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

Summary Dysregulation of hydrogen sulphide (H2S) producing enzymes has been related to hypertensive pregnancy, and H2S donor, sodium hydrosulphide (NaHS) exerts antihypertensive effects, modulates angiogenic factors production and acts as an antioxidant. Moreover, reduction in nitric oxide (NO) bioa...

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Veröffentlicht in:Clinical and experimental pharmacology & physiology 2018-11, Vol.45 (11), p.1118-1127
Hauptverfasser: Possomato‐Vieira, Jose S., Chimini, Jessica S., Silva, Maria L. S., Dias‐Junior, Carlos A.
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container_issue 11
container_start_page 1118
container_title Clinical and experimental pharmacology & physiology
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creator Possomato‐Vieira, Jose S.
Chimini, Jessica S.
Silva, Maria L. S.
Dias‐Junior, Carlos A.
description Summary Dysregulation of hydrogen sulphide (H2S) producing enzymes has been related to hypertensive pregnancy, and H2S 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 H2S 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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S. ; Dias‐Junior, Carlos A.</creator><creatorcontrib>Possomato‐Vieira, Jose S. ; Chimini, Jessica S. ; Silva, Maria L. S. ; Dias‐Junior, Carlos A.</creatorcontrib><description>Summary Dysregulation of hydrogen sulphide (H2S) producing enzymes has been related to hypertensive pregnancy, and H2S 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 H2S 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. 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S.</creatorcontrib><creatorcontrib>Dias‐Junior, Carlos A.</creatorcontrib><title>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</title><title>Clinical and experimental pharmacology &amp; physiology</title><addtitle>Clin Exp Pharmacol Physiol</addtitle><description>Summary Dysregulation of hydrogen sulphide (H2S) producing enzymes has been related to hypertensive pregnancy, and H2S 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 H2S 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. 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S. ; Dias‐Junior, Carlos A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3710-b881b6cfab1520e79c32ac054279fdc143462254fa82f6cd00dd628d55e5bdec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acetic acid</topic><topic>Acetylcholine</topic><topic>Angiogenesis</topic><topic>Antihypertensives</topic><topic>Antioxidants</topic><topic>Aorta</topic><topic>Bioavailability</topic><topic>Blood pressure</topic><topic>Efficiency</topic><topic>Fetuses</topic><topic>Hydrogen sulfide</topic><topic>hydrogen sulphide</topic><topic>Hyperreactivity</topic><topic>Hypersensitivity</topic><topic>Hypertension</topic><topic>hypertenstion in pregnancy</topic><topic>Nitric oxide</topic><topic>Parameters</topic><topic>Phenylephrine</topic><topic>Placenta</topic><topic>Pregnancy</topic><topic>Pressure effects</topic><topic>Rats</topic><topic>Saline solutions</topic><topic>Sodium</topic><topic>Thorax</topic><topic>vascular reactivity</topic><topic>Weight</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Possomato‐Vieira, Jose S.</creatorcontrib><creatorcontrib>Chimini, Jessica S.</creatorcontrib><creatorcontrib>Silva, Maria L. S.</creatorcontrib><creatorcontrib>Dias‐Junior, Carlos A.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical and experimental pharmacology &amp; physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Possomato‐Vieira, Jose S.</au><au>Chimini, Jessica S.</au><au>Silva, Maria L. S.</au><au>Dias‐Junior, Carlos A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>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</atitle><jtitle>Clinical and experimental pharmacology &amp; physiology</jtitle><addtitle>Clin Exp Pharmacol Physiol</addtitle><date>2018-11</date><risdate>2018</risdate><volume>45</volume><issue>11</issue><spage>1118</spage><epage>1127</epage><pages>1118-1127</pages><issn>0305-1870</issn><eissn>1440-1681</eissn><abstract>Summary Dysregulation of hydrogen sulphide (H2S) producing enzymes has been related to hypertensive pregnancy, and H2S 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 H2S 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.</abstract><cop>Australia</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29927503</pmid><doi>10.1111/1440-1681.13000</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-0348-6144</orcidid></addata></record>
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source Wiley Journals
subjects Acetic acid
Acetylcholine
Angiogenesis
Antihypertensives
Antioxidants
Aorta
Bioavailability
Blood pressure
Efficiency
Fetuses
Hydrogen sulfide
hydrogen sulphide
Hyperreactivity
Hypersensitivity
Hypertension
hypertenstion in pregnancy
Nitric oxide
Parameters
Phenylephrine
Placenta
Pregnancy
Pressure effects
Rats
Saline solutions
Sodium
Thorax
vascular reactivity
Weight
title 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
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