Relationship between adiponectin and nitrite in healthy and preeclampsia pregnancies

Eleuterio, Nibia Mariana; Palei, Ana C.; Machado, Jackeline de Souza Rangel; Tanus‐Santos, Jose E.; Cavalli, Ricardo de Carvalho; Sandrim, Valéria C.

doi:10.1016/j.cca.2013.04.027

Cited by 29 publications

(18 citation statements)

References 26 publications

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“…Taken together, these results show that the combined administration of nitrite and sildenafil is not advantageous compared with sildenafil alone, because sildenafil alone protected against hypertension and fetal growth restriction without increase cGMP levels in HP + S group, thus, suggesting that sildenafil effects in hypertension in pregnancy were not dependent of NO and cGMP. Thereby, our present results provide preclinical evidences to support the use of sildenafil in women with hypertension-in-pregnancy with features of preeclampsia (Trapani et al, 2016), even though preeclamptic women have shown reduced NO formation compared to healthy pregnant women (Ehsanipoor et al, 2013;Eleuterio et al, 2013;Schiessl et al, 2006;Tranquilli et al, 2004;Wang et al, 2015).…”

Section: Discussionsupporting

confidence: 59%

Maternal hypertension and feto-placental growth restriction is reversed by sildenafil: Evidence of independent effects of circulating nitric oxide levels

Gonçalves-Rizzi

Possomato-Vieira

Nascimento

et al. 2018

European Journal of Pharmacology

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Sildenafil has shown nitric oxide (NO)-independent pleiotropic effects, however the mechanisms involved are unclear. We investigated the protective effects of sildenafil against hypertension in pregnancy and feto-placental growth restriction induced by NO inhibition, and if sodium nitrite-derived NO formation influences sildenafil effects. We evaluated the plasmatic levels of NO metabolites, cyclic guanosine monophosphate (cGMP), oxidative stress and myeloperoxidase, which are involved in endothelial dysfunction during hypertension in pregnancy. Also, we performed in vitro experiments to examine cell viability and NO synthesis in human umbilical vein endothelial cells (HUVECs) cultures incubated with plasma from healthy or hypertensive pregnant rats treated (or not) with both drugs, either alone or in association. Sildenafil blunted hypertension in pregnancy and protected against feto-placental growth restriction induced by NO inhibition and these effects of sildenafil alone were similar to those presented by its association with sodium nitrite. Protective effects of sildenafil were observed even with low plasmatic NO levels and were not followed by increases in cGMP levels. Also, sildenafil, but not sodium nitrite, blunted the increases in myeloperoxidase activity. Both drugs (isolated or in association) presented antioxidant effects. Plasma from hypertensive pregnant rats treated with sildenafil, but not sodium nitrite alone, increased the viability of HUVECs. NO synthesis in HUVECs cultures was increased with plasma from rats treated with both drugs. We conclude that sildenafil effects are not dependent of circulating NO levels in hypertension and feto-placental growth restriction. These findings may reflect a protection against myeloperoxidase and pro-oxidant activation in hypertension in pregnancy.

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Section: Discussionsupporting

confidence: 59%

Maternal hypertension and feto-placental growth restriction is reversed by sildenafil: Evidence of independent effects of circulating nitric oxide levels

Gonçalves-Rizzi

Possomato-Vieira

Nascimento

et al. 2018

European Journal of Pharmacology

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“…A reduction in endogenous nitric oxide (NO) bioavailability in hypertensive pregnancy is supported by several studies and interactions between H 2 S and NO have been described before . Indeed, a previous study from our group suggested H 2 S and NO interaction in hypertension‐in‐pregnancy, thus, we aimed to investigate the antihypertensive effects and changes in feto‐placental parameters exerted by NaHS in hypertension‐in‐pregnancy.…”

Section: Introductionmentioning

confidence: 79%

Increases in placental nitric oxide, but not nitric oxide‐mediated relaxation, underlie the improvement in placental efficiency and antihypertensive effects of hydrogen sulphide donor in hypertensive pregnancy

Possomato-Vieira

Chimini

Silva

et al. 2018

Clin Exp Pharma Physio

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Dysregulation of hydrogen sulphide (H S) producing enzymes has been related to hypertensive pregnancy, and H S donor, sodium hydrosulphide (NaHS) exerts antihypertensive effects, modulates angiogenic factors production and acts as an antioxidant. Moreover, reduction in nitric oxide (NO) bioavailability is related to hypertensive pregnancy and H S may interact with NO, modulating its production. We aimed to investigate the NaHS effects in hypertension-in-pregnancy and also in feto-placental parameters. Female Wistar rats (200-250 g) were mated and desoxycorticosterone acetate injections followed by replacement of water by 0.9% saline solution were used to induce hypertensive pregnancy. Rats were divided into four groups: normal pregnant (Norm-Preg), pregnant + NaHS (Preg+NaHS), hypertensive pregnant (HTN-Preg) and HTN-Preg+NaHS. Systolic blood pressure was increased in HTN-Preg and this increase was blunted in HTN-Preg+NaHS. Fetal and placental weights were decreased in HTN-Preg animals, while fetal growth restriction was improved in HTN-Preg+NaHS. Placental weight was lower in HTN-Preg+NaHS than in HTN-Preg; however, placental efficiency was re-established in HTN-Preg+NaHS rats. We observed that a partial contribution of placental NO, but not changes in anti-angiogenic factors may mediate the increases in placental efficiency in HTN-Preg+NaHS. HTN-Preg presented thoracic aorta hyperreactivity to phenylephrine while NaHS treatment blunted this hyperreactivity, which seems not to be related to NO-mediated relaxation induced by acetylcholine. Therefore, changes in vascular responsiveness promoted by NaHS treatment may underlie the beneficial effects in systolic blood pressure and feto-placental parameters in our study.

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“…NO is required vascular alterations during normal pregnancy to support the increased blood volume [28]. NO deficiency has been shown to impair the vasorelaxation in human and animal models of PE [29–31] and increased NO bioavailability could contribute to improve maternal and fetal outcomes.…”

Section: Endothelial Dysfunction Is a Common Thread That Could Contrimentioning

confidence: 99%

Pathophysiology and Current Clinical Management of Preeclampsia

et al. 2017

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Preeclampsia is characterized by blood pressure greater than 140/90 mmHg in the second half of pregnancy. This disease is a major contributor to preterm and low birth weight babies. The early delivery of the baby, which becomes necessary for maintaining maternal well-being, makes pre-eclampsia the leading cause for preterm labor and infant mortality and morbidity. Currently, there is no cure for this pregnancy disorder. The current clinical management of PE is hydralazine with labetalol and magnesium sulfate to slow disease progression and prevent maternal seizure, and hopefully prolong the pregnancy. This review will highlight factors implicated in the pathophysiology of preeclampsia and current treatments for the management of this disease.

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Relationship between adiponectin and nitrite in healthy and preeclampsia pregnancies

Abstract: Our findings showed higher levels of adiponectin and lower nitrite levels in PE compared to HP, and these levels were positively correlated in HP and in PE presenting lower concentrations of ADMA.

Cited by 29 publications

References 26 publications

Maternal hypertension and feto-placental growth restriction is reversed by sildenafil: Evidence of independent effects of circulating nitric oxide levels

Maternal hypertension and feto-placental growth restriction is reversed by sildenafil: Evidence of independent effects of circulating nitric oxide levels

Increases in placental nitric oxide, but not nitric oxide‐mediated relaxation, underlie the improvement in placental efficiency and antihypertensive effects of hydrogen sulphide donor in hypertensive pregnancy

Pathophysiology and Current Clinical Management of Preeclampsia

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