NO donors-relaxation is impaired in aorta from hypertensive rats due to a reduced involvement of K+ channels and sarcoplasmic reticulum Ca2+-ATPase

Bonaventura, Daniella; Lima, Renata Galvão de; Silva, Roberto Santana da; Bendhack, Lusiane Maria

doi:10.1016/j.lfs.2011.07.022

Cited by 21 publications

(12 citation statements)

References 50 publications

(58 reference statements)

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“…Vascular relaxation sensitivity to ODQ inhibition is an indicative of a predominant mechanism of heme site mediated activation of sGC, whereas resistance toward ODQ suggests the possible presence of alternative mechanisms of vasorelaxation. In the concentration of 1 lM, ODQ abolished the relaxation induced by TERPY [25] and 15-ANE [21] in 2K-1C aortas. These results differ from what is observed in SHR aortas, where the concentration-response curves to TERPY and SNP, are shifted to the right in the presence of ODQ (1 lM), but were not abolished (Fig.…”

Section: Discussionmentioning

confidence: 85%

Hypotensive and vasorelaxing effects of the new NO-donor [Ru(terpy)(bdq)NO+]3+ in spontaneously hypertensive rats

et al. 2012

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Drugs that release nitric oxide (NO) usually have limitations due to their harmful effects. Sodium nitroprusside (SNP) induces a rapid hypotension that leads to reflex tachycardia, which could be an undesirable effect in patients with heart disease, a common feature of hypertension. The nitrosyl ruthenium complex [Ru(terpy)(bdq)NO(+)](3+) (TERPY) is a NO donor that is less potent than SNP in denuded aortic rings. This study evaluated the hypotension and vasorelaxation induced by this NO donor in Wistar (W) and spontaneously hypertensive rats (SHR) and compared to the results obtained with SNP. Differently from the hypotension induced by SNP, the action of TERPY was slow, long lasting and it did not lead to reflex tachycardia in both groups. The hypotension induced by the NO-donors was more potent in SHR than in W. TERPY induced relaxation with similar efficacy to SNP, although its potency is lower in both strains. The relaxation induced by TERPY is similar in W and SHR, but SNP is more potent and efficient in SHR. The relaxation induced by TERPY is partially dependent on guanylate cyclase in SHR aorta. The NO released from the NO donors measured with DAF-2 DA by confocal microscopy shows that TERPY releases similar amounts of NO in W and SHR, while SNP releases more NO in SHR aortic rings.

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Section: Discussionmentioning

confidence: 85%

Hypotensive and vasorelaxing effects of the new NO-donor [Ru(terpy)(bdq)NO+]3+ in spontaneously hypertensive rats

et al. 2012

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“…Endothelial dysfunction involves decreased production or bioavailability of endogenous nitric oxide (NO) and it is associated with hypertension [1,2] as well as other cardiovascular diseases [3][4][5][6].…”

Section: Introdutionmentioning

confidence: 99%

In vitro Treatment with cis-[Ru(H-dcbpy-)2(Cl)(NO)] Improves the Endothelial Function in Aortic Rings with Endothelial Dysfunction

et al. 2015

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Purpose: The ruthenium complex cis-[Ru(H-dcbpy-)2(Cl)(NO)] (DCBPY) is a nitric oxide (NO) donor and studies suggested that the ruthenium compounds can inactivate O2-. The aim of this study is to test if DCBPY can revert and/or prevent the endothelial dysfunction. Methods: Normotensive (2K) and hypertensive (2K-1C) wistar rats were used. To vascular reactivity study, thoracic aortas were isolated, rings with intact endothelium were incubated with: DCBPY: 0.1; 1 and 10μM, DCBPY plus hydroxocobalin (NO scavenger) or tempol during 30 minutes, and concentration effect curves to acetylcholine were performed. The potency values (pD2) and maximum effect (ME) were analyzed. The O2- was generated using hypoxantine xantine oxidase and the reduction of cytochrome c, NO consumption by O2- and the effect in avoid NO consumption was measured. Results: In 2K-1C DCBPY at 0.1; 1 or 10μM improved the relaxation endothelium dependent induced by acetylcholine in aortic rings compared to control 2K-1C, and also improved ME. In rings from 2K incubation with DCBPY (0.1; 1.0 and 10 μM) did not change pD2 or ME. Incubation with 0.1 μM of DCBPY plus hydroxocobalamin did not modify the potency and ME in 2K-1C compared to DCBPY (0.1 μM). DCBPY and SOD inhibits the reduction of cytochrome c and inhibited the NO consumption by O2-, showing that O2- has been removed from the solution. Conclusion: Our results suggest that DCBPY at a lower concentration (0.1 µM) is not an NO generator, but can inactivate superoxide and improves the endothelial function. This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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“…However, vasodilation induced by these agents differs in the experimental models of hypertension. In renal hypertensive rats, TERPY-induced vasodilation is impaired when compared with 2-kidney sham-operated rats (Rodrigues et al, 2007Bonaventura et al, 2011). However, in spontaneously hypertensive rats it is not altered as compared with normotensive Wistar rats (Munhoz et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Mechanisms underlying the hypotensive and vasodilator effects of Ru(terpy)(bdq)NO]3+, a nitric oxide donor, differ between normotensive and spontaneously hypertensive rats

Potje

Munhoz

Perassa

et al. 2014

European Journal of Pharmacology

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NO donors-relaxation is impaired in aorta from hypertensive rats due to a reduced involvement of K+ channels and sarcoplasmic reticulum Ca2+-ATPase

Abstract: Taken together, our results provide evidences that in this model of hypertension, impaired K(+) channels activation by TERPY and SERCA activation by SNP may contribute to decreased vasodilatation.

Cited by 21 publications

References 50 publications

Hypotensive and vasorelaxing effects of the new NO-donor [Ru(terpy)(bdq)NO+]3+ in spontaneously hypertensive rats

Hypotensive and vasorelaxing effects of the new NO-donor [Ru(terpy)(bdq)NO+]3+ in spontaneously hypertensive rats

In vitro Treatment with cis-[Ru(H-dcbpy-)2(Cl)(NO)] Improves the Endothelial Function in Aortic Rings with Endothelial Dysfunction

Mechanisms underlying the hypotensive and vasodilator effects of Ru(terpy)(bdq)NO]3+, a nitric oxide donor, differ between normotensive and spontaneously hypertensive rats

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