Cardiac and vascular effects of nitric oxide synthase inhibition in lipopolysaccharide-treated rats

2000 ◽  
Vol 406 (2) ◽  
pp. 257-264 ◽  
Author(s):  
Qixian Shan ◽  
Jean-Pierre Bourreau
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Vascular Effects ◽  
Oxide Synthase

Vascular effects of LPS in mice deficient in expression of the gene for inducible nitric oxide synthase

1998 ◽  
Vol 275 (2) ◽  
pp. H416-H421 ◽  
Author(s):  
Carol A. Gunnett ◽  
Yi Chu ◽  
Donald D. Heistad ◽  
Angela Loihl ◽  
Frank M. Faraci
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Carotid Arteries ◽  
Inos Mrna ◽  
Wild Type ◽  
Vascular Effects ◽  
Contractile Responses ◽  
Vasomotor Function ◽  
Oxide Synthase ◽  
Deficient Mice

The inducible isoform of nitric oxide synthase (iNOS) is expressed after systemic administration of lipopolysaccharide (LPS). The importance of expression of iNOS in blood vessels is poorly defined. Because nitric oxide from iNOS may alter vasomotor function, we examined effects of LPS on vasomotor function in carotid arteries from iNOS-deficient mice. We studied contraction of the carotid artery from wild-type and iNOS-deficient mice in vitro 12 h after injection of LPS (20 mg/kg ip). Contractile responses to PGF2α (3–30 μM) and thromboxane A2 analog (U-46619; 3–100 nM) were evaluated using vascular rings from mice treated with vehicle or LPS. Maximum force of contraction generated by rings in response to PGF2α was 0.39 ± 0.02 and 0.25 ± 0.01 (SE) g ( n = 14) in vehicle and LPS-treated wild-type mice, respectively ( P < 0.001 vs. vehicle). Thus LPS reduced constrictor responses in wild-type mice. Thiocitrulline and aminoguanidine (inhibitors of iNOS) improved contractile responses from LPS-treated wild-type vessels. Indomethacin also improved constrictor responses in arteries from wild-type mice injected with LPS. In contrast, contraction of the carotid arteries in response to PGF2α and U-46619 was not impaired in LPS-treated iNOS-deficient mice, and contraction was not altered by inhibitors of iNOS. Expression of iNOS mRNA was confirmed using RT-PCR in carotid arteries from wild-type mice after injection of LPS but not vehicle. PCR products for iNOS were not observed in iNOS-deficient mice. These findings provide the first direct evidence that iNOS mediates impairment of vascular contraction after treatment with LPS.

scholarly journals Influence of hypertension on nitric oxide synthase expression and vascular effects of lipopolysaccharide in rat mesenteric arteries

2000 ◽  
Vol 131 (2) ◽  
pp. 185-194 ◽  
Author(s):  
Ana M Briones ◽  
María J Alonso ◽  
Jesús Marín ◽  
Gloria Balfagón ◽  
Mercedes Salaices
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mesenteric Arteries ◽  
Vascular Effects ◽  
Oxide Synthase

scholarly journals Intracoronary Genistein Acutely Increases Coronary Blood Flow in Anesthetized Pigs through β-Adrenergic Mediated Nitric Oxide Release and Estrogenic Receptors

Endocrinology ◽  
2008 ◽  
Vol 149 (5) ◽  
pp. 2678-2687 ◽  
Author(s):  
Elena Grossini ◽  
Claudio Molinari ◽  
David A. S. G. Mary ◽  
Francesca Uberti ◽  
Philippe Primo Caimmi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Coronary Blood Flow ◽  
Adrenergic Receptors ◽  
Primary Effect ◽  
No Production ◽  
Concomitant Treatment ◽  
Vascular Effects ◽  
Oxide Synthase

