Alterations in aortic vascular reactivity to angiotensin 1–7 in 17-β-estradiol-treated female SD rats

2006 ◽  
Vol 133 (1-3) ◽  
pp. 62-67 ◽  
Author(s):  
Justin L. Grobe ◽  
Michael J. Katovich
Keyword(s):  
Vascular Reactivity ◽  
Sd Rats ◽  
Aortic Vascular Reactivity

In Vitro Alteration of Aortic Vascular Reactivity in Hypertension Induced by ChronicNG-Nitro-l-Arginine Methyl Ester

Hypertension ◽  
1996 ◽  
Vol 28 (3) ◽  
pp. 361-366 ◽  
Author(s):  
Daniel Henrion ◽  
Fiona J. Dowell ◽  
Bernard I. Levy ◽  
Jean-Baptiste Michel
Keyword(s):  
Methyl Ester ◽  
Vascular Reactivity ◽  
Aortic Vascular Reactivity

Effects of sex hormone levels on aortic vascular reactivity and variables associated with the metabolic syndrome in sucrose-fed female rats

2008 ◽  
Vol 86 (1-2) ◽  
pp. 25-35 ◽  
Author(s):  
Israel Pérez-Torres ◽  
Mohammed El Hafidi ◽  
Oscar Infante ◽  
Guadalupe Baños
Keyword(s):  
Metabolic Syndrome ◽  
Vascular Reactivity ◽  
Hormone Treatment ◽  
Female Rats ◽  
Serum Triglycerides ◽  
Intact Control ◽  
The Metabolic Syndrome ◽  
Sucrose Diet ◽  
Aortic Vascular Reactivity ◽  
Intact Rats

We studied the effect of varying levels of sex hormones, induced by ovariectomy and administration of testosterone or estradiol, on aortic reactivity in female rats with metabolic syndrome (MS) induced by a sucrose diet. Vasoreactivity of aortic rings, blood pressure, intra-abdominal fat, serum triglycerides, nitrates and nitrites, and TBARS were evaluated. Intact MS and ovariectomized MS had higher BP than intact control (C) and ovariectomized C, respectively; estradiol administration decreased BP in ovariectomized MS but not in ovariectomized C. Triglycerides and fat were both higher in MS. Triglycerides were not modified by surgery or hormone treatment, but ovariectomy increased fat. When ovariectomy was combined with hormones, however, fat was reduced to the level of intact rats. Ovariectomy decreased, but hormones increased, serum nitrates and nitrites. Vasoconstriction was larger in intact MS and ovariectomized MS + testosterone aortas than in intact C and ovariectomized C + testosterone, respectively. Vasodilation was reduced in intact MS and ovariectomized MS + testosterone compared with intact C, ovariectomized C + testosterone, ovariectomized MS, and ovariectomized MS + estradiol. The results suggest endothelial dysfunction in intact MS and ovariectomized MS + testosterone, but protection by ovariectomy + estradiol in MS due to hormones. Indomethacin reduced all contractions, but the effect was greater in estradiol-treated rats. l-NAME increased contractility, more in the ovariectomized C and MS groups and less in the estradiol-treated groups.

scholarly journals The triterpenoid alpha, beta-amyrin prevents the impaired aortic vascular reactivity in high-fat diet-induced obese mice

2017 ◽  
Vol 390 (10) ◽  
pp. 1029-1039 ◽  
Author(s):  
Flávia Almeida Santos ◽  
Karine Maria Martins Bezerra Carvalho ◽  
Francisco José Batista-Lima ◽  
Paulo Iury Gomes Nunes ◽  
Ana Flávia Seraine Custódio Viana ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Vascular Reactivity ◽  
Obese Mice ◽  
High Fat ◽  
Alpha Beta ◽  
Aortic Vascular Reactivity

Altered aortic vascular reactivity in the unpredictable chronic mild stress model of depression in mice

