Hypertension from Carotid Occlusion Decreases Renal Papillary Plasma Flow, Hypotension from Hemorrhage Increases It, an Autoregulatory Paradox
Renal papillary plasma flow was tested during acute increases and decreases of perfusion pressure using the 125I-labelled albumin technique. Increases of pressure were attained through ligation of carotid arteries; decreases of pressure through modest hemorrhage. In 12 control rats with blood pressu...
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| Veröffentlicht in: | Hypertension Research 1996, Vol.19(1), pp.17-22 |
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| creator | Ganguli, Mukul Tobian, Louis |
| description | Renal papillary plasma flow was tested during acute increases and decreases of perfusion pressure using the 125I-labelled albumin technique. Increases of pressure were attained through ligation of carotid arteries; decreases of pressure through modest hemorrhage. In 12 control rats with blood pressure of 144mmHg, the papillary plasma flow averaged 21.5ml per 100g papilla per min. In 12 rats after ligation of carotid arteries, blood pressure rose from 143mmHg to 172, a 20% increase. The papillary plasma flow in these rats with acute hypertension averaged 17.9ml per 100g papilla per min, a 17% decrease (p |
| doi_str_mv | 10.1291/hypres.19.17 |
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Increases of pressure were attained through ligation of carotid arteries; decreases of pressure through modest hemorrhage. In 12 control rats with blood pressure of 144mmHg, the papillary plasma flow averaged 21.5ml per 100g papilla per min. In 12 rats after ligation of carotid arteries, blood pressure rose from 143mmHg to 172, a 20% increase. The papillary plasma flow in these rats with acute hypertension averaged 17.9ml per 100g papilla per min, a 17% decrease (p<0.025). In another 12 rats after bleeding 1% of body weight over a period of 10min, blood pressure dropped from 146mmHg to 104, a 29% decrease. The papillary plasma flow in these rats with acute hypotension averaged 26.0ml per 100g papilla per min, a 21% increase (p<0.025). The decrease in papillary plasma flow during acute hypertension strongly suggests an increased vascular resistance of the descending vasa recta, while the increase in papillary plasma flow during acute hypotension suggests that vasodilatation occurred in these vessels. This dilatation may be produced by the local release of prostaglandins or other vasoactive substances. Thus, the renal papilla appears to "overshoot" its autoregulation of plasma flow, with actual reduced flow during an acute blood pressure rise and increased flow during an acute blood pressure fall, an enigmatic over-compensation. (Hypertens Res 1996; 19: 17-22)</description><identifier>ISSN: 0916-9636</identifier><identifier>EISSN: 1348-4214</identifier><identifier>DOI: 10.1291/hypres.19.17</identifier><identifier>PMID: 8829819</identifier><language>eng</language><publisher>England: The Japanese Society of Hypertension</publisher><subject>Animals ; Blood Pressure - physiology ; carotid ligation ; Carotid Stenosis - complications ; Carotid Stenosis - physiopathology ; Hematocrit ; hemorrhage ; Hemorrhage - complications ; Hemorrhage - physiopathology ; Homeostasis - physiology ; hypertension ; Hypertension - etiology ; Hypertension - physiopathology ; hypotension ; Hypotension - etiology ; Hypotension - physiopathology ; Kidney Medulla - blood supply ; Male ; Rats ; Rats, Sprague-Dawley ; Renal Circulation - physiology ; renal papillary autoregulation ; Sodium - metabolism ; Urea - metabolism ; Vascular Resistance - physiology</subject><ispartof>Hypertension Research, 1996, Vol.19(1), pp.17-22</ispartof><rights>The Japanese Society of Hypertension</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3967-31c38aa9bbc861d2032de1c9cb9c0b48495352c061dc19abc55612aebb7e799f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,1877,4010,27900,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8829819$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ganguli, Mukul</creatorcontrib><creatorcontrib>Tobian, Louis</creatorcontrib><title>Hypertension