Renin Activity ◽  
Vascular Lesions ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

1. Renal and cerebral vascular lesions occurred more often and earlier in spontaneously hypertensive rats (SHR) given a high salt diet than in SHR given a normal diet. 2. Kidney renin activity was low during high salt loading; the kidney renin activity of rats with hypertensive renal vascular lesions was moderately elevated. Kidney renin activity or cathepsin D activities were higher in stroke-prone SHR (SHRSP) aged 9 months than in stroke-resistant SHR (SHRSR). 3. β-Glucuronidase, cathepsin D and deoxyribonuclease activities were greater in the kidney of Wistar/Kyoto (WK) rats or SHR when there were hypertensive vascular lesions. These three enzyme activities were also greater in the aorta of SHR aged 13–14 months than in the aorta of WK rats. 4. It was supposed that kidney renin activity and lysosomal enzyme activities were related to hypertensive vascular lesions.

Further analysis of cell membrane changes in genetic hypertension in rats by diphenylhexatriene fluorescence polarization

1984 ◽  
Vol 66 (6) ◽  
pp. 717-723 ◽  
Author(s):  
I. Aracon-Birlouez ◽  
T. Montenay-Carestier ◽  
M. A. Devynck
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Erythrocyte Membranes ◽  
Shr Rats ◽  
Erythrocyte Ghosts ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Platelet Membranes ◽  
Wistar Kyoto ◽  
Membrane Changes

1. Fluorescence Dolarization of dbhenvlhexa-triene embedded in membranes was used as an index of ‘microviscosity’ in platelets and ervthro—cyte ghosts of spontaneously hypertensive rats of the Okamoto-Aoki strain (SHR), Wistar-Kyoto strain (WKY) and of the hypertension-prone and -resistant Sabra strains (SBH and SBN), and the original Sabra strain (SB). 2. Microviscosity was increased both in erythrocyte ghosts and platelet membranes of male but not female SHR rats compared with WKY rats and in hypertension-prone Sabra rats compared with the original Sabra rats. 3. Acute and chronic salt loading increased the microviscosity of platelet membranes in all strains of rats but had no effect on the erythrocyte membranes. 4. Microviscosities of vesicles made of lipids extracted from SHR and WKY erythrocyte ghosts were similar. This supports the hypothesis that membrane proteins play a major role in the differences in microviscosity observed in SHR rats.

scholarly journals Thromboxane A2 Receptor Antagonist (ONO-8809) Attenuates the Renal Disorders Caused by Salt-Overload in Stroke-Prone Spontaneously Hypertensive Rats

2021 ◽  
Author(s):  
Yusuke Nagatani ◽  
Toshihide Higashino ◽  
Kosho Kinoshita ◽  
Hideaki Higashino
Keyword(s):  
Gene Expression ◽  
Spontaneously Hypertensive Rats ◽  
Salt Intake ◽  
Thromboxane A2 ◽  
High Salt ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Spontaneously Hypertensive ◽  
Oxidative Stresses ◽  
High Salt Intake

Background. Epidemiological and clinical studies demonstrated that excessive salt intake causes severe hypertension and exacerbated organ derangement such as chronic kidney disease (CKD). In this study, we focused on evaluating histological and gene-expression findings in the kidney using stroke-prone spontaneously hypertensive rats (SHRSP) with high-salt intake and thromboxane A2/ prostaglandin H2 receptor (TPR) blocker ONO-8809. Methods. SHRSP aged 6 weeks were divided into three groups eating normal chow containing 0.4% NaCl, 2.0%NaCl, or 2.0%NaCl +ONO-8809 (0.6mg/kg p.o. daily). Histological analyses with immunohistochemistry and a gene-expression assay with a DNA kidney microarray were performed after 8 weeks. Results. The following changes were observed with high-salt intake. Glomerular sclerotic changes were remarkably observed in the juxtaglomerular cortex areas. ED1, MCP-1, nitrotyrosine, and HIF-1α staining areas were increased in the glomeruli and interstitial portion. Tbxa2r which encodes TPR, Prcp, and Car7 were significantly underexpressed in the kidney. The plasma 8-isoprostane level was significantly elevated, and was attenuated with ONO-8809 treatment. Conclusion. TXA2 and oxidative stresses exaggerated renal dysfunction in salt-loading SHRSP, and ONO-8809 as a TPR blocker suppressed these changes. Therefore, ONO-8809 is a candidate drug to prevent CKD for hypertensive patients associated with high-salt intake.

Alteration in sialidase and other glycosidase activities in the kidney of spontaneously hypertensive rats: persistence after preventive treatment with hydralazine

1988 ◽  
Vol 66 (7) ◽  
pp. 884-888 ◽  
Author(s):  
L. Cohen-Forterre ◽  
A. M. Grigorova-Borsos ◽  
C. Falcy ◽  
G. Mansour ◽  
G. Mozere ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Enzyme Activities ◽  
Spontaneously Hypertensive Rats ◽  
Specific Activity ◽  
Blood Pressure Level ◽  
Preventive Treatment ◽  
Kidney Cortex ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto

