Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats
1 Division of Cardiovascular Medicine, Department of Internal Medicine, University of California, Davis, California 95616; and 2 Departments of Kinesiology and of Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506 We hypothesized that nitric oxide (NO) opposes ANG II-induced...
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| creator | Symons, J. David Stebbins, Charles L Musch, Timothy I |
| description | 1 Division of Cardiovascular
Medicine, Department of Internal Medicine, University of California,
Davis, California 95616; and
2 Departments of Kinesiology and
of Anatomy and Physiology, Kansas State University, Manhattan,
Kansas 66506
We hypothesized that nitric oxide (NO) opposes ANG II-induced
increases in arterial pressure and reductions in renal, splanchnic, and
skeletal muscle vascular conductance during dynamic exercise in normal
and heart failure rats. Regional blood flow and vascular conductance
were measured during treadmill running before (unblocked exercise) and
after 1 ) ANG II
AT 1 -receptor blockade (losartan, 20 mg/kg ia), 2 ) NO synthase (NOS)
inhibition
[ N G -nitro- L -arginine
methyl ester ( L -NAME); 10 mg/kg
ia], or 3 ) ANG II
AT 1 -receptor blockade + NOS
inhibition (combined blockade). Renal conductance during unblocked
exercise (4.79 ± 0.31 ml · 100 g 1 · min 1 · mmHg 1 )
was increased after ANG II
AT 1 -receptor blockade (6.53 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 )
and decreased by NOS inhibition (2.12 ± 0.20 ml · 100 g 1 · min 1 · mmHg 1 )
and combined inhibition (3.96 ± 0.57 ml · 100 g 1 · min 1 · mmHg 1 ;all
P |
| doi_str_mv | 10.1152/jappl.1999.87.2.574 |
| format | Article |
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Medicine, Department of Internal Medicine, University of California,
Davis, California 95616; and
2 Departments of Kinesiology and
of Anatomy and Physiology, Kansas State University, Manhattan,
Kansas 66506
We hypothesized that nitric oxide (NO) opposes ANG II-induced
increases in arterial pressure and reductions in renal, splanchnic, and
skeletal muscle vascular conductance during dynamic exercise in normal
and heart failure rats. Regional blood flow and vascular conductance
were measured during treadmill running before (unblocked exercise) and
after 1 ) ANG II
AT 1 -receptor blockade (losartan, 20 mg/kg ia), 2 ) NO synthase (NOS)
inhibition
[ N G -nitro- L -arginine
methyl ester ( L -NAME); 10 mg/kg
ia], or 3 ) ANG II
AT 1 -receptor blockade + NOS
inhibition (combined blockade). Renal conductance during unblocked
exercise (4.79 ± 0.31 ml · 100 g 1 · min 1 · mmHg 1 )
was increased after ANG II
AT 1 -receptor blockade (6.53 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 )
and decreased by NOS inhibition (2.12 ± 0.20 ml · 100 g 1 · min 1 · mmHg 1 )
and combined inhibition (3.96 ± 0.57 ml · 100 g 1 · min 1 · mmHg 1 ;all
P < 0.05 vs. unblocked). In heart
failure rats, renal conductance during unblocked exercise (5.50 ± 0.66 ml · 100 g 1 · min 1 · mmHg 1 )
was increased by ANG II
AT 1 -receptor blockade (8.48 ± 0.83 ml · 100 g 1 · min 1 · mmHg 1 )
and decreased by NOS inhibition (2.68 ± 0.22 ml · 100 g 1 · min 1 · mmHg 1 ;
both P < 0.05 vs. unblocked), but it
was unaltered during combined inhibition (4.65 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 ).
Because our findings during combined blockade could be predicted from
the independent actions of NO and ANG II, no interaction was apparent
between these two substances in control or heart failure animals. In
skeletal muscle, L -NAME-induced
reductions in conductance, compared with unblocked exercise
( P < 0.05), were abolished during
combined inhibition in heart failure but not in control rats. These
observations suggest that ANG II causes vasoconstriction in skeletal
muscle that is masked by NO-evoked dilation in animals with heart
failure. Because reductions in vascular conductance between unblocked
exercise and combined inhibition were less than would be predicted from
the independent actions of NO and ANG II, an interaction exists between
these two substances in heart failure rats.
