scholarly journals Effects of Monosodium Glutamate-Induced Obesity in Spontaneously Hypertensive Rats vs. Wistar Kyoto Rats: Serum Leptin and Blood Flow to Brown Adipose Tissue.

2000 ◽  
Vol 23 (5) ◽  
pp. 503-510 ◽  
Author(s):  
Masanori IWASE ◽  
Kojiro ICHIKAWA ◽  
Kenji TASHIRO ◽  
Kenzo IINO ◽  
Noriyasu SHINOHARA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Spontaneously Hypertensive Rats ◽  
Monosodium Glutamate ◽  
Hypertensive Rats ◽  
Serum Leptin ◽  
Spontaneously Hypertensive ◽  
Brown Adipose ◽  
Wistar Kyoto

scholarly journals Mutant Wars2 Gene in Spontaneously Hypertensive Rats Impairs Brown Adipose Tissue Function and Predisposes to Visceral Obesity

2017 ◽  
pp. 917-924 ◽  
Author(s):  
M. PRAVENEC ◽  
V. ZÍDEK ◽  
V. LANDA ◽  
P. MLEJNEK ◽  
J. ŠILHAVÝ ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Glucose Metabolism ◽  
Brown Adipose Tissue ◽  
Quantitative Trait ◽  
Spontaneously Hypertensive Rats ◽  
Glucose Oxidation ◽  
Trna Synthetase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Brown Adipose

Brown adipose tissue (BAT) plays an important role in lipid and glucose metabolism in rodents and possibly also in humans. Identification of genes responsible for BAT function would shed light on underlying pathophysiological mechanisms of metabolic disturbances. Recent linkage analysis in the BXH/HXB recombinant inbred (RI) strains, derived from Brown Norway (BN) and spontaneously hypertensive rats (SHR), identified two closely linked quantitative trait loci (QTL) associated with glucose oxidation and glucose incorporation into BAT lipids in the vicinity of Wars2 (tryptophanyl tRNA synthetase 2 (mitochondrial)) gene on chromosome 2. The SHR harbors L53F WARS2 protein variant that was associated with reduced angiogenesis and Wars2 thus represents a prominent positional candidate gene. In the current study, we validated this candidate as a quantitative trait gene (QTG) using transgenic rescue experiment. SHR-Wars2 transgenic rats with wild type Wars2 gene when compared to SHR, showed more efficient mitochondrial proteosynthesis and increased mitochondrial respiration, which was associated with increased glucose oxidation and incorporation into BAT lipids, and with reduced weight of visceral fat. Correlation analyses in RI strains showed that increased activity of BAT was associated with amelioration of insulin resistance in muscle and white adipose tissue. In summary, these results demonstrate important role of Wars2 gene in regulating BAT function and consequently lipid and glucose metabolism.

scholarly journals Novel acute stressor effects on interscapular brown adipose tissue sympathetic inervation and UCP-1 content in chronically isolated and spontaneously hypertensive rats

2011 ◽  
Vol 63 (3) ◽  
pp. 589-596
Author(s):  
Iva Lakic ◽  
Tamara Drenca ◽  
Jelena Djordjevic ◽  
P. Vujovic ◽  
N. Jasnic ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Spontaneously Hypertensive Rats ◽  
Acute Stress ◽  
Uncoupling Protein ◽  
Stress Conditions ◽  
Hypertensive Rats ◽  
Interscapular Brown Adipose Tissue ◽  
Spontaneously Hypertensive ◽  
Brown Adipose

Interscapular brown adipose tissue (IBAT) is an energy storing organ involved in the maintenance of homeostasis in stress conditions when the balance of energy supplies is disturbed. The major regulator of IBAT activity is the sympathetic nervous system (SNS). Since genetic background is responsible for the individual differences in neuroendocrine stress responsivity, spontaneously hypertensive rats (SHR) that have a genetically increased general sympathetic output are a useful model for studying adaptive processes in stress conditions. Our aim was to test the effect of acute and/or chronic exposure to various stressors (thermal-cold, psychophysical-immobilization and psychosocial-isolation) on IBAT SNS and the metabolic activity in SHR, by measuring the number of monoamine-containing nerve endings and uncoupling protein-1 (UCP-1) content. The obtained results show that the IBAT SNS activity of unstressed SHR was stimulated by the administration of a single acute or chronic stressor and was independent of the duration or type of stressor, while chronic pre-stress of isolation suppressed further the SNS reaction to novel acute stress exposure. The IBAT UCP-1 content followed SNS changes, suggesting that this system is dominant in the regulation of IBAT metabolic rate 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.

