Vascular reactivity and flow-pressure curve in isolated kidneys from rats with N-nitro-L-arginine methyl ester-induced hypertension

1996 ◽  
Vol 14 (3) ◽  
pp. 373-379 ◽  
Author(s):  
F??lix Vargas ◽  
Antonio Osuna ◽  
Antonio Fern??ndez-Rivas
Keyword(s):  
Methyl Ester ◽  
Vascular Reactivity ◽  
Pressure Curve ◽  
Induced Hypertension ◽  
Flow Pressure ◽  
Isolated Kidneys

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

Vascular and Antioxidant Effects of an Aqueous Mentha cordifolia Extract in Experimental NG-Nitro-L-arginine Methyl Ester-Induced Hypertension

2014 ◽  
Vol 69 (1-2) ◽  
pp. 35-45 ◽  
Author(s):  
Poungrat Pakdeechote ◽  
Parichat Prachaney ◽  
Warinee Berkban ◽  
Upa Kukongviriyapan ◽  
Veerapol Kukongviriyapan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Methyl Ester ◽  
Thoracic Aorta ◽  
Wall Thickness ◽  
Vascular Remodeling ◽  
Oxidative Stress Markers ◽  
Sectional Area ◽  
Cross Sectional ◽  
Stress Markers ◽  
Induced Hypertension

The effect of an aqueous Mentha cordifolia (MC) extract on the haemodynamic status, vascular remodeling, function, and oxidative status in NG-nitro-L-arginine methyl ester (L-NAME)-induced hypertension was investigated. Male Sprague-Dawley rats were given L-NAME [50 mg/(kg body weight (BW) d)] in their drinking water for 5 weeks and were treated by intragastric administration with the MC extract [200 mg/(kgBWd)] for 2 consecutive weeks. Quercetin [25 mg/(kg BW d)] was used as a positive control. The effects of the MC extract on the haemodynamic status, thoracic aortic wall thickness, and oxidative stress markers were determined, and the vasorelaxant activity of the MC extract was tested in isolated mesenteric vascular beds in rats. Significant increases in the mean arterial pressure (MAP), heart rate (HR), hind limb vascular resistance (HVR), wall thickness, and cross-sectional area of the thoracic aorta, as well as oxidative stress markers were found in the LNAME- treated group compared to the control (P<0.05). MAP, HVR, wall thickness, cross-sectional area of the thoracic aorta, plasma malondialdehyde (MDA), and vascular superoxide anion production were significantly reduced in L-NAME hypersensitive rats treated with the MC extract or quercetin. Furthermore, the MC extract induced vasorelaxation in the pre-constricted mesenteric vascular bed with intact and denuded endothelium of normotensive and hypertensive rats. Our results suggest that the MC extract exhibits an antihypertensive effect via its antioxidant capacity, vasodilator property, and reduced vascular remodeling.

Effect of magnesium supplementation on blood pressure and vascular reactivity in nitric oxide synthase inhibition-induced hypertension model

2015 ◽  
Vol 37 (8) ◽  
pp. 633-642 ◽  
Author(s):  
Filiz Basralı ◽  
Günnur Koçer ◽  
Pınar Ülker Karadamar ◽  
Seher Nasırcılar Ülker ◽  
Leyla Satı ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Vascular Reactivity ◽  
Magnesium Supplementation ◽  
Induced Hypertension ◽  
Oxide Synthase

Effects of exercise training on the vascular reactivity of the whole kidney circulation in rabbits

2004 ◽  
Vol 97 (2) ◽  
pp. 683-688 ◽  
Author(s):  
Roger De Moraes ◽  
Giovanni Gioseffi ◽  
Antonio C. L. Nóbrega ◽  
Eduardo Tibiriçá
Keyword(s):  
Exercise Training ◽  
Vascular Reactivity ◽  
Perfusion Pressure ◽  
Rabbit Kidney ◽  
Constant Flow ◽  
Renal Circulation ◽  
New Zealand White Rabbits ◽  
Vascular Beds ◽  
Renal Vascular ◽  
Isolated Kidneys