from Carotid Occlusion Decreases Renal Papillary Plasma Flow, Hypotension from Hemorrhage Increases It, an Autoregulatory Paradox</title><title>Hypertension Research</title><addtitle>Hypertension Research</addtitle><description>Renal papillary plasma flow was tested during acute increases and decreases of perfusion pressure using the 125I-labelled albumin technique. Increases of pressure were attained through ligation of carotid arteries; decreases of pressure through modest hemorrhage. In 12 control rats with blood pressure of 144mmHg, the papillary plasma flow averaged 21.5ml per 100g papilla per min. In 12 rats after ligation of carotid arteries, blood pressure rose from 143mmHg to 172, a 20% increase. The papillary plasma flow in these rats with acute hypertension averaged 17.9ml per 100g papilla per min, a 17% decrease (p<0.025). In another 12 rats after bleeding 1% of body weight over a period of 10min, blood pressure dropped from 146mmHg to 104, a 29% decrease. The papillary plasma flow in these rats with acute hypotension averaged 26.0ml per 100g papilla per min, a 21% increase (p<0.025). The decrease in papillary plasma flow during acute hypertension strongly suggests an increased vascular resistance of the descending vasa recta, while the increase in papillary plasma flow during acute hypotension suggests that vasodilatation occurred in these vessels. This dilatation may be produced by the local release of prostaglandins or other vasoactive substances. Thus, the renal papilla appears to "overshoot" its autoregulation of plasma flow, with actual reduced flow during an acute blood pressure rise and increased flow during an acute blood pressure fall, an enigmatic over-compensation. (Hypertens Res 1996; 19: 17-22)</description><subject>Animals</subject><subject>Blood Pressure - physiology</subject><subject>carotid ligation</subject><subject>Carotid Stenosis - complications</subject><subject>Carotid Stenosis - physiopathology</subject><subject>Hematocrit</subject><subject>hemorrhage</subject><subject>Hemorrhage - complications</subject><subject>Hemorrhage - physiopathology</subject><subject>Homeostasis - physiology</subject><subject>hypertension</subject><subject>Hypertension - etiology</subject><subject>Hypertension - physiopathology</subject><subject>hypotension</subject><subject>Hypotension - etiology</subject><subject>Hypotension - physiopathology</subject><subject>Kidney Medulla - blood supply</subject><subject>Male</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Renal Circulation - physiology</subject><subject>renal papillary autoregulation</subject><subject>Sodium - metabolism</subject><subject>Urea - metabolism</subject><subject>Vascular Resistance - physiology</subject><issn>0916-9636</issn><issn>1348-4214</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkE1r20AQhpfQkjppbr0W9tST5Wq0-tg5BjeJDYGE0p7FaDWOFSStuivR-E_kN3cbq4ZeZmCelwfmFeITxCtIEL7uD4NjvwJcQXEmFqBSHaUJpO_EIkbII8xV_kFceP8cx4nOEM7FudYJasCFeN0cBnYj976xvdw528k1OTs2tXwwpp3ezt_YOCbPXn7nnlr5SEPTtuQO8rEl35G8be3vpQwq-59pw511bk9PLLf9P8V2XErq5fU0WsdPU0thBxE5qu3LR_F-R63nq3lfip-3Nz_Wm-j-4W67vr6PjMK8iBQYpYmwqozOoU5ildQMBk2FJq5SnWKmssTEgRlAqkyW5ZAQV1XBBeJOXYovR-_g7K-J_Vh2jTccnurZTr4sNCjMsjQEl8egcdZ7x7tycE0XXi8hLv_WXx7rLwFLKEL88-ydqo7rU3juO_CbI3_2Y6jlxMmNjWl5lgFi8iacR3HiZk-u5F79Ad5Fnfs</recordid><startdate>1996</startdate><enddate>1996</enddate><creator>Ganguli, Mukul</creator><creator>Tobian, Louis</creator><general>The Japanese Society of Hypertension</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>1996</creationdate><title>Hypertension from Carotid Occlusion Decreases Renal Papillary Plasma Flow, Hypotension from Hemorrhage Increases It, an Autoregulatory Paradox</title><author>Ganguli, Mukul ; Tobian, Louis</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3967-31c38aa9bbc861d2032de1c9cb9c0b48495352c061dc19abc55612aebb7e799f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Animals</topic><topic>Blood Pressure - physiology</topic><topic>carotid ligation</topic><topic>Carotid