scholarly journals Different effects of arginine vasopressin on high-mobility group box 1 expression in astrocytes isolated from stroke-prone spontaneously hypertensive rats and congenic SHRpch1_18 rats

2016 ◽  
Vol 97 (2) ◽  
pp. 97-106 ◽  
Author(s):  
Kazuo Yamagata ◽  
Natumi Sone ◽  
Sari Suguyama ◽  
Toru Nabika
Keyword(s):  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
High Mobility ◽  
High Mobility Group ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Greater high-mobility group box 1 in male compared with female spontaneously hypertensive rats worsens renal ischemia–reperfusion injury

2020 ◽  
Vol 134 (13) ◽  
pp. 1751-1762 ◽  
Author(s):  
Riyaz Mohamed ◽  
Olga Rafikova ◽  
Paul M. O’Connor ◽  
Jennifer C. Sullivan
Keyword(s):  
Cell Death ◽  
Spontaneously Hypertensive Rats ◽  
Ischemia Reperfusion ◽  
High Mobility ◽  
Renal Ischemia ◽  
Tubular Cell ◽  
High Mobility Group ◽  
Tubular Damage ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Abstract Renal ischemia is the most common cause of acute kidney injury. Damage-associated molecular patterns (DAMPs) initiate an inflammatory response and contribute to ischemia–reperfusion (IR) injury in males, yet the contribution of DAMPs to IR injury in females is unknown. The goal of the current study was to test the hypothesis that males have greater increases in the DAMP high-mobility group box 1 (HMGB1), worsening injury compared with females. Thirteen-week-old male and female spontaneously hypertensive rats (SHR) were subjected to sham or 45-min warm bilateral ischemia followed by 24 h of reperfusion before measurement of HMGB1 and renal function. Additional SHR were pre-treated with control (IgG) or HMGB1 neutralizing antibody (300 µg/rat) 1 h prior to renal ischemia. Blood, urine and kidneys were harvested 24 h post-IR for histological and Western blot analyses. Initial studies confirmed that IR resulted in greater increases in renal HMGB1 in male SHR compared with females. Greater renal HMGB1 in male SHR post-IR resulted in greater increases in serum TNF-α and renal IL-1β, neutrophil infiltration and tubular cell death. Neutralization of HMGB1 attenuated IR-induced increases in plasma creatinine, blood urea nitrogen (BUN), inflammation, tubular damage and tubular cell death only in male SHR. In conclusion, our data demonstrate that there is a sex difference in the contribution of HMGB1 to IR-induced injury, where males exhibit greater increases in HMGB1-mediated renal injury in response to IR compared with females.

Renal Hemodynamics in Young and Old Spontaneously Hypertensive Rats during Intrarenal Infusion of Arginine Vasopressin

2001 ◽  
Vol 24 (3) ◽  
pp. 176-184 ◽  
Author(s):  
Rolf E.F. Christiansen ◽  
Anca B. Roald ◽  
Camilla Gjerstad ◽  
Olav Tenstad ◽  
Bjarne M. Iversen
Keyword(s):  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
Renal Hemodynamics ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Mitogenic Events Induced by Vasopressin in Aortic Fibroblasts from Spontaneously Hypertensive Rats

1993 ◽  
Vol 85 (1) ◽  
pp. 57-61 ◽  
Author(s):  
Ding Liang Zhu ◽  
Thierry Herembert ◽  
Pierre Marche
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
Thymidine Incorporation ◽  
Inositol Phosphate ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Kinase C ◽  
Wistar Kyoto

