Cardiovascular alterations at different stages of hypertension development during ethanol consumption: Time-course of vascular and autonomic changes

The aim of the present work was to establish a time-course correlation between vascular and autonomic changes that contribute to the development of hypertension during ethanol ingestion in rats. For this, male Wistar rats were subjected to the intake of increasing ethanol concentrations in their dri...

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Veröffentlicht in:Toxicology and applied pharmacology 2014-10, Vol.280 (2), p.245-255
Hauptverfasser: Crestani, Carlos C., Lopes da Silva, Andréia, Scopinho, América A., Ruginsk, Silvia G., Uchoa, Ernane T., Correa, Fernando M.A., Elias, Lucila L.K., Antunes-Rodrigues, José, Resstel, Leonardo B.M.
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container_issue 2
container_start_page 245
container_title Toxicology and applied pharmacology
container_volume 280
creator Crestani, Carlos C.
Lopes da Silva, Andréia
Scopinho, América A.
Ruginsk, Silvia G.
Uchoa, Ernane T.
Correa, Fernando M.A.
Elias, Lucila L.K.
Antunes-Rodrigues, José
Resstel, Leonardo B.M.
description The aim of the present work was to establish a time-course correlation between vascular and autonomic changes that contribute to the development of hypertension during ethanol ingestion in rats. For this, male Wistar rats were subjected to the intake of increasing ethanol concentrations in their drinking water during four weeks. Ethanol effects were investigated at the end of each week. Mild hypertension was already observed at the first week of treatment, and a progressive blood pressure increase was observed along the evaluation period. Increased pressor response to phenylephrine was observed from first to fourth week. α1-adrenoceptor protein in the mesenteric bed was enhanced at the first week, whereas β2-adrenoceptor protein in the aorta was reduced after the second week. In the third week, ethanol intake facilitated the depressor response to sodium nitroprusside, whereas in the fourth week it reduced nitrate content in aorta and increased it plasma. The bradycardic component of the baroreflex was impaired, whereas baroreflex tachycardia was enhanced at the third and fourth weeks. AT1A receptor and C-type natriuretic peptide (CNP) mRNAs in the nucleus tractus solitarius were increased at the fourth week. These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption. Additionally, baroreflex changes are possibly mediated by alterations in angiotensinergic mechanisms and CNP content within the brainstem, which contribute to maintaining the hypertensive state in later phases of ethanol ingestion. Facilitated vascular responsiveness to nitric oxide seems to counteract ethanol-induced hypertension. •Mild hypertension was observed during the entire period of ethanol ingestion.•Ethanol facilitated vascular reactivity to vasoactive agents.•Changes in baroreflex activity contribute to ethanol-evoked hypertension.•Plasma and aortic nitrate content was affected by ethanol consumption.•Ethanol changed AT1A receptor and CNP in the nucleus tractus solitaries.
doi_str_mv 10.1016/j.taap.2014.08.012
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AT1A receptor and C-type natriuretic peptide (CNP) mRNAs in the nucleus tractus solitarius were increased at the fourth week. These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption. Additionally, baroreflex changes are possibly mediated by alterations in angiotensinergic mechanisms and CNP content within the brainstem, which contribute to maintaining the hypertensive state in later phases of ethanol ingestion. 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Arterial hypotension ; Baroreflex ; Baroreflex - drug effects ; Baroreflex - physiology ; Biological and medical sciences ; Blood and lymphatic vessels ; BLOOD PRESSURE ; Blood Pressure - drug effects ; Cardiology. Vascular system ; CONCENTRATION RATIO ; DRINKING WATER ; ETHANOL ; Heart Rate - drug effects ; HYPERTENSION ; Hypertension - etiology ; Hypertension - physiopathology ; INGESTION ; Male ; Medical sciences ; MESSENGER-RNA ; Natriuretic Peptide, C-Type - genetics ; Nitrate ; NITRATES ; NITRIC OXIDE ; Nitric Oxide - physiology ; Nitroprusside - pharmacology ; Nucleus tractus solitarius ; PEPTIDES ; Phenylephrine - pharmacology ; RATS ; Rats, Wistar ; Receptor, Angiotensin, Type 1 - genetics ; RECEPTORS ; SODIUM ; Toxicology ; Vascular reactivity</subject><ispartof>Toxicology and applied pharmacology, 2014-10, Vol.280 (2), p.245-255</ispartof><rights>2014 Elsevier Inc.