Loading…
Effects of Angiotensin II on the Cardiac Responses to Sympathetic Nerve Stimulation in Dogs
In anesthetized dogs with the left cardiac sympathetic nerves and both vagal nerves intact, angiotensin II (All) induced a substantial, dose-dependent increase in arterial blood pressure and small increments in cardiac cycle length and ventricular contractile force. In dogs in which the cardiac symp...
Saved in:
Published in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 1983-01, Vol.5 (1), p.26-33 |
---|---|
Main Authors: | , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c4775-80e877e68b06d58a37126025e029bcb48bc7f94b14a53e02380570b4af0caf803 |
---|---|
cites | |
container_end_page | 33 |
container_issue | 1 |
container_start_page | 26 |
container_title | Hypertension (Dallas, Tex. 1979) |
container_volume | 5 |
creator | FURUKAWA, YASUYUKI SCIPIONE, PAUL LEVY, MATTHEW N |
description | In anesthetized dogs with the left cardiac sympathetic nerves and both vagal nerves intact, angiotensin II (All) induced a substantial, dose-dependent increase in arterial blood pressure and small increments in cardiac cycle length and ventricular contractile force. In dogs in which the cardiac sympathetic and vagal nerves had been interrupted, All produced similar increases in blood pressure and larger increases in contractile force, but it decreased the cardiac cycle length. In both groups of dogs, All augmented substantially the positive inotropic responses to sympathetic nerve stimulation, but it enhanced the positive chronotropic responses only slightly. However, AH did not appreciably prolong the cardiac responses to sympathetic nerve stimulation, nor did it alter signifi-cantly the cardiac responses to norepinephrine infusions. Hence, at the dosage levels used, All probably did not inhibit the neuronal uptake of norepinephrine appreciably nor did it enhance the responsiveness of the cardiac effector sites to norepinephrine. Therefore, the potentiation of the cardiac responses to sympathetic nerve stimulation by All in these experiments was probably achieved principally by facilitating norepinephrine release from the adrenergic nerve terminals in the heart. |
doi_str_mv | 10.1161/01.hyp.5.1.26 |
format | article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_80350236</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>80350236</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4775-80e877e68b06d58a37126025e029bcb48bc7f94b14a53e02380570b4af0caf803</originalsourceid><addsrcrecordid>eNo9kM1P3DAQxS3Uim6BI0ckn3pL6klsxzmihZaVUIv4kKh6sBzvhE1J4mA7Rfvf16tddS6jee_33mEIOQeWA0j4yiDfbKdc5JAX8ogsQBQ840KWH8iCQc2zGuD5E_kcwh_GgHNeHZNjqbjiUizI7-u2RRsDdS29HF86F3EM3UhXK-pGGjdIl8avO2PpPYbJjQEDjY4-bIfJJDd2lv5A_xfpQ-yGuTexS7GUv3Iv4ZR8bE0f8OywT8jTt-vH5U12-_P7anl5m1leVSJTDFVVoVQNk2uhTFlBIVkhkBV1YxuuGlu1NW-AG1EmsVRMVKzhpmXWtIqVJ-TLvnfy7m3GEPXQBYt9b0Z0c9AJESkmE5jtQetdCB5bPfluMH6rgendMzUDffPrTgsNutjxF4fiuRlw_Z8-fC_5fO-_uz6iD6_9_I5eb9D0caNZGl5IlUGtSgbpynaSKP8BdHl-ng</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>80350236</pqid></control><display><type>article</type><title>Effects of Angiotensin II on the Cardiac Responses to Sympathetic Nerve Stimulation in Dogs</title><source>EZB Electronic Journals Library</source><creator>FURUKAWA, YASUYUKI ; SCIPIONE, PAUL ; LEVY, MATTHEW N</creator><creatorcontrib>FURUKAWA, YASUYUKI ; SCIPIONE, PAUL ; LEVY, MATTHEW N</creatorcontrib><description>In anesthetized dogs with the left cardiac sympathetic nerves and both vagal nerves intact, angiotensin II (All) induced a substantial, dose-dependent increase in arterial blood pressure and small increments in cardiac cycle length and ventricular contractile force. In dogs in which the cardiac sympathetic and vagal nerves had been interrupted, All produced similar increases in blood pressure and larger increases in contractile force, but it decreased the cardiac cycle length. In both groups of dogs, All augmented substantially the positive inotropic responses to sympathetic nerve stimulation, but it enhanced the positive chronotropic responses only slightly. However, AH did not appreciably prolong the cardiac responses to sympathetic nerve stimulation, nor did it alter signifi-cantly the cardiac responses to norepinephrine infusions. Hence, at the dosage levels used, All probably did not inhibit the neuronal uptake of norepinephrine appreciably nor did it enhance the responsiveness of the cardiac effector sites to norepinephrine. Therefore, the potentiation of the cardiac responses to sympathetic nerve stimulation by All in these experiments was probably achieved principally by facilitating norepinephrine release from the adrenergic nerve terminals in the heart.