scholarly journals Chemokine-like Receptor 1 in Brain of Spontaneously Hypertensive Rats Mediates Systemic Hypertension

2021 ◽  
Vol 22 (21) ◽  
pp. 11812
Author(s):  
Atsunori Yamamoto ◽  
Kosuke Otani ◽  
Muneyoshi Okada ◽  
Hideyuki Yamawaki
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Western Blotting ◽  
Spontaneously Hypertensive Rats ◽  
Biologically Active ◽  
Systemic Hypertension ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Peripheral Protein ◽  
Wistar Kyoto

Adipocytokine chemerin is a biologically active molecule secreted from adipose tissue. Chemerin elicits a variety of functions via chemokine-like receptor 1 (CMKLR1). The cardiovascular center in brain that regulates blood pressure (BP) is involved in pathophysiology of systemic hypertension. Thus, we explored the roles of brain chemerin/CMKLR1 on regulation of BP in spontaneously hypertensive rats (SHR). For this aim, we examined effects of intracerebroventricular (i.c.v.) injection of CMKLR1 small interfering (si)RNA on both systemic BP as measured by tail cuff system and protein expression in paraventricular nucleus (PVN) of SHR as determined by Western blotting. We also examined both central and peripheral protein expression of chemerin by Western blotting. Systolic BP of SHR but not normotensive Wistar Kyoto rats (WKY) was decreased by CMKLR1 siRNA. The decrease of BP by CMKLR1 siRNA persisted for 3 days. Protein expression of CMKLR1 in PVN of SHR tended to be increased compared with WKY, which was suppressed by CMKLR1 siRNA. Protein expression of chemerin in brain, peripheral plasma, and adipose tissue was not different between WKY and SHR. In summary, we for the first time revealed that the increased protein expression of CMKLR1 in PVN is at least partly responsible for systemic hypertension in SHR.

Cerebral artery responses to pressure and flow in uremic hypertensive and spontaneously hypertensive rats

2003 ◽  
Vol 284 (4) ◽  
pp. H1212-H1216 ◽  
Author(s):  
D. I. New ◽  
A. M. S. Chesser ◽  
R. C. Thuraisingham ◽  
M. M. Yaqoob
Keyword(s):  
Blood Flow ◽  
Cerebral Artery ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Hypertensive Rats ◽  
Independent Manner ◽  
Spontaneously Hypertensive ◽  
Cerebral Blood Flow Autoregulation ◽  
Wistar Kyoto ◽  
Normotensive Control

Impaired cerebral blood flow autoregulation is seen in uremic hypertension, whereas in nonuremic hypertension autoregulation is shifted toward higher perfusion pressure. The cerebral artery constricts in response to a rise in either lumen pressure or flow; we examined these responses in isolated middle cerebral artery segments from uremic Wistar-Kyoto rats (WKYU), normotensive control rats (WKYC), and spontaneously hypertensive rats (SHR). Pressure-induced (myogenic) constriction developed at 100 mmHg; lumen flow was then increased in steps from 0 to 98 μl/min. Some vessels were studied after endothelium ablation. Myogenic constriction was significantly lower in WKYU (28 ± 2.9%) compared with both WKYC (39 ± 2.5%, P = 0.035) and SHR (40 ± 3.1%, P = 0.018). Flow caused constriction of arteries from all groups in an endothelium-independent manner. The response to flow was similar in WKYU and WKYC, whereas SHR displayed increased constriction compared with WKYU ( P < 0.001) and WKYC ( P < 0.001). We conclude that cerebral myogenic constriction is decreased in WKYU, whereas flow-induced constriction is enhanced in SHR.