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2014 Elsevier Inc. 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For this, male Wistar rats were subjected to the intake of increasing ethanol concentrations in their drinking water during four weeks. Ethanol effects were investigated at the end of each week. Mild hypertension was already observed at the first week of treatment, and a progressive blood pressure increase was observed along the evaluation period. Increased pressor response to phenylephrine was observed from first to fourth week. α1-adrenoceptor protein in the mesenteric bed was enhanced at the first week, whereas β2-adrenoceptor protein in the aorta was reduced after the second week. In the third week, ethanol intake facilitated the depressor response to sodium nitroprusside, whereas in the fourth week it reduced nitrate content in aorta and increased it plasma. The bradycardic component of the baroreflex was impaired, whereas baroreflex tachycardia was enhanced at the third and fourth weeks. AT1A receptor and C-type natriuretic peptide (CNP) mRNAs in the nucleus tractus solitarius were increased at the fourth week. These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption. Additionally, baroreflex changes are possibly mediated by alterations in angiotensinergic mechanisms and CNP content within the brainstem, which contribute to maintaining the hypertensive state in later phases of ethanol ingestion. Facilitated vascular responsiveness to nitric oxide seems to counteract ethanol-induced hypertension. •Mild hypertension was observed during the entire period of ethanol ingestion.•Ethanol facilitated vascular reactivity to vasoactive agents.•Changes in baroreflex activity contribute to ethanol-evoked hypertension.•Plasma and aortic nitrate content was affected by ethanol consumption.•Ethanol changed AT1A receptor and CNP in the nucleus tractus solitaries.</description><subject>60 APPLIED LIFE SCIENCES</subject><subject>Adrenoceptor</subject><subject>Alcohol Drinking - adverse effects</subject><subject>Alcohol Drinking - physiopathology</subject><subject>Alcoholism and acute alcohol poisoning</subject><subject>Animals</subject><subject>AORTA</subject><subject>Arterial hypertension. 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Arterial hypotension</topic><topic>Baroreflex</topic><topic>Baroreflex - drug effects</topic><topic>Baroreflex - physiology</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>BLOOD PRESSURE</topic><topic>Blood Pressure - drug effects</topic><topic>Cardiology. Vascular system</topic><topic>CONCENTRATION RATIO</topic><topic>DRINKING WATER</topic><topic>ETHANOL</topic><topic>Heart Rate - drug effects</topic><topic>HYPERTENSION</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>INGESTION</topic><topic>Male</topic><topic>Medical sciences</topic><topic>MESSENGER-RNA</topic><topic>Natriuretic Peptide, C-Type - genetics</topic><topic>Nitrate</topic><topic>NITRATES</topic><topic>NITRIC OXIDE</topic><topic>Nitric Oxide - physiology</topic><topic>Nitroprusside - pharmacology</topic><topic>Nucleus tractus solitarius</topic><topic>PEPTIDES</topic><topic>Phenylephrine - pharmacology</topic><topic>RATS</topic><topic>Rats, Wistar</topic><topic>Receptor, Angiotensin, Type 1 - genetics</topic><topic>RECEPTORS</topic><topic>SODIUM</topic><topic>Toxicology</topic><topic>Vascular reactivity</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Crestani, Carlos C.</creatorcontrib><creatorcontrib>Lopes da Silva, Andréia</creatorcontrib><creatorcontrib>Scopinho, América A.</creatorcontrib><creatorcontrib>Ruginsk, Silvia G.</creatorcontrib><creatorcontrib>Uchoa, Ernane T.</creatorcontrib><creatorcontrib>Correa, Fernando M.A.</creatorcontrib><creatorcontrib>Elias, Lucila L.K.</creatorcontrib><creatorcontrib>Antunes-Rodrigues, José</creatorcontrib><creatorcontrib>Resstel, Leonardo B.M.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>OSTI.GOV</collection><jtitle>Toxicology and applied pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Crestani, Carlos C.