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.5.1.26</identifier><identifier>PMID: 6848465</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Angiotensin II - pharmacology ; Animals ; Blood Pressure - drug effects ; Dogs ; Dose-Response Relationship, Drug ; Electric Stimulation ; Heart Rate - drug effects ; Myocardial Contraction - drug effects ; Sympathetic Nervous System - physiology</subject><ispartof>Hypertension (Dallas, Tex. 1979), 1983-01, Vol.5 (1), p.26-33</ispartof><rights>1983 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4775-80e877e68b06d58a37126025e029bcb48bc7f94b14a53e02380570b4af0caf803</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6848465$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>FURUKAWA, YASUYUKI</creatorcontrib><creatorcontrib>SCIPIONE, PAUL</creatorcontrib><creatorcontrib>LEVY, MATTHEW N</creatorcontrib><title>Effects of Angiotensin II on the Cardiac Responses to Sympathetic Nerve Stimulation in Dogs</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>In anesthetized dogs with the left cardiac sympathetic nerves and both vagal nerves intact, angiotensin II (All) induced a substantial, dose-dependent increase in arterial blood pressure and small increments in cardiac cycle length and ventricular contractile force. In dogs in which the cardiac sympathetic and vagal nerves had been interrupted, All produced similar increases in blood pressure and larger increases in contractile force, but it decreased the cardiac cycle length. In both groups of dogs, All augmented substantially the positive inotropic responses to sympathetic nerve stimulation, but it enhanced the positive chronotropic responses only slightly. However, AH did not appreciably prolong the cardiac responses to sympathetic nerve stimulation, nor did it alter signifi-cantly the cardiac responses to norepinephrine infusions. Hence, at the dosage levels used, All probably did not inhibit the neuronal uptake of norepinephrine appreciably nor did it enhance the responsiveness of the cardiac effector sites to norepinephrine. Therefore, the potentiation of the cardiac responses to sympathetic nerve stimulation by All in these experiments was probably achieved principally by facilitating norepinephrine release from the adrenergic nerve terminals in the heart.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Blood Pressure - drug effects</subject><subject>Dogs</subject><subject>Dose-Response Relationship, Drug</subject><subject>Electric Stimulation</subject><subject>Heart Rate - drug effects</subject><subject>Myocardial Contraction - drug effects</subject><subject>Sympathetic Nervous System - physiology</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1983</creationdate><recordtype>article</recordtype><recordid>eNo9kM1P3DAQxS3Uim6BI0ckn3pL6klsxzmihZaVUIv4kKh6sBzvhE1J4mA7Rfvf16tddS6jee_33mEIOQeWA0j4yiDfbKdc5JAX8ogsQBQ840KWH8iCQc2zGuD5E_kcwh_GgHNeHZNjqbjiUizI7-u2RRsDdS29HF86F3EM3UhXK-pGGjdIl8avO2PpPYbJjQEDjY4-bIfJJDd2lv5A_xfpQ-yGuTexS7GUv3Iv4ZR8bE0f8OywT8jTt-vH5U12-_P7anl5m1leVSJTDFVVoVQNk2uhTFlBIVkhkBV1YxuuGlu1NW-AG1EmsVRMVKzhpmXWtIqVJ-TLvnfy7m3GEPXQBYt9b0Z0c9AJESkmE5jtQetdCB5bPfluMH6rgendMzUDffPrTgsNutjxF4fiuRlw_Z8-fC_5fO-_uz6iD6_9_I5eb9D0caNZGl5IlUGtSgbpynaSKP8BdHl-ng</recordid><startdate>198301</startdate><enddate>198301</enddate><creator>FURUKAWA, YASUYUKI</creator><creator>SCIPIONE, PAUL</creator><creator>LEVY, MATTHEW N</creator><general>American Heart Association, Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>198301</creationdate><title>Effects of