Stenosis - complications</topic><topic>Carotid Stenosis - physiopathology</topic><topic>Hematocrit</topic><topic>hemorrhage</topic><topic>Hemorrhage - complications</topic><topic>Hemorrhage - physiopathology</topic><topic>Homeostasis - physiology</topic><topic>hypertension</topic><topic>Hypertension - etiology</topic><topic>Hypertension - physiopathology</topic><topic>hypotension</topic><topic>Hypotension - etiology</topic><topic>Hypotension - physiopathology</topic><topic>Kidney Medulla - blood supply</topic><topic>Male</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Renal Circulation - physiology</topic><topic>renal papillary autoregulation</topic><topic>Sodium - metabolism</topic><topic>Urea - metabolism</topic><topic>Vascular Resistance - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ganguli, Mukul</creatorcontrib><creatorcontrib>Tobian, Louis</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 Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ganguli, Mukul</au><au>Tobian, Louis</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypertension from Carotid Occlusion Decreases Renal Papillary Plasma Flow, Hypotension from Hemorrhage Increases It, an Autoregulatory Paradox</atitle><jtitle>Hypertension Research</jtitle><addtitle>Hypertension Research</addtitle><date>1996</date><risdate>1996</risdate><volume>19</volume><issue>1</issue><spage>17</spage><epage>22</epage><pages>17-22</pages><issn>0916-9636</issn><eissn>1348-4214</eissn><abstract>Renal papillary plasma flow was tested during acute increases and decreases of perfusion pressure using the 125I-labelled albumin technique. Increases of pressure were attained through ligation of carotid arteries; decreases of pressure through modest hemorrhage. In 12 control rats with blood pressure of 144mmHg, the papillary plasma flow averaged 21.5ml per 100g papilla per min. In 12 rats after ligation of carotid arteries, blood pressure rose from 143mmHg to 172, a 20% increase. The papillary plasma flow in these rats with acute hypertension averaged 17.9ml per 100g papilla per min, a 17% decrease (p<0.025). In another 12 rats after bleeding 1% of body weight over a period of 10min, blood pressure dropped from 146mmHg to 104, a 29% decrease. The papillary plasma flow in these rats with acute hypotension averaged 26.0ml per 100g papilla per min, a 21% increase (p<0.025). The decrease in papillary plasma flow during acute hypertension strongly suggests an increased vascular resistance of the descending vasa recta, while the increase in papillary plasma flow during acute hypotension suggests that vasodilatation occurred in these vessels. This dilatation may be produced by the local release of prostaglandins or other vasoactive substances. Thus, the renal papilla appears to "overshoot" its autoregulation of plasma flow, with actual reduced flow during an acute blood pressure rise and increased flow during an acute blood pressure fall, an enigmatic over-compensation. (Hypertens Res 1996; 19: 17-22)</abstract><cop>England</cop><pub>The Japanese Society of Hypertension</pub><pmid>8829819</pmid><doi>10.1291/hypres.19.17</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension Research, 1996, Vol.19(1), pp.17-22 |
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| source | J-STAGE Free; MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Blood Pressure - physiology carotid ligation Carotid Stenosis - complications Carotid Stenosis - physiopathology Hematocrit hemorrhage Hemorrhage - complications Hemorrhage - physiopathology Homeostasis - physiology hypertension Hypertension - etiology Hypertension - physiopathology hypotension Hypotension - etiology Hypotension - physiopathology Kidney Medulla - blood supply Male Rats Rats, Sprague-Dawley Renal Circulation - physiology renal papillary autoregulation Sodium - metabolism Urea - metabolism Vascular Resistance - physiology |
| title | Hypertension from Carotid Occlusion Decreases Renal Papillary Plasma Flow, Hypotension from Hemorrhage Increases It, an Autoregulatory Paradox |
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