Various studies have suggested that the phytoestrogen genistein has beneficial cardioprotective and vascular effects. However, there has been scarce information regarding the primary effect of genistein on coronary blood flow and its mechanisms including estrogen receptors, autonomic nervous system, and nitric oxide (NO). The present study was planned to determine the primary effect of genistein on coronary blood flow and the mechanisms involved. In anesthetized pigs, changes in left anterior descending coronary artery caused by intracoronary infusion of genistein at constant heart rate and arterial pressure were assessed using ultrasound flowmeters. In 25 pigs, genistein infused at 0.075 mg/min increased coronary blood flow by about 16.3%. This response was graded in a further five pigs by increasing the infused dose of the genistein between 0.007 and 0.147 mg/min. In the 25 pigs, blockade of cholinergic receptors (iv atropine; five pigs) and α-adrenergic receptors (iv phentolamine; five pigs) did not abolish the coronary response to genistein, whose effects were prevented by blockade of β2-adrenergic receptors (iv butoxamine; five pigs), nitric oxide synthase (intracoronary Nω-nitro-l-arginine methyl ester; five pigs) and estrogenic receptors (ERs; ERα/ERβ; intracoronary fulvestrant; five pigs). In porcine aortic endothelial cells, genistein induced the phosphorylation of endothelial nitric oxide synthase and NO production through ERK 1/2, Akt, and p38 MAPK pathways, which was prevented by the concomitant treatment by butoxamine and fulvestrant. In conclusion, genistein primarily caused coronary vasodilation the mechanism of which involved ERα/ERβ and the release of NO through vasodilatory β2-adrenoreceptor effects.

scholarly journals Endothelial Metabolism of Angiotensin II to Angiotensin III, not Angiotensin (1–7), Augments the Vasorelaxation Response in Adrenal Cortical Arteries

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4768-4776 ◽  
Author(s):  
Phillip G. Kopf ◽  
William B. Campbell
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ang Ii ◽  
Peptide Fragments ◽  
Vascular Effects ◽  
Basal Tone ◽  
Angiotensin Iii ◽  
Adrenal Vasculature ◽  
Ang Iv ◽  
Oxide Synthase

Hyperaldosteronism is linked to the development and progression of several different cardiovascular diseases. Angiotensin (Ang) II increases aldosterone secretion and adrenal blood flow. Ang II peptide fragments are produced by various peptidases, and these Angs have diverse and vital physiologic roles. Due to the uncharacteristic vasorelaxation of adrenal arteries by Ang II, we tested the hypothesis that Ang II metabolism contributes to its relaxant activity in adrenal arteries. Metabolism of Angs by bovine adrenal cortical arteries and isolated bovine adrenal vascular cells was measured by liquid chromatography-mass spectrometry. The primary Ang metabolites of adrenal arteries are Ang III and Ang (1–7), with Ang IV produced to a lesser extent. Bovine microvascular endothelial cells produced a similar metabolic profile to adrenal arteries, whereas bovine adrenal artery smooth muscle cells exhibited less metabolism. In preconstricted adrenal arteries, Ang II caused relaxation in picomolar concentrations and constrictions at 10nM. Ang-converting enzyme 2 inhibition augmented this relaxation response, whereas aminopeptidase inhibition did not. Ang III was equipotent to Ang II in relaxing adrenal arteries. Ang IV did not cause relaxation. Nitric oxide synthase inhibition enhanced Ang II-induced constriction of adrenal arteries. Aminopeptidase inhibition increased the concentration range for Ang II-induced constriction of adrenal arteries. Ang III and Ang IV did not change the basal tone but caused constriction of adrenal arteries with nitric oxide synthase inhibition. These data indicate that Ang II metabolism modulates the vascular effects of Ang II in the adrenal vasculature.

scholarly journals Essential Role of Endothelial Nitric Oxide Synthase in Vascular Effects of Erythropoietin

Hypertension ◽  
2007 ◽  
Vol 49 (5) ◽  
pp. 1142-1148 ◽  
Author(s):  
Livius V. d’Uscio ◽  
Leslie A. Smith ◽  
Anantha V. Santhanam ◽  
Darcy Richardson ◽  
Karl A. Nath ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Essential Role ◽  
Vascular Effects ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

1996 ◽  
Vol 54 ◽  
pp. 786-787
Author(s):  
Chi-Ming Wei ◽  
Margarita Bracamonte ◽  
Shi-Wen Jiang ◽  
Richard C. Daly ◽  
Christopher G.A. McGregor ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Cardiac Tissues ◽  
Mammalian Tissues ◽  
End Stage Heart Failure ◽  
End Stage ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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