Resetting of renal blood flow autoregulation in spontaneously hypertensive rats

1987 ◽  
Vol 252 (3) ◽  
pp. F480-F486 ◽  
Author(s):  
B. M. Iversen ◽  
I. Sekse ◽  
J. Ofstad
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Spontaneously Hypertensive Rats ◽  
Lower Pressure ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Pressure Limit ◽  
Wistar Kyoto ◽  
Renal Vascular ◽  
Renal Blood Flow Autoregulation

Renal blood flow (RBF) autoregulation was examined in untreated 10- and 40-wk-old spontaneously hypertensive rats (SHR) [mean arterial pressure (MAP) 125 +/- 4 and 167 +/- 7 mmHg] and in captopril-treated (7 days) 10- and 40-wk-old SHR (88 +/- 7 and 112 +/- 5 mmHg). Age-matched Wistar-Kyoto rats (WKY) were used as controls (MAP 91 +/- 3 and 104 +/- 2 mmHg). The study was carried out in rats with and without acute uninephrectomy. In 10-wk-old acutely uninephrectomized animals, the lower pressure limit of autoregulation was 78 +/- 4 mmHg in WKY, 102 +/- 5 mmHg in SHR (P less than 0.02), and 78 +/- 7 mmHg in captopril-treated SHR (P greater than 0.10). The renal vascular resistance (RVR) was significantly elevated at the lower pressure limit of RBF autoregulation in untreated SHR (P less than 0.02) but became normal after treatment (P greater than 0.10). Neither uninephrectomy nor variation of RBF between different batches seemed to influence the lower pressure limit of RBF autoregulation. In 40-wk-old acutely nephrectomized animals, the lower pressure limit of RBF autoregulation in WKY was 85 +/- 4 mmHg, 128 +/- 3 mmHg in SHR (P less than 0.001), and 101 +/- 5 mmHg in captopril-treated SHR (P less than 0.01). RVR at the lower pressure limit was increased in untreated SHR (P less than 0.01), but fell to normal values during captopril treatment. Neither the uninephrectomy nor variation of RBF between different batches of rats seemed to influence the lower pressure limit of RBF autoregulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Impaired hemodynamics and endothelial vasomotor function via endoperoxide-mediated vasoconstriction in the carotid artery of spontaneously hypertensive rats

2009 ◽  
Vol 296 (4) ◽  
pp. H1038-H1047 ◽  
Author(s):  
Steven G. Denniss ◽  
James W. E. Rush
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Spontaneously Hypertensive Rats ◽  
Contractile Activity ◽  
Body Wave ◽  
Large Artery ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Vasomotor Function ◽  
Wistar Kyoto

The fact that endothelium removal increases diameter and compliance in the common carotid artery (CCA) of spontaneously hypertensive rats (SHR) and that improving CCA endothelium-dependent vasorelaxation has been shown to normalize a reduced systolic blood flow through the SHR CCA compared with normotensive Wistar-Kyoto rats (WKY) suggests that endothelial vasomotor dysfunction may be linked to altered large artery hemodynamics in hypertension. The experiments herein were designed to further investigate WKY and SHR CCA hemodynamics and endothelium-dependent vasomotor functions. It was hypothesized that CCA blood flow and conductance would be reduced throughout the cardiac cycle in SHR and that endothelium-dependent contractile activity would impair SHR CCA vasorelaxation. We report that mean, maximal systolic, and diastolic blood flow was reduced in SHR vs. WKY CCA, as was vascular conductance. Pressure was augmented in SHR CCA and accompanied by late systolic flow augmentation so that total flow during systole was indeed no different between strains, possibly explained by earlier lower body wave reflection. While ACh stimulation in isolated precontracted WKY CCA caused a robust nitric oxide (NO)-mediated vasorelaxation, endothelium-dependent, cyclooxygenase (COX)-mediated contractile activity stimulated by high ACh concentration impaired NO- and non-NO/non-COX-mediated vasorelaxation in precontracted SHR CCA. In quiescent CCA, this endothelium-dependent contractile response was COX-1 and thromboxane-prostanoid receptor mediated and modulated by the availability of NO. These data collectively suggest that endothelium-dependent, COX-mediated endoperoxide signaling in the CCA of SHR may elicit vasoconstriction, which could shift the mechanical properties of this conduit artery and contribute to reduced CCA blood flow in vivo.

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