L -NAME-induced increases in
arterial pressure during treadmill running were attenuated
( P < 0.05) similarly in both groups
by combined inhibition. These findings indicate that NO opposes ANG
II-induced increases in arterial pressure and in renal and
skeletal muscle resistance during dynamic exercise.
regional blood flow; vascular resistance; vascular conductance; N G -nitro- L -arginine
methyl ester; losartan</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/jappl.1999.87.2.574</identifier><identifier>PMID: 10444615</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Anatomy & physiology ; Angiotensin II - chemistry ; Angiotensin Receptor Antagonists ; Animals ; Biological and medical sciences ; Blood pressure ; Blood Pressure - drug effects ; Blood vessels ; Cardiology. Vascular system ; Exercise ; Female ; Gases ; Heart ; Heart Diseases - physiopathology ; Heart failure ; Heart failure, cardiogenic pulmonary edema, cardiac enlargement ; Heart Rate - drug effects ; Losartan - pharmacology ; Medical sciences ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - chemistry ; Nitric Oxide Synthase - antagonists & inhibitors ; Physical Conditioning, Animal - physiology ; Rats ; Rats, Wistar ; Receptor, Angiotensin, Type 1 ; Receptor, Angiotensin, Type 2 ; Regional Blood Flow - drug effects ; Rodents</subject><ispartof>Journal of applied physiology (1985), 1999-08, Vol.87 (2), p.574-581</ispartof><rights>1999 INIST-CNRS</rights><rights>Copyright American Physiological Society Aug 1999</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-aba031d176d02527f49993d42f00c242fd0a33f01fdae5279ec3dbdc8745c83d3</citedby><cites>FETCH-LOGICAL-c499t-aba031d176d02527f49993d42f00c242fd0a33f01fdae5279ec3dbdc8745c83d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3040,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1897686$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10444615$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Symons, J. David</creatorcontrib><creatorcontrib>Stebbins, Charles L</creatorcontrib><creatorcontrib>Musch, Timothy I</creatorcontrib><title>Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>1 Division of Cardiovascular
Medicine, Department of Internal Medicine, University of California,
Davis, California 95616; and
2 Departments of Kinesiology and
of Anatomy and Physiology, Kansas State University, Manhattan,
Kansas 66506
We hypothesized that nitric oxide (NO) opposes ANG II-induced
increases in arterial pressure and reductions in renal, splanchnic, and
skeletal muscle vascular conductance during dynamic exercise in normal
and heart failure rats. Regional blood flow and vascular conductance
were measured during treadmill running before (unblocked exercise) and
after 1 ) ANG II
AT 1 -receptor blockade (losartan, 20 mg/kg ia), 2 ) NO synthase (NOS)
inhibition
[ N G -nitro- L -arginine
methyl ester ( L -NAME); 10 mg/kg
ia], or 3 ) ANG II
AT 1 -receptor blockade + NOS
inhibition (combined blockade). Renal conductance during unblocked
exercise (4.79 ± 0.31 ml · 100 g 1 · min 1 · mmHg 1 )
was increased after ANG II
AT 1 -receptor blockade (6.53 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 )
and decreased by NOS inhibition (2.12 ± 0.20 ml · 100 g 1 · min 1 · mmHg 1 )
and combined inhibition (3.96 ± 0.57 ml · 100 g 1 · min 1 · mmHg 1 ;all
P < 0.05 vs. unblocked). In heart
failure rats, renal conductance during unblocked exercise (5.50 ± 0.66 ml · 100 g 1 · min 1 · mmHg 1 )
was increased by ANG II
AT 1 -receptor blockade (8.48 ± 0.83 ml · 100 g 1 · min 1 · mmHg 1 )
and decreased by NOS inhibition (2.68 ± 0.22 ml · 100 g 1 · min 1 · mmHg 1 ;
both P < 0.05 vs. unblocked), but it
was unaltered during combined inhibition (4.65 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 ).
Because our findings during combined blockade could be predicted from
the independent actions of NO and ANG II, no interaction was apparent
between these two substances in control or heart failure animals. In
skeletal muscle, L -NAME-induced
reductions in conductance, compared with unblocked exercise
( P < 0.05), were abolished during
combined inhibition in heart failure but not in control rats. These
observations suggest that ANG II causes vasoconstriction in skeletal
muscle that is masked by NO-evoked dilation in animals with heart
failure. Because reductions in vascular conductance between unblocked
exercise and combined inhibition were less than would be predicted from
the independent actions of NO and ANG II, an interaction exists between
these two substances in heart failure rats.