Exercise training is known to improve vasodilating mechanisms mediated by endothelium-dependent relaxing factors in the cardiac and skeletal muscle vascular beds. However, the effects of exercise training on visceral vascular reactivity, including the renal circulation, are still unclear. We used the experimental model of the isolated perfused rabbit kidney, which involves both the renal macro- and microcirculation, to test the hypothesis that exercise training improves vasodilator mechanisms in the entire renal circulation. New Zealand White rabbits were pen confined (Sed; n = 24) or treadmill trained (0% grade) for 5 days/wk at a speed of 18 m/min during 60 min over a 12-wk period (ExT; n = 24). Kidneys isolated from Sed and ExT rabbits were continuously perfused in a nonrecirculating system under conditions of constant flow and precontracted with norepinephrine (NE). We assessed the effects of exercise training on renal vascular reactivity using endothelial-dependent [acetylcholine (ACh) and bradykinin (BK)] and -independent [sodium nitroprusside (SNP)] vasodilators. ACh induced marked and dose-related vasodilator responses in kidneys from Sed rabbits, the reduction in perfusion pressure reaching 41 ± 8% ( n = 6; P < 0.05). In the kidneys from ExT rabbits, vasodilation induced by ACh was significantly enhanced to 54 ± 6% ( n = 6; P < 0.05). In contrast, BK-induced renal vasodilation was not enhanced by training [19 ± 8 and 13 ± 4% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P > 0.05)]. Continuous perfusion of isolated kidneys from ExT animals with Nω-nitro-l-arginine methyl ester (l-NAME; 300 μM), an inhibitor of nitric oxide (NO) biosynthesis, completely blunted the additional vasodilation elicited by ACh [reduction in perfusion pressure of 54 ± 6 and 38 ± 5% for ExT and l-NAME + ExT, respectively ( n = 6; P < 0.05)]. On the other hand, l-NAME infusion did not affect ACh-induced vasodilation in Sed animals. Exercise training also increased renal vasodilation induced by SNP [36 ± 7 and 45 ± 10% reduction in perfusion pressure for Sed and ExT rabbits, respectively ( n = 6; P < 0.05)]. It is concluded that exercise training alters the rabbit kidney vascular reactivity, enhancing endothelium-dependent and -independent renal vasodilation. This effect seems to be related not only to an increased bioavailability of NO but also to the enhanced responsiveness of the renal vascular smooth muscle to NO.

scholarly journals Antihypertensive effect of methanol leaf extract of Anacardium occidentale against L‐Nitro Arginine Methyl Ester (L‐NAME)‐induced hypertension in male Wistar rats

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Adebowale Benard Saba ◽  
Adedeji Kolawole Adebayo ◽  
Ademola Adetokunbo Oyagbemi ◽  
Temidayo Olutayo Omobowale ◽  
Olufunke Eunice Ola-Davies ◽  
...  
Keyword(s):  
Methyl Ester ◽  
Wistar Rats ◽  
Leaf Extract ◽  
Antihypertensive Effect ◽  
Anacardium Occidentale ◽  
Induced Hypertension ◽  
Male Wistar Rats

Study on Numerical Simulation and Performance of the Secondary Throttle Choke Used in the Oil Field

2013 ◽  
Vol 712-715 ◽  
pp. 1201-1204
Author(s):  
Hai Feng Zhao ◽  
Yan Xu
Keyword(s):  
Numerical Simulation ◽  
Pressure Change ◽  
Simulation Method ◽  
Differential Pressure ◽  
Oil Field ◽  
Pressure Curve ◽  
Flow Pressure ◽  
Flow Changes ◽  
And Performance ◽  
Main Factor

The numerical simulation method is adopted to calculate the flow field of the secondary throttle choke used in the oil field. The relationships among the flow of the secondary throttle choke, differential pressure and diameters are studied. The results of numerical simulation coincide with the experiment values, which verify that the method is correct. The results show that the flow increases with the increasing of differential pressure of the throttle choke at both ends, but the increment of the flow gradually decreases. The structure could maintain the flow not to change basically when differential pressure change in a certain scope. When the throttle diameter turns out to be small, the flow decreases, and flow-pressure curve gradually becomes aclinic. Compared with the first-class throttle diameter, the second-class throttle diameter is the main factor which effects flow changes.

Effect of Viscum articulatum Burm. (Loranthaceae) in Nω-nitro-l-arginine methyl ester induced hypertension and renal dysfunction

2012 ◽  
Vol 142 (2) ◽  
pp. 467-473 ◽  
Author(s):  
Sagar S. Bachhav ◽  
Mukesh S. Bhutada ◽  
Savita D. Patil ◽  
Bhavana Baser ◽  
Kishor B. Chaudhari
Keyword(s):  
Methyl Ester ◽  
Renal Dysfunction ◽  
Induced Hypertension

Androgen-receptor defect abolishes sex differences in nitric oxide and reactivity to vasopressin in rat aorta

