scholarly journals Nobiletin, A Citrus Flavonoid, Suppresses SPC-induced Abnormal Vascular Contraction

2021 ◽  
Vol 70 (1) ◽  
pp. 29-35
Author(s):  
Kenji MIYANARI
Keyword(s):  
2003 ◽  
Vol 285 (3) ◽  
pp. R542-R551 ◽  
Author(s):  
Jason A. Payne ◽  
Jane F. Reckelhoff ◽  
Raouf A. Khalil

The incidence of hypertension increases during the late stages of aging; however, the vascular mechanisms involved are unclear. We investigated whether the late stages of aging are associated with impaired nitric oxide (NO)-mediated vascular relaxation and enhanced vascular contraction and whether oxidative stress plays a role in the age-related vascular changes. Aging (16 mo) male spontaneously hypertensive rats (SHR) nontreated or treated for 8 mo with the antioxidant tempol (1 mM in drinking water) or vitamin E (E; 5,000 IU/kg chow) and vitamin C (C; 100 mg · kg-1· day-1in drinking water) and adult (12 wk) male SHR were used. After the arterial pressure was measured, aortic strips were isolated from the rats for measurement of isometric contraction. The arterial pressure and phenylephrine (Phe)-induced vascular contraction were enhanced, and the ACh-induced vascular relaxation and nitrite/nitrate production were reduced in aging compared with adult rats. In aging rats, the arterial pressure was nontreated (188 ± 4), tempol-treated (161 ± 6), and E + C-treated (187 ± 1 mmHg). Phe (10-5M) caused an increase in active stress in nontreated aging rats (14.3 ± 1.0) that was significantly ( P < 0.05) reduced in tempol-treated (9.0 ± 0.7) and E + C-treated rats (9.8 ± 0.6 × 104N/m2). ACh produced a small relaxation of Phe contraction in nontreated aging rats that was enhanced ( P < 0.05) in tempol- and E + C-treated rats. l-NAME (10-4M), inhibitor of NO synthase, or ODQ (10-5M), inhibitor of cGMP production in smooth muscle, inhibited ACh relaxation and enhanced Phe contraction in tempol- and E + C-treated but not the nontreated aging rats. ACh-induced vascular nitrite/nitrate production was not different in nontreated, tempol- and E + C-treated aging rats. Relaxation of Phe contraction with sodium nitroprusside, an exogenous NO donor, was smaller in aging than adult rats but was not different between nontreated, tempol- and E + C-treated aging rats. Thus, during the late stages of aging in SHR rats, an age-related inhibition of a vascular relaxation pathway involving not only NO production by endothelial cells but also the bioavailability of NO and the smooth muscle response to NO is partially reversed during chronic treatment with the antioxidants tempol and vitamins E and C. The data suggest a role for oxidative stress in the reduction of vascular relaxation and thereby the promotion of vascular contraction and hypertension during the late stages of aging.


2018 ◽  
Vol 19 (12) ◽  
pp. 3942 ◽  
Author(s):  
Ali Mahdi ◽  
Tong Jiao ◽  
Yahor Tratsiakovich ◽  
Jiangning Yang ◽  
Claes-Göran Östenson ◽  
...  

Purinergic signaling may be altered in diabetes accounting for endothelial dysfunction. Uridine adenosine tetraphosphate (Up4A), a novel dinucleotide substance, regulates vascular function via both purinergic P1 and P2 receptors (PR). Up4A enhances vascular contraction in isolated arteries of diabetic rats likely through P2R. However, the precise involvement of PRs in endothelial dysfunction and the vasoconstrictor response to Up4A in diabetes has not been fully elucidated. We tested whether inhibition of PRs improved endothelial function and attenuated Up4A-mediated vascular contraction using both aortas and mesenteric arteries of type 2 diabetic (T2D) Goto Kakizaki (GK) rats vs. control Wistar (WT) rats. Endothelium-dependent (EDR) but not endothelium-independent relaxation was significantly impaired in both aortas and mesenteric arteries from GK vs. WT rats. Non-selective inhibition of P1R or P2R significantly improved EDR in aortas but not mesenteric arteries from GK rats. Inhibition of A1R, P2X7R, or P2Y6R significantly improved EDR in aortas. Vasoconstrictor response to Up4A was enhanced in aortas but not mesenteric arteries of GK vs. WT rats via involvement of A1R and P2X7R but not P2Y6R. Depletion of major endothelial component nitric oxide enhanced Up4A-induced aortic contraction to a similar extent between WT and GK rats. No significant differences in protein levels of A1R, P2X7R, and P2Y6R in aortas from GK and WT rats were observed. These data suggest that altered PR sensitivity accounts for endothelial dysfunction in aortas in diabetes. Modulating PRs may represent a potential therapy for improving endothelial function.


2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Amanda Oliveira ◽  
Fernanda Priviero ◽  
R. Webb ◽  
Kenia Nunes
Keyword(s):  

2003 ◽  
Vol 138 (5) ◽  
pp. 745-750 ◽  
Author(s):  
Rachel L Matz ◽  
Maria Alvarez de Sotomayor ◽  
Christa Schott ◽  
Ramaroson Andriantsitohaina

Author(s):  
Dr Mark Harrison

4.1 General principles, 512 4.2 Specific tissues, 513 • 5 stages: ▪ Haemostasis ▪ Inflammation ▪ Reconstruction ▪ Epithelialization ▪ Maturation • Primary haemostasis - local vascular contraction and platelet plug formation • Activation of the clotting cascade • Prepares the wound for healing...


2016 ◽  
Vol 12 (6) ◽  
pp. 587-596 ◽  
Author(s):  
Mecit Orhan Uludag ◽  
Ebru Hicdurmaz ◽  
Sevtap Han ◽  
Suzan Emel Usanmaz ◽  
Nurettin Abacioglu ◽  
...  

2003 ◽  
Vol 59 (1) ◽  
pp. 82-87 ◽  
Author(s):  
Anna-Karin Wihlborg ◽  
Johnny Slätt ◽  
Xiangyang Sun ◽  
Xiao-He Zhao ◽  
Jan Bergman ◽  
...  

1994 ◽  
Vol 64 ◽  
pp. 249
Author(s):  
Taijiro Enoki ◽  
Shigeo Kobayashi ◽  
Soichi Miwa ◽  
Tomoh Masaki

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