L -NAME-induced increases in
arterial pressure during treadmill running were attenuated
( P < 0.05) similarly in both groups
by combined inhibition. These findings indicate that NO opposes ANG
II-induced increases in arterial pressure and in renal and
skeletal muscle resistance during dynamic exercise.
regional blood flow; vascular resistance; vascular conductance; N G -nitro- L -arginine
methyl ester; losartan</description><subject>Anatomy & physiology</subject><subject>Angiotensin II - chemistry</subject><subject>Angiotensin Receptor Antagonists</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood pressure</subject><subject>Blood Pressure - drug effects</subject><subject>Blood vessels</subject><subject>Cardiology. Vascular system</subject><subject>Exercise</subject><subject>Female</subject><subject>Gases</subject><subject>Heart</subject><subject>Heart Diseases - physiopathology</subject><subject>Heart failure</subject><subject>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</subject><subject>Heart Rate - drug effects</subject><subject>Losartan - pharmacology</subject><subject>Medical sciences</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - chemistry</subject><subject>Nitric Oxide Synthase - antagonists & inhibitors</subject><subject>Physical Conditioning, Animal - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor, Angiotensin, Type 1</subject><subject>Receptor, Angiotensin, Type 2</subject><subject>Regional Blood Flow - drug effects</subject><subject>Rodents</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kd-LEzEQx4MoXj39CwQJIvrUNT92N5tHOTwtHPhyPoc0mW1T0mRNslz735teKx6CT8PMfL4zw3wRektJQ2nHPu_0NPmGSimbQTSs6UT7DC1qhy1pT-hztBhER5aiG8QVepXzjhDath19ia4oadu2p90CwSoUSNoUF0PGaygPAAHrsHGxQMgu4NWqphYHV5IzOB6cBWzn5MIGwwGScRlwxUJMe-0f0S3oVPConZ8T4KRLfo1ejNpneHOJ1-jn7df7m-_Lux_fVjdf7pamlbIs9VoTTi0VvSWsY2KsVclty0ZCDKvBEs35SOhoNdS-BMPt2ppBtJ0ZuOXX6ON57pTirxlyUXuXDXivA8Q5q17KXnSMV_D9P-AuzinU2xRjjPYDJbRC_AyZFHNOMKopub1OR0WJOlmgHi1QJwvUIBRT1YKqencZPa_3YJ9ozj-vwIcLoLPRfkw61Cf-5QYp-qGv2KcztnWb7YNLoKbtMbvo4-Z4Wvx0I_8_eTt7fw-HcpL8UajJjvw3hV2xjg</recordid><startdate>19990801</startdate><enddate>19990801</enddate><creator>Symons, J. David</creator><creator>Stebbins, Charles L</creator><creator>Musch, Timothy I</creator><general>Am Physiological Soc</general><general>American Physiological Society</general><scope>IQODW</scope><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>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19990801</creationdate><title>Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats</title><author>Symons, J. David ; Stebbins, Charles L ; Musch, Timothy I</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-aba031d176d02527f49993d42f00c242fd0a33f01fdae5279ec3dbdc8745c83d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Anatomy & physiology</topic><topic>Angiotensin II - chemistry</topic><topic>Angiotensin Receptor Antagonists</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood pressure</topic><topic>Blood Pressure - drug effects</topic><topic>Blood vessels</topic><topic>Cardiology. Vascular system</topic><topic>Exercise</topic><topic>Female</topic><topic>Gases</topic><topic>Heart</topic><topic>Heart Diseases - physiopathology</topic><topic>Heart failure</topic><topic>Heart failure, cardiogenic pulmonary edema, cardiac enlargement</topic><topic>Heart Rate - drug effects</topic><topic>Losartan - pharmacology</topic><topic>Medical sciences</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - chemistry</topic><topic>Nitric Oxide Synthase - antagonists & inhibitors</topic><topic>Physical Conditioning, Animal - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor, Angiotensin, Type 1</topic><topic>Receptor, Angiotensin, Type 2</topic><topic>Regional Blood Flow - drug effects</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Symons, J. David</creatorcontrib><creatorcontrib>Stebbins, Charles L</creatorcontrib><creatorcontrib>Musch, Timothy I</creatorcontrib><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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Symons, J. David</au><au>Stebbins, Charles L</au><au>Musch, Timothy I</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>1999-08-01</date><risdate>1999</risdate><volume>87</volume><issue>2</issue><spage>574</spage><epage>581</epage><pages>574-581</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>1 Division of Cardiovascular