2011 ◽  
Vol 103 (5) ◽  
pp. 540-546 ◽  
Author(s):  
Elsa Isingrini ◽  
Alexandre Surget ◽  
Catherine Belzung ◽  
Jean-Louis Freslon ◽  
Jefferson Frisbee ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Stress Model ◽  
Unpredictable Chronic Mild Stress ◽  
Aortic Vascular Reactivity

Exercise training alters aortic vascular reactivity in hypothyroid rats

1995 ◽  
Vol 268 (4) ◽  
pp. H1428-H1435 ◽  
Author(s):  
M. D. Delp ◽  
R. M. McAllister ◽  
M. H. Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Exercise Training ◽  
Vascular Reactivity ◽  
Peripheral Resistance ◽  
Abdominal Aortic ◽  
Vasoconstrictor Response ◽  
Agonist Concentration ◽  
Aortic Vascular Reactivity

Hypothyroidism induces a number of cardiovascular adaptations in rats, including decreases in blood flow to high-oxidative skeletal muscle and increases in total peripheral resistance. Conversely, exercise training results in elevations in blood flow to high-oxidative skeletal muscle and decreases in vascular resistance. The purpose of this study was to determine whether hypothyroidism induces changes in the vasomotor responses of arterial vessels and whether exercise training modifies these responses. Rats were divided into three groups, sedentary euthyroid (S-Eut), sedentary hypothyroid (S-Hypo), and exercise-trained hypothyroid (ET-Hypo). Responses to vasoactive compounds were examined in vitro using abdominal aortic rings. Maximal isometric contractile tension (g/mm2) evoked by KCl and norepinephrine (NE) were not different among groups. However, sensitivity to KCl [agonist concentration producing 50% of maximal vasoconstrictor response (EC50; in mM): S-Eut, 21.1 +/- 1.1; S-Hypo, 35.7 +/- 2.7; ET-Hypo, 43.8 +/- 2.0] and to NE [EC50 (in M): S-Eut, 4.0 x 10(-8) +/- 2.3 x 10(-8); S-Hypo, 8.3 x 10(-8) +/- 3.4 x 10(-8); ET-Hypo, 3.6 x 10(-7) +/- 1.1 x 10(-7)] was different among groups, and in the order S-Eut > S-Hypo > ET-Hypo. Maximal vasodilator responses induced by acetylcholine (10(-7) M NE preconstriction) were lower in rings from S-Hypo animals than those from S-Eut and ET-Hypo rats. Dilatory responses induced by sodium nitroprusside (SNP) with the same NE preconstriction were not different among groups. However, with a 10(-4) M NE preconstriction, maximal dilatory responses induced by SNP were lower in vessels from hypothyroid animals. Dilatory responses to forskolin (10(-4) M NE preconstriction) were not different among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary vascular reactivity in Fischer rats

1991 ◽  
Vol 70 (4) ◽  
pp. 1861-1866 ◽  
Author(s):  
L. S. He ◽  
S. W. Chang ◽  
N. F. Voelkel
Keyword(s):  
Salt Solution ◽  
Vascular Reactivity ◽  
Genetic Difference ◽  
Oxidant Stress ◽  
Ang Ii ◽  
Vascular Control ◽  
Sd Rats ◽  
Rat Lungs ◽  
Alveolar Hypoxia ◽  
Isolated Lungs

We previously reported that Fischer (F) rat lungs developed more extensive injury when challenged with oxidants than age-matched Sprague-Dawley (SD) rat lungs. We now describe a reduced pulmonary vascular response to alveolar hypoxia and angiotensin II (ANG II) in F compared with SD rats. The comparative studies were performed with isolated lungs perfused with salt solution or blood, catheter-implanted awake rats, and isolated main pulmonary arterial rings. Isolated lungs from F rats perfused with either blood or salt solution had reduced vasoconstriction in comparison with lungs from SD rats when exposed to alveolar hypoxia or challenged with ANG II. Instrumented awake F rats had a smaller mean increase in total pulmonary vascular resistance (PVR) than SD rats (35 vs. 94 mmHg.min.l-1, P less than 0.05) when challenged with 8% oxygen. The contractile response of isolated pulmonary artery but not thoracic aortic rings to KCl and ANG II was reduced in F compared with SD rats. In addition, F rats exposed to 4 wk of hypobaric hypoxia developed less pulmonary hypertension and right ventricular hypertrophy (when corrected for the hematocrit) than SD rats. We conclude that the oxidant stress-sensitive inbred F rat strain is characterized by a lung vascular bed that is relatively unresponsive to vasoconstricting stimuli. The mechanism underlying this genetic difference in lung vascular control remains to be defined.