</au><au>Lopes da Silva, Andréia</au><au>Scopinho, América A.</au><au>Ruginsk, Silvia G.</au><au>Uchoa, Ernane T.</au><au>Correa, Fernando M.A.</au><au>Elias, Lucila L.K.</au><au>Antunes-Rodrigues, José</au><au>Resstel, Leonardo B.M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardiovascular alterations at different stages of hypertension development during ethanol consumption: Time-course of vascular and autonomic changes</atitle><jtitle>Toxicology and applied pharmacology</jtitle><addtitle>Toxicol Appl Pharmacol</addtitle><date>2014-10-15</date><risdate>2014</risdate><volume>280</volume><issue>2</issue><spage>245</spage><epage>255</epage><pages>245-255</pages><issn>0041-008X</issn><eissn>1096-0333</eissn><coden>TXAPA9</coden><abstract>The aim of the present work was to establish a time-course correlation between vascular and autonomic changes that contribute to the development of hypertension during ethanol ingestion in rats. For this, male Wistar rats were subjected to the intake of increasing ethanol concentrations in their drinking water during four weeks. Ethanol effects were investigated at the end of each week. Mild hypertension was already observed at the first week of treatment, and a progressive blood pressure increase was observed along the evaluation period. Increased pressor response to phenylephrine was observed from first to fourth week. α1-adrenoceptor protein in the mesenteric bed was enhanced at the first week, whereas β2-adrenoceptor protein in the aorta was reduced after the second week. In the third week, ethanol intake facilitated the depressor response to sodium nitroprusside, whereas in the fourth week it reduced nitrate content in aorta and increased it plasma. The bradycardic component of the baroreflex was impaired, whereas baroreflex tachycardia was enhanced at the third and fourth weeks. AT1A receptor and C-type natriuretic peptide (CNP) mRNAs in the nucleus tractus solitarius were increased at the fourth week. These findings suggest that increased vascular responsiveness to vasoconstrictor agents is possibly a link factor in the development and maintenance of the progressive hypertension induced by ethanol consumption. Additionally, baroreflex changes are possibly mediated by alterations in angiotensinergic mechanisms and CNP content within the brainstem, which contribute to maintaining the hypertensive state in later phases of ethanol ingestion. Facilitated vascular responsiveness to nitric oxide seems to counteract ethanol-induced hypertension. •Mild hypertension was observed during the entire period of ethanol ingestion.•Ethanol facilitated vascular reactivity to vasoactive agents.•Changes in baroreflex activity contribute to ethanol-evoked hypertension.•Plasma and aortic nitrate content was affected by ethanol consumption.•Ethanol changed AT1A receptor and CNP in the nucleus tractus solitaries.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>25151222</pmid><doi>10.1016/j.taap.2014.08.012</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record>
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source MEDLINE; Access via ScienceDirect (Elsevier)
subjects 60 APPLIED LIFE SCIENCES
Adrenoceptor
Alcohol Drinking - adverse effects
Alcohol Drinking - physiopathology
Alcoholism and acute alcohol poisoning
Animals
AORTA
Arterial hypertension. Arterial hypotension
Baroreflex
Baroreflex - drug effects
Baroreflex - physiology
Biological and medical sciences
Blood and lymphatic vessels
BLOOD PRESSURE
Blood Pressure - drug effects
Cardiology. Vascular system
CONCENTRATION RATIO
DRINKING WATER
ETHANOL
Heart Rate - drug effects
HYPERTENSION
Hypertension - etiology
Hypertension - physiopathology
INGESTION
Male
Medical sciences
MESSENGER-RNA
Natriuretic Peptide, C-Type - genetics
Nitrate
NITRATES
NITRIC OXIDE
Nitric Oxide - physiology
Nitroprusside - pharmacology
Nucleus tractus solitarius
PEPTIDES
Phenylephrine - pharmacology
RATS
Rats, Wistar
Receptor, Angiotensin, Type 1 - genetics
RECEPTORS
SODIUM
Toxicology
Vascular reactivity
title Cardiovascular alterations at different stages of hypertension development during ethanol consumption: Time-course of vascular and autonomic changes
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