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Background of Increased Flow Resistance and Vascular Reactivity in Spontaneously Hypertensive Rats
The hindquarters of a spontaneously hypertensive rat (SHR) and a matched normotensive control rat (NCR) were perfused at a constant rate of flow with oxygenated plasma substitute in 15 paired experiments. As is the case in the entire systemic vascular bed (Folkow et al. 1969), flow resistance was ra...
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Published in: | Acta physiologica Scandinavica 1970-09, Vol.80 (1), p.93-106 |
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description | The hindquarters of a spontaneously hypertensive rat (SHR) and a matched normotensive control rat (NCR) were perfused at a constant rate of flow with oxygenated plasma substitute in 15 paired experiments. As is the case in the entire systemic vascular bed (Folkow et al. 1969), flow resistance was raised even during maximal dilatation in SHR (p |
doi_str_mv | 10.1111/j.1748-1716.1970.tb04773.x |
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As is the case in the entire systemic vascular bed (Folkow et al. 1969), flow resistance was raised even during maximal dilatation in SHR (p<0.001), almost in proportion to their raised blood pressure. Graded noradrenaline (NA) infusions showed identical NA “thresholds”, while SHR displayed a steeper curve, relating log NA dose to resistance response (p<0.001) and a greater maximal contractile strength of the resistance vessels (p<0.001). These characteristics of the resistance curves for SHR and NCR were compared with those mathematically deduced for two hypothetical vessels, identical except for the presence in one of them of a 30 per cent increase of its media thickness encroaching upon its lumen even at complete relaxation. In all essential points the relationships between the two sets of curves were the same while no other type of vascular change, structural or functional, could alone reproduce all the characteristics of the SHR curve. The results therefore suggest the presence of an increased contractile wall mass in the systemic resistance vessels of SHR encroaching upon their lumina even during maximal dilatation. Without necessitating any increased smooth muscle activity the haemodynamic effects of the proposed structural change can largely alone account for the raised resistance and increased vascular “reactivity” in SHR.</description><identifier>ISSN: 0001-6772</identifier><identifier>EISSN: 1365-201X</identifier><identifier>DOI: 10.1111/j.1748-1716.1970.tb04773.x</identifier><identifier>PMID: 5475335</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Animals ; Blood Pressure ; Blood Vessels - drug effects ; Blood Vessels - physiopathology ; Dilatation ; Hypertension - physiopathology ; Norepinephrine - pharmacology ; Perfusion ; Rats ; Vascular Resistance</subject><ispartof>Acta physiologica Scandinavica, 1970-09, Vol.80 (1), p.93-106</ispartof><rights>1970 Scandinavian Physiological Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4733-5d2a2e56becd0465276ade5174c56d488c3b9b19ffbeca2bbb53ccdc15c7e0173</citedby><cites>FETCH-LOGICAL-c4733-5d2a2e56becd0465276ade5174c56d488c3b9b19ffbeca2bbb53ccdc15c7e0173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fj.1748-1716.1970.tb04773.x$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fj.1748-1716.1970.tb04773.x$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1415,27922,27923,46047,46471</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/5475335$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Folkow, Björn</creatorcontrib><creatorcontrib>Hallbäck, Margareta</creatorcontrib><creatorcontrib>Lundgren, Yen</creatorcontrib><creatorcontrib>Weiss, Lilian</creatorcontrib><title>Background of Increased Flow Resistance and Vascular Reactivity in Spontaneously Hypertensive Rats</title><title>Acta physiologica Scandinavica</title><addtitle>Acta Physiol Scand</addtitle><description>The hindquarters of a spontaneously hypertensive rat (SHR) and a matched normotensive control rat (NCR) were perfused at a constant rate of flow with oxygenated plasma substitute in 15 paired experiments. As is the case in the entire systemic vascular bed (Folkow et al. 1969), flow resistance was raised even during maximal dilatation in SHR (p<0.001), almost in proportion to their raised blood pressure. Graded noradrenaline (NA) infusions showed identical NA “thresholds”, while SHR displayed a steeper curve, relating log NA dose to resistance response (p<0.001) and a greater maximal contractile strength of the resistance vessels (p<0.001). These characteristics of the resistance curves for SHR and NCR were compared with those mathematically deduced for two hypothetical vessels, identical except for the presence in one of them of a 30 per cent increase of its media thickness encroaching upon its lumen even at complete relaxation. In all essential points the relationships between the two sets of curves were the same while no other type of vascular change, structural or functional, could alone reproduce all the characteristics of the SHR curve. The results therefore suggest the presence of an increased contractile wall mass in the systemic resistance vessels of SHR encroaching upon their lumina even during maximal dilatation. Without necessitating any increased smooth muscle activity the haemodynamic effects of the proposed structural change can largely alone account for the raised resistance and increased vascular “reactivity” in SHR.