Tributyltin chloride disrupts aortic vascular reactivity and increases reactive oxygen species production in female rats

2017 ◽  
Vol 24 (31) ◽  
pp. 24509-24520 ◽  
Author(s):  
Carolina Falcão Ximenes ◽  
Samya Mere Lima Rodrigues ◽  
Priscila Lang Podratz ◽  
Eduardo Merlo ◽  
Julia Fernandez Puñal de Araújo ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Production ◽  
Vascular Reactivity ◽  
Reactive Oxygen ◽  
Female Rats ◽  
Oxygen Species ◽  
Tributyltin Chloride ◽  
Species Production ◽  
Aortic Vascular Reactivity

Abstract W P358: SOD overexpression Accounts for the Neurovascular Protection in Rats Following Ischemic Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Maha Coucha ◽  
Weiguo Li ◽  
Mohammed Abdelsaid ◽  
Sherif Hafez ◽  
Susan C Fagan ◽  
...  
Keyword(s):  
Infarct Size ◽  
Vascular Reactivity ◽  
Ischemia Reperfusion ◽  
Experimental Studies ◽  
Neurological Deficits ◽  
Myogenic Response ◽  
Transgenic Rats ◽  
Stroke Outcomes ◽  
Sd Rats ◽  
Neurovascular Protection

Acute hyperglycemic stroke (AHS) is associated with poor stroke outcomes and functional recovery. We recently showed that myogenic response; the ability of blood vessels to maintain adequate blood flow despite changes in pressure; was impaired after AHS. Experimental studies showed that acute elevation of blood glucose at stroke onset enhances oxidative stress that impairs effective reperfusion. Copper/zinc-superoxide dismutase (SOD1), an antioxidant enzyme that catalyzes the dismutation of superoxide into oxygen and hydrogen peroxide, has been shown to be highly protective against ischemia/reperfusion injury (IRI). Yet, the mechanism by which SOD1 improves stroke outcomes is still unresolved. Hypothesis: SOD1 overexpression improves cerebral myogenic behavior leading to neurovascular protection after AHS Methods: Wild-type Sprague Dawley (SD) and human SOD1 transgenic rats (n=6-8) were subjected to 30 min middle cerebral artery occlusion (MCAO)/45 min or 24 hr reperfusion. Hyperglycemia was induced by intraperitoneal injection of 40 % glucose solution 10 min before procedure. Myogenic tone of isolated MCAs, infarct size, edema and neurological deficits were determined. Results: IRI impaired myogenic response of MCAs isolated from SD rats compared to sham (***p<0.001). Normoglycemic and hyperglycemic SOD1 rats maintained a well developed myogenic response after IRI. Infarct size and edema were significantly reduced in the SOD1 transgenic rats compared to SD rats (**p<0.01). SOD1 overexpression significantly improved beam walk score and grip strength deficit compared to SD rats (*p<0.05). Hyperglycemic SOD1 transgenic rats showed smaller infarct size and edema (**p<0.01) and experienced improved neurological behavior (*p<0.05) compared to hyperglycemic SD rats. Conclusions: We provide evidence that SOD1 overexpression preserves the myogenic behavior of MCAs achieving neurovascular protection in conditions associated with poor stroke outcomes. Further studies are required to unravel the exact mechanism by which SOD exerts its beneficial role on vascular reactivity, and to identify new therapeutic targets for stroke management.

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