2001 ◽  
Vol 91 (6) ◽  
pp. 2602-2610 ◽  
Author(s):  
John N. Stallone ◽  
Ronald L. Salisbury ◽  
Clifford T. Fulton
Keyword(s):  
Nitric Oxide ◽  
Androgen Receptor ◽  
Methyl Ester ◽  
Thoracic Aorta ◽  
Vascular Reactivity ◽  
Rat Aorta ◽  
Maximal Response ◽  
Maximal Contraction ◽  
Rat Thoracic Aorta ◽  
Recessive Defect

Contractions of rat thoracic aorta to vasopressin (VP) are threefold higher in females (F) than in males (M), primarily because nitric oxide (NO) attenuation of contraction is greater in M. To determine the role of the androgen receptor (AR) in this mechanism, vascular reactivity to VP was examined in thoracic aorta of the testicular-feminized male (Tfm) rat, which has an X-linked, recessive defect in AR function in affected M. Maximal contraction of normal aortas to VP was fourfold higher in F (4,128 ± 291 mg/mg ring wt) than in M (971 ± 133 mg); maximal response of Tfm (3,967 ± 253 mg) was similar to that of normal F. N G-nitro-l-arginine methyl ester increased maximal response to VP threefold in M but had no effect in F or Tfm. In contrast, maximal contraction of normal aortas to phenylephrine was 43% higher in M (4,011 ± 179 mg) than in F (2,809 ± 78 mg); maximal response of Tfm (2,716 ± 126 mg) was similar to that of normal F. N G-nitro-l-arginine methyl ester increased maximal response to phenylephrine by >50% in F and Tfm but had no effect in M. Maximal contractile response to 80 mM KCl did not differ among M, F, or Tfm. Thus androgens and normal vascular AR function are important in the greater NO-mediated attenuation of reactivity to VP in M than in F rat aorta, which may involve specific modulation of endothelial VP signal transduction pathways and NO release by androgens. These data also establish the importance of the Tfm rat as a model to study the effects of androgens on cardiovascular function.

TNF-α enhances contraction and inhibits endothelial NO-cGMP relaxation in systemic vessels of pregnant rats

2002 ◽  
Vol 283 (1) ◽  
pp. R130-R143 ◽  
Author(s):  
Jena B. Giardina ◽  
Gachavis M. Green ◽  
Kathy L. Cockrell ◽  
Joey P. Granger ◽  
Raouf A. Khalil
Keyword(s):  
Vascular Reactivity ◽  
Pregnancy Induced Hypertension ◽  
Vascular Relaxation ◽  
Sprague Dawley ◽  
Direct Role ◽  
Pregnant Rats ◽  
No Donor ◽  
Vascular Contraction ◽  
Tnf Α ◽  
Induced Hypertension

Tumor necrosis factor-α (TNF-α) is elevated in the plasma of preeclamptic women and may have a role in pregnancy-induced hypertension. However, whether the hemodynamic effects of TNF-α reflect the direct effects on vascular reactivity is unclear. We tested the hypothesis that TNF-α impairs endothelium-dependent relaxation and enhances vascular contraction in systemic vessels of pregnant rats. We measured isometric contraction in aortic strips isolated from virgin and pregnant Sprague-Dawley rats (nontreated vs. treated for 2 h with 10–1,000 pg/ml TNF-α). In endothelium-intact vascular strips, TNF-α caused greater enhancement of phenylephrine (Phe) contraction in pregnant than virgin rats. TNF-α caused significant inhibition of ACh- and bradykinin-induced vascular relaxation and nitrite/nitrate production that were more prominent in pregnant than virgin rats. N G-nitro-l-arginine methyl ester [l-NAME, 100 μM, an inhibitor of nitric oxide (NO) synthase] or 1H-[1,2,4]oxadiazolo[4,3]-quinoxalin-1-one (ODQ, 1 μM, an inhibitor of cGMP production in smooth muscle) inhibited ACh relaxation and enhanced Phe contraction in nontreated but to a lesser extent in TNF-α-treated vessels, particularly those of pregnant rats. Endothelium removal enhanced Phe contraction in nontreated but not TNF-α-treated vessels, especially those of pregnant rats. Relaxation of Phe contraction with the NO donor sodium nitroprusside was not different between nontreated and TNF-α-treated vessels. Thus TNF-α enhances vascular contraction and inhibits endothelium-dependent NO-cGMP-mediated vascular relaxation in systemic vessels, particularly those of pregnant rats. The results support a direct role for TNF-α as a possible mediator of increased vascular resistance associated with pregnancy-induced hypertension.

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