Angiotensin II on the Cardiac Responses to Sympathetic Nerve Stimulation in Dogs</title><author>FURUKAWA, YASUYUKI ; SCIPIONE, PAUL ; LEVY, MATTHEW N</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4775-80e877e68b06d58a37126025e029bcb48bc7f94b14a53e02380570b4af0caf803</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1983</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Blood Pressure - drug effects</topic><topic>Dogs</topic><topic>Dose-Response Relationship, Drug</topic><topic>Electric Stimulation</topic><topic>Heart Rate - drug effects</topic><topic>Myocardial Contraction - drug effects</topic><topic>Sympathetic Nervous System - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>FURUKAWA, YASUYUKI</creatorcontrib><creatorcontrib>SCIPIONE, PAUL</creatorcontrib><creatorcontrib>LEVY, MATTHEW N</creatorcontrib><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><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>FURUKAWA, YASUYUKI</au><au>SCIPIONE, PAUL</au><au>LEVY, MATTHEW N</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of Angiotensin II on the Cardiac Responses to Sympathetic Nerve Stimulation in Dogs</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>1983-01</date><risdate>1983</risdate><volume>5</volume><issue>1</issue><spage>26</spage><epage>33</epage><pages>26-33</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><abstract>In anesthetized dogs with the left cardiac sympathetic nerves and both vagal nerves intact, angiotensin II (All) induced a substantial, dose-dependent increase in arterial blood pressure and small increments in cardiac cycle length and ventricular contractile force. In dogs in which the cardiac sympathetic and vagal nerves had been interrupted, All produced similar increases in blood pressure and larger increases in contractile force, but it decreased the cardiac cycle length. In both groups of dogs, All augmented substantially the positive inotropic responses to sympathetic nerve stimulation, but it enhanced the positive chronotropic responses only slightly. However, AH did not appreciably prolong the cardiac responses to sympathetic nerve stimulation, nor did it alter signifi-cantly the cardiac responses to norepinephrine infusions. Hence, at the dosage levels used, All probably did not inhibit the neuronal uptake of norepinephrine appreciably nor did it enhance the responsiveness of the cardiac effector sites to norepinephrine. Therefore, the potentiation of the cardiac responses to sympathetic nerve stimulation by All in these experiments was probably achieved principally by facilitating norepinephrine release from the adrenergic nerve terminals in the heart.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>6848465</pmid><doi>10.1161/01.hyp.5.1.26</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 0194-911X |
ispartof | Hypertension (Dallas, Tex. 1979), 1983-01, Vol.5 (1), p.26-33 |
issn | 0194-911X 1524-4563 |
language | eng |
recordid | cdi_proquest_miscellaneous_80350236 |
source | EZB Electronic Journals Library |
subjects | Angiotensin II - pharmacology Animals Blood Pressure - drug effects Dogs Dose-Response Relationship, Drug Electric Stimulation Heart Rate - drug effects Myocardial Contraction - drug effects Sympathetic Nervous System - physiology |
title | Effects of Angiotensin II on the Cardiac Responses to Sympathetic Nerve Stimulation in Dogs |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-07T15%3A32%3A09IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Effects%20of%20Angiotensin%20II%20on%20the%20Cardiac%20Responses%20to%20Sympathetic%20Nerve%20Stimulation%20in%20Dogs&rft.jtitle=Hypertension%20(Dallas,%20Tex.%201979)&rft.au=FURUKAWA,%20YASUYUKI&rft.date=1983-01&rft.volume=5&rft.issue=1&rft.spage=26&rft.epage=33&rft.pages=26-33&rft.issn=0194-911X&rft.eissn=1524-4563&rft_id=info:doi/10.1161/01.hyp.5.1.26&rft_dat=%3Cproquest_cross%3E80350236%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c4775-80e877e68b06d58a37126025e029bcb48bc7f94b14a53e02380570b4af0caf803%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=80350236&rft_id=info:pmid/6848465&rfr_iscdi=true |