Medicine, Department of Internal Medicine, University of California,
Davis, California 95616; and
2 Departments of Kinesiology and
of Anatomy and Physiology, Kansas State University, Manhattan,
Kansas 66506
We hypothesized that nitric oxide (NO) opposes ANG II-induced
increases in arterial pressure and reductions in renal, splanchnic, and
skeletal muscle vascular conductance during dynamic exercise in normal
and heart failure rats. Regional blood flow and vascular conductance
were measured during treadmill running before (unblocked exercise) and
after 1 ) ANG II
AT 1 -receptor blockade (losartan, 20 mg/kg ia), 2 ) NO synthase (NOS)
inhibition
[ N G -nitro- L -arginine
methyl ester ( L -NAME); 10 mg/kg
ia], or 3 ) ANG II
AT 1 -receptor blockade + NOS
inhibition (combined blockade). Renal conductance during unblocked
exercise (4.79 ± 0.31 ml · 100 g 1 · min 1 · mmHg 1 )
was increased after ANG II
AT 1 -receptor blockade (6.53 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 )
and decreased by NOS inhibition (2.12 ± 0.20 ml · 100 g 1 · min 1 · mmHg 1 )
and combined inhibition (3.96 ± 0.57 ml · 100 g 1 · min 1 · mmHg 1 ;all
P < 0.05 vs. unblocked). In heart
failure rats, renal conductance during unblocked exercise (5.50 ± 0.66 ml · 100 g 1 · min 1 · mmHg 1 )
was increased by ANG II
AT 1 -receptor blockade (8.48 ± 0.83 ml · 100 g 1 · min 1 · mmHg 1 )
and decreased by NOS inhibition (2.68 ± 0.22 ml · 100 g 1 · min 1 · mmHg 1 ;
both P < 0.05 vs. unblocked), but it
was unaltered during combined inhibition (4.65 ± 0.51 ml · 100 g 1 · min 1 · mmHg 1 ).
Because our findings during combined blockade could be predicted from
the independent actions of NO and ANG II, no interaction was apparent
between these two substances in control or heart failure animals. In
skeletal muscle, L -NAME-induced
reductions in conductance, compared with unblocked exercise
( P < 0.05), were abolished during
combined inhibition in heart failure but not in control rats. These
observations suggest that ANG II causes vasoconstriction in skeletal
muscle that is masked by NO-evoked dilation in animals with heart
failure. Because reductions in vascular conductance between unblocked
exercise and combined inhibition were less than would be predicted from
the independent actions of NO and ANG II, an interaction exists between
these two substances in heart failure rats.
L -NAME-induced increases in
arterial pressure during treadmill running were attenuated
( P < 0.05) similarly in both groups
by combined inhibition. These findings indicate that NO opposes ANG
II-induced increases in arterial pressure and in renal and
skeletal muscle resistance during dynamic exercise.
regional blood flow; vascular resistance; vascular conductance; N G -nitro- L -arginine
methyl ester; losartan</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>10444615</pmid><doi>10.1152/jappl.1999.87.2.574</doi><tpages>8</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 8750-7587 |
| ispartof | Journal of applied physiology (1985), 1999-08, Vol.87 (2), p.574-581 |
| issn | 8750-7587 1522-1601 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_69967523 |
| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Anatomy & physiology Angiotensin II - chemistry Angiotensin Receptor Antagonists Animals Biological and medical sciences Blood pressure Blood Pressure - drug effects Blood vessels Cardiology. Vascular system Exercise Female Gases Heart Heart Diseases - physiopathology Heart failure Heart failure, cardiogenic pulmonary edema, cardiac enlargement Heart Rate - drug effects Losartan - pharmacology Medical sciences NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - chemistry Nitric Oxide Synthase - antagonists & inhibitors Physical Conditioning, Animal - physiology Rats Rats, Wistar Receptor, Angiotensin, Type 1 Receptor, Angiotensin, Type 2 Regional Blood Flow - drug effects Rodents |
| title | Interactions between angiotensin II and nitric oxide during exercise in normal and heart failure rats |
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