</description><subject>Animals</subject><subject>Blood Pressure</subject><subject>Blood Vessels - drug effects</subject><subject>Blood Vessels - physiopathology</subject><subject>Dilatation</subject><subject>Hypertension - physiopathology</subject><subject>Norepinephrine - pharmacology</subject><subject>Perfusion</subject><subject>Rats</subject><subject>Vascular Resistance</subject><issn>0001-6772</issn><issn>1365-201X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1970</creationdate><recordtype>article</recordtype><recordid>eNqVkF1P2zAUhi00VDrGT0CydrG7ZP6I45SLSS1aWxDdELCPO8t2TlDaNOnsBJp_j6tU3M83ln2e8x77QegzJTEN6-s6pjLJIippGtOJJHFrSCIlj_cnaEx5KiJG6N8PaEwIoVEqJTtDH71fhyPPGBuhkUik4FyMkZlpu3l2TVfnuCnwTW0daA85nlfNK34AX_pW1xawDsBv7W1XaRfutW3Ll7LtcVnjx11TBwiazlc9XvY7cC3UvnwB_KBb_wmdFrrycHHcz9Gv-fen62V093Nxcz29i2wiOY9EzjQDkRqwOUlSwWSqcxDhp1akeZJllpuJoZOiCIRmxhjBrc0tFVYCoZKfoy9D7s41_zrwrdqW3kJVDU9TWSJpxqkI4NUAWtd476BQO1dutesVJeogWK3VQbA6CFYHweooWO1D8-VxSme2kL-3Ho2G-reh_lpW0P9HspreL6cTHgKiISCYh_17gHYblUouhfrzY6FmM_Z0e7taqRV_A8YCnMQ</recordid><startdate>197009</startdate><enddate>197009</enddate><creator>Folkow, Björn</creator><creator>Hallbäck, Margareta</creator><creator>Lundgren, Yen</creator><creator>Weiss, Lilian</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope></search><sort><creationdate>197009</creationdate><title>Background of Increased Flow Resistance and Vascular Reactivity in Spontaneously Hypertensive Rats</title><author>Folkow, Björn ; Hallbäck, Margareta ; Lundgren, Yen ; Weiss, Lilian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4733-5d2a2e56becd0465276ade5174c56d488c3b9b19ffbeca2bbb53ccdc15c7e0173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1970</creationdate><topic>Animals</topic><topic>Blood Pressure</topic><topic>Blood Vessels - drug effects</topic><topic>Blood Vessels - physiopathology</topic><topic>Dilatation</topic><topic>Hypertension - physiopathology</topic><topic>Norepinephrine - pharmacology</topic><topic>Perfusion</topic><topic>Rats</topic><topic>Vascular Resistance</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Folkow, Björn</creatorcontrib><creatorcontrib>Hallbäck, Margareta</creatorcontrib><creatorcontrib>Lundgren, Yen</creatorcontrib><creatorcontrib>Weiss, Lilian</creatorcontrib><collection>Istex</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><jtitle>Acta physiologica Scandinavica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Folkow, Björn</au><au>Hallbäck, Margareta</au><au>Lundgren, Yen</au><au>Weiss, Lilian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Background of Increased Flow Resistance and Vascular Reactivity in Spontaneously Hypertensive Rats</atitle><jtitle>Acta physiologica Scandinavica</jtitle><addtitle>Acta Physiol Scand</addtitle><date>1970-09</date><risdate>1970</risdate><volume>80</volume><issue>1</issue><spage>93</spage><epage>106</epage><pages>93-106</pages><issn>0001-6772</issn><eissn>1365-201X</eissn><abstract>The hindquarters of a spontaneously hypertensive rat (SHR) and a matched normotensive control rat (NCR) were perfused at a constant rate of flow with oxygenated plasma substitute in 15 paired experiments. As is the case in the entire systemic vascular bed (Folkow et al. 1969), flow resistance was raised even during maximal dilatation in SHR (p<0.001), almost in proportion to their raised blood pressure. Graded noradrenaline (NA) infusions showed identical NA “thresholds”, while SHR displayed a steeper curve, relating log NA dose to resistance response (p<0.001) and a greater maximal contractile strength of the resistance vessels (p<0.001). These characteristics of the resistance curves for SHR and NCR were compared with those mathematically deduced for two hypothetical vessels, identical except for the presence in one of them of a 30 per cent increase of its media thickness encroaching upon its lumen even at complete relaxation. In all essential points the relationships between the two sets of curves were the same while no other type of vascular change, structural or functional, could alone reproduce all the characteristics of the SHR curve. The results therefore suggest the presence of an increased contractile wall mass in the systemic resistance vessels of SHR encroaching upon their lumina even during maximal dilatation. Without necessitating any increased smooth muscle activity the haemodynamic effects of the proposed structural change can largely alone account for the raised resistance and increased vascular “reactivity” in SHR.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>5475335</pmid><doi>10.1111/j.1748-1716.1970.tb04773.x</doi><tpages>14</tpages></addata></record> |
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subjects | Animals Blood Pressure Blood Vessels - drug effects Blood Vessels - physiopathology Dilatation Hypertension - physiopathology Norepinephrine - pharmacology Perfusion Rats Vascular Resistance |
title | Background of Increased Flow Resistance and Vascular Reactivity in Spontaneously Hypertensive Rats |
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