Altered Vascular Reactivity in Isolated Aortic Rings from Potassium-adapted Wistar Rats

2006 ◽  
Vol 2 (2) ◽  
pp. 193-200 ◽  
Author(s):  
R.I. Ozolua ◽  
E.E.I. Omogbai . ◽  
A.B. Ebeigbe .
2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
A. C. Keller ◽  
L. A. Knaub ◽  
R. L. Scalzo ◽  
S. E. Hull ◽  
A. E. Johnston ◽  
...  

In the vasculature, sedentary behavior leads to endothelial abnormalities, resulting in elevated cardiovascular disease risk. Endothelial nitric oxide synthase (eNOS) aberrations characterize endothelial dysfunction; eNOS also regulates mitochondrial function. We hypothesized that sepiapterin (a precursor to eNOS cofactor tetrahydrobiopterin (BH4)) supplementation would improve endothelium-dependent vascular relaxation in sedentary animals via modulation of NOS function and mitochondrial activity. Sedentary male Wistar rats were fed ad libitum for a total of 10 weeks. Sepiapterin was administered in diet during the final 5 weeks. Intraperitoneal insulin and glucose tolerance tests (IP-ITT/IP-GTT) were conducted at baseline and endpoint. Aorta was assessed for vasoreactivity and mitochondrial respiration. Insulin tolerance, determined by IP-ITT, significantly improved in rats treated with sepiapterin (p<0.05, interaction of time and treatment). Acetylcholine- (ACh-) driven vasodilation was significantly greater in aorta from sepiapterin-treated rats as compared with control (76.4% versus 54.9% of phenylephrine contraction at 20 μM ACh, p<0.05). Sepiapterin treatment resulted in significantly elevated state 3 (9.00 oxygen pmol/sec∗mg versus 8.17 oxygen pmol/sec∗mg, p<0.05) and 4 (7.28 oxygen pmol/sec∗mg versus 5.86 oxygen pmol/sec∗mg, p<0.05) aortic mitochondrial respiration with significantly lower respiratory control ratio (p<0.05) during octanoylcarnitine-driven respiration. Vasodilation and insulin sensitivity were improved through targeting NOS via sepiapterin supplementation.


2007 ◽  
Vol 7 (S1) ◽  
Author(s):  
Angelina Zanesco ◽  
Camila de Moraes ◽  
AP Davel ◽  
LV Rossoni ◽  
Gilberto de Nucci ◽  
...  

2009 ◽  
pp. 917-920
Author(s):  
M Žaloudíková ◽  
M Vízek ◽  
J Herget

We investigated the influence of oxygenation of in vitro lung preparation on the pulmonary vascular reactivity. Small pulmonary vessels isolated from adult male Wistar rats exposed for 4 days to hypoxia (FiO2 = 0.1, group CH) were compared with those of normoxic controls (group N). The bath in the chamber of small vessel myograph was saturated with gas mixture containing either 21 % or 95 % of O2 with 5 % CO2 and we measured the reactions of vessels to acute hypoxic challenge with 0 % O2 or to PGF2α. We did not observe any difference of the contractile responses between both groups when the normoxic conditions were set in the bath. When the bath oxygenation was increased to 95 % O2, the contractions induced by hypoxic challenge and PGF2α decreased in chronically hypoxic rats and did not change in normoxic controls. We hypothesize that reduced reactivity of vessels from hypoxic rats in hyperoxia results from the effect of chronic hypoxia on Ca2+ signaling in the vascular smooth muscle, which is modulated by increased free radical production during the exposure to chronic hypoxia and further hyperoxia.


2006 ◽  
Vol 38 (Supplement) ◽  
pp. S3-S4
Author(s):  
Angelina Zanesco ◽  
Camila de Moraes ◽  
Mario Angelo Claudino ◽  
Carla Franco Penteado ◽  
Emerielle C. Vanzela ◽  
...  

Author(s):  
Ana Paula Davel ◽  
Gisele Kruger Couto ◽  
Camilla Ferreira Wenceslau ◽  
Emilia Cristina Peres ◽  
Fabiano Elias Xavier ◽  
...  

AbstractThe purpose of this study was to compare the effect of long-term ouabain treatment on the vascular reactivity and NaMale Wistar rats were treated with ouabain (~8.0 µg/day, subcutaneously) or vehicle for 5 and 20 weeks, and spontaneously hypertensive rats (SHRs) for 5 weeks. Vasoconstrictor response to phenylephrine (10The phenylephrine-induced contraction was reduced, whereas the relaxation to KCl was enhanced in the aorta of ouabain-treated Wistar rats and SHRs. In both strains, endothelial modulation of α-adrenergic response was enhanced, related to an increased NO and reduced COX-derived vasoconstrictor factor modulation. Aortas from 20-week ouabain-treated Wistar rats showed reduced COX-2 and enhanced eNOS protein expression. In SHRs, 5-week ouabain treatment reduced COX-2 and increased nNOS protein expression.The results suggest that long-term ouabain treatment reduces the α-adrenergic response of aorta from normotensive rats and SHRs, associated with an increase of NO synthesis, reduced COX-2-derived vasoconstrictor factors, and enhanced ouabain-sensitive Na


2017 ◽  
Vol 61 (1) ◽  
pp. 32-38
Author(s):  
Ioana-Cristina Coman ◽  
Horia Paunescu ◽  
Alina Cristina Stamate ◽  
Alina Popa Cherecheanu ◽  
Isabel Ghita ◽  
...  

Author(s):  
Igor Souza-Silva ◽  
Cristiane de Paula ◽  
Lucas Bolais-Ramos ◽  
Anderson Santos ◽  
Filipe da Silva ◽  
...  

Background and purpose: Bradykinin [BK-(1-9)] is an endogenous nonapeptide involved in multiple physiological and pathological processes. A long-held belief is that peptide fragments of BK-(1-9) are biologically inactive. Here, we have tested the biological activities of BK-(1-9) and two major peptide fragments in human and animal systems. Experimental Approach: Levels of BK peptides in male Wistar rat plasma were quantified by mass spectrometric methods. Nitric oxide was quantified in human, mouse and rat cells, and loaded with DAF-FM. We used aortic rings from adult male Wistar rats to test vascular reactivity. Changes in blood pressure and heart rate were measured in conscious adult male Wistar rats. Key results: Plasma levels of BK-(1-7) and BK-(1-5) in rats were increased following infusion of BK-(1-9). All tested peptides induced NO production in all cell types tested. However, unlike BK-(1-9), NO production elicited by BK-(1-7) or BK-(1-5) was not inhibited by B or B receptor antagonists. BK-(1-7) or BK-(1-5) also induced concentration-dependent vasorelaxation of aortic rings, without involving B or B receptors. In vivo, either intravenous or intra-arterial administration of BK-(1-7) or BK-(1-5) induced similar hypotension response. Conclusions and implications: BK-(1-7) and BK-(1-5) are endogenous peptides present in plasma. They are formed, at least partially, through the BK-(1-9) proteolysis. BK-related peptide fragments show biological activity, not mediated by B or B receptors. These BK-fragments could constitute new, active components of the kallikrein-kinin system.


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