Because kidney microangiopathy with capillary basement membrane thickening has been reported in spontaneous hypertension, we have studied the activities of three lysosomal glycosidases able to degrade the carbohydrate moieties of basement membrane constituents in the kidney cortex of 12-week-old spontaneously hypertensive rats (SHR) and age-matched normotensive Wistar Kyoto rats (WKY). These activities were also determined in SHR and WKY treated from 6 to 12 weeks of age with hydralazine (mean dose, 18 mg/kg per day in drinking water). Sialidase specific activity on sialyl-α2-3-[3H]lactitol was markedly decreased in the kidney of untreated SHR, 40% activity remaining relative to that found in untreated age-matched WKY (p < 0.001). β-Galactosidase specific activity on p-nitrophenyl-β-D-galactoside was also decreased, 86% activity remaining relative to that found in untreated WKY (p < 0.001). Glucosyl-galactosyl-hydroxylysyl glucohydrolase specific activity on glucosyl-galactosyl-hydroxylysine was equally diminished, 74% activity remaining relative to that found in untreated age-matched WKY (p < 0.001). In contrast, the activities of two control glycosidases inactive on the carbohydrate moieties of basement membrane constituents, α-glucosidase assayed with p-nitrophenyl-α-D-glucoside as substrate and β-glucosidase assayed with p-nitrophenyl-β-D-glucoside as substrate, were significantly increased. All the alterations in enzyme activities observed in the kidney of SHR were also present in the long-term treated normotensive SHR. No effect of the hydralazine treatment on the three enzyme activities investigated could be demonstrated in the WKY. Thus the alterations observed in the kidneys of SHR appear to be independent of blood pressure level.

Salt loading augments vascular responses to indomethacin in stroke-prone SHR

1982 ◽  
Vol 243 (3) ◽  
pp. H360-H364
Author(s):  
T. Imaizumi ◽  
A. Takeshita ◽  
T. Ashihara ◽  
M. Nakamura
Keyword(s):  
Vascular Resistance ◽  
Prostaglandin E1 ◽  
Salt Intake ◽  
High Salt ◽  
Salt Loading ◽  
Salt Diet ◽  
Spontaneously Hypertensive ◽  
High Salt Intake ◽  
Endogenous Prostaglandins ◽  
Wistar Kyoto

We examined whether endogenous prostaglandins (PGs) participated in control of hindquarters vascular resistance during salt loading in stroke-prone spontaneously hypertensive rates (SHR-SP). SHR-SP and Wistar-Kyoto rats (WKY) were fed either a normal (0.3% NaCl) or high (8% NaCl) salt diet for 5 wk. High salt increased blood pressure and hindquarter vascular resistance (VR) in SHR-SP (P less than 0.01) but not in WKY. Indomethacin given intravenously increased hindquarter VR in SHR-SP during high salt as well as during normal salt (P less than 0.01) but not in either group of WKY. In SHR-SP the increase in hindquarter VR by PG synthesis inhibitors were two times greater during high salt than during normal salt (P less than 0.01). In addition, hindquarter vasodilatation by bradykinin was greater (P less than 0.05) in SHR-SP during high salt than that during normal salt, but vasodilatation by prostaglandin E1 or nitroglycerin was not different between the two groups. These results suggest that vascular synthesis of endogenous PGs was greater in SHR-SP during high salt than that during normal salt. Increased endogenous PGs may play an important role in the regulation of hindquarter VR during high salt intake in SHR-SP.

Enhanced Sympathetic Activity Caused by Salt Loading in Spontaneously Hypertensive Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 171s-173s ◽  
Author(s):  
R. Dietz ◽  
A. Schoumig ◽  
W. Rascher ◽  
R. Strasser ◽  
W. Kubler
Keyword(s):  
Sympathetic Activity ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Salt Loading ◽  
Plasma Adrenaline ◽  
Spontaneously Hypertensive ◽  
Noradrenaline Concentration ◽  
Wistar Kyoto ◽  
Distinct Increase ◽  
Stimulation Of

1. Salt loading accelerates and increases the rise in blood pressure (spSH) in stroke-prone spontaneously hypertensive rats, but not in Wistar-Kyoto (WK) rats. 2. In both strains a slight increase in plasma volume was obtained during salt loading. 3. Salt loading caused a distinct increase in plasma noradrenaline concentration in spSH rats, but a slight decrease in WK rats. Plasma adrenaline and dopamine concentrations remained unaffected. 4. Exposure to cold resulted in a more marked stimulation of sympathoadrenal and sympathoneuronal activity in salt-loaded spSH rats than in spSH rats on a normal sodium diet. 5. It is concluded that salt loading results in a further increase of the already elevated sympathetic activity in spSH rats.

Antibody-Sensitive Renin of Adrenal and Resistance Vessels is Markedly Elevated in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 187s-189s ◽  
Author(s):  
Mitsuhide Naruse ◽  
Tadashi Inagami
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Resistance Vessels ◽  
Significant Difference ◽  
Mesenteric Vessels ◽  
Wistar Kyoto

1. Three-week-old spontaneously hypertensive rats (SHR) showed markedly elevated specific renin activity in the adrenal and the mesenteric vessels compared with control Wistar-Kyoto (WKY)rats. 2. In 17-week-old SHR with established hypertension, adrenal renin remained markedly elevated over that of WKY rats, whereas no significant difference was observed in renin of the mesenteric vessels. 3. The specific renin activity of the aorta showed no significant difference compared with that of WKY rats at 3 or 17 weeks of age. 4. These results suggest possible involvement of adrenal and vascular renin in the pathogenesis of hypertension in SHR.

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.

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