1. To further explore the mechanisms of arterial growth, we investigated the signalling pathways through which arginine-vasopressin acts as a mitogen in cultured adventitial aortic fibroblasts of the spontaneously hypertensive rat, and we examined the mechanisms involved in the hyperresponsiveness to arginine-vasopressin of fibroblasts from spontaneously hypertensive rats compared with fibroblasts from Wistar-Kyoto rats. 2. Arginine-vasopressin-induced [3H]thymidine incorporation was used to determine the peptide mitogenicity. Arginine-vasopressin-triggered hydrolysis of phosphoinositides by phospholipase C was evaluated by measuring [3H]inositol phosphate formation. The role of protein kinase C and protein tyrosine kinases in arginine-vasopressin mitogenicity was assessed by stimulating the cells with arginine-vasopressin in the presence of 12-O-tetradecanoylphorbol 13-acetate and tyrphostin (a tyrosine kinase inhibitor), respectively. 3. Arginine-vasopressin-induced DNA synthesis was completely abolished in confluent cells, whereas [3H]inositol phosphate formation was only reduced. The presence of 12-O-tetradecanoylphorbol 13-acetate markedly decreased arginine-vasopressin-induced [3H]thymidine incorporation in fibroblasts from spontaneously hypertensive rats and was without effect in fibroblasts from Wistar-Kyoto rats. Tyrphostin abolished arginine-vasopressin-induced [3H]thymidine incorporation in a dose-dependent manner and did not affect the formation of inositol phosphates. 4. These results indicate that phospholipase C activation is not sufficient for arginine-vasopressin-induced mitogenesis. They also suggest that (i) tyrosine kinase activation is a necessary step in the transduction of the arginine-vasopressin mitogenic signal, and (ii) protein kinase C participates in the increased mitogenic potency of arginine-vasopressin in spontaneously hypertensive rats.

Reduced Synthesis of [Arginine]Vasopressin in Spontaneously Hypertensive Rats

1982 ◽  
Vol 63 (s8) ◽  
pp. 117s-119s ◽  
Author(s):  
W. Rascher ◽  
R. E. Lang ◽  
B. Fink ◽  
D. Ganten ◽  
TH. Unger ◽  
...  
Keyword(s):  
Brain Stem ◽  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
Severe Dehydration ◽  
Hypertensive Rats ◽  
Brain Areas ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Wistar Kyoto ◽  
The Brain

1. In 12 week-old stroke-prone spontaneously hypertensive (SPSH) rats and in normotensive Wistar-Kyoto (WKY) rats plasma concentration of [arginine]vasopressin (AVP) and the AVP content in various brain areas were measured by radioimmunoassay. 2. In hydrated SPSH rats plasma AVP was lower than in WKY rats. In the hypothalamus and in the brain stem, but not in the pituitary, the content of AVP was reduced. 3. After a dehydration period of 48 h plasma AVP rose similarly in both SPSH and WKY rats. However, in the pituitary the AVP content was significantly lower in SPSH than in WKY rats. In the hypothalamus and in the brain stem, AVP content was not significantly influenced by dehydration. 4. It is concluded that in the hydrated stage the secretion of AVP and its synthesis in the hypothalamus are reduced in SPSH rats. However, the SPSH rats still respond satisfactorily to the strong stimulus of severe dehydration.

Vasopressin withdrawal produces hypotension in the spontaneously hypertensive rat

1985 ◽  
Vol 249 (1) ◽  
pp. H193-H197 ◽  
Author(s):  
E. K. Chiu ◽  
J. R. McNeill
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Pressor Agent

In spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto controls (WKY), prolonged intravenous infusions of either arginine vasopressin (AVP, 8 mU X kg-1 X min-1) or phenylephrine (PE, 20 nmol X kg-1 X min-1) resulted in similar rises in arterial pressure. Heart rate fell greatly in the WKY but not in the SHR. Withdrawal of the PE infusion resulted in moderate decreases in blood pressure and increases in heart rate; these responses were similar in SHR and WKY. At 5 h after PE withdrawal, blood pressure and heart rate returned to basal values. In contrast, withdrawal of the AVP infusion was associated with greater falls in blood pressure and rises in heart rate. Blood pressure and heart rate in both the SHR and the WKY at 5 h after AVP were significantly different from their respective basal values. The effects of AVP withdrawal on either blood pressure or heart rate were significantly greater in the SHR than in the WKY. At 5 h after the withdrawal of AVP, blood pressure in the SHR was reduced to normotensive levels. These results suggest that the withdrawal effect was specific to AVP, was more marked in the SHR, and might not result from only the rise in blood pressure seen during the intravenous infusion of the pressor agent.

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