Role of the native kidney in experimental post-transplantation hypertension
Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensiv...
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| Autor*in: |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1996 |
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| Umfang: |
6 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Pflügers Archiv - 1868, 431(1996) vom: Juni, Seite 971-976 |
| Übergeordnetes Werk: |
volume:431 ; year:1996 ; month:06 ; pages:971-976 ; extent:6 |
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| 520 | |a Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. | ||
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(DE-627)NLEJ201007886 DE-627 ger DE-627 rakwb eng Role of the native kidney in experimental post-transplantation hypertension 1996 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. Springer Online Journal Archives 1860-2002 Sander, Steffen oth Ehrig, Burghard oth Rettig, R. oth in Pflügers Archiv 1868 431(1996) vom: Juni, Seite 971-976 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:431 year:1996 month:06 pages:971-976 extent:6 http://dx.doi.org/10.1007/s004240050093 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 431 1996 6 971-976 6 |
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(DE-627)NLEJ201007886 DE-627 ger DE-627 rakwb eng Role of the native kidney in experimental post-transplantation hypertension 1996 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. Springer Online Journal Archives 1860-2002 Sander, Steffen oth Ehrig, Burghard oth Rettig, R. oth in Pflügers Archiv 1868 431(1996) vom: Juni, Seite 971-976 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:431 year:1996 month:06 pages:971-976 extent:6 http://dx.doi.org/10.1007/s004240050093 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 431 1996 6 971-976 6 |
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(DE-627)NLEJ201007886 DE-627 ger DE-627 rakwb eng Role of the native kidney in experimental post-transplantation hypertension 1996 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. Springer Online Journal Archives 1860-2002 Sander, Steffen oth Ehrig, Burghard oth Rettig, R. oth in Pflügers Archiv 1868 431(1996) vom: Juni, Seite 971-976 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:431 year:1996 month:06 pages:971-976 extent:6 http://dx.doi.org/10.1007/s004240050093 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 431 1996 6 971-976 6 |
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(DE-627)NLEJ201007886 DE-627 ger DE-627 rakwb eng Role of the native kidney in experimental post-transplantation hypertension 1996 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. Springer Online Journal Archives 1860-2002 Sander, Steffen oth Ehrig, Burghard oth Rettig, R. oth in Pflügers Archiv 1868 431(1996) vom: Juni, Seite 971-976 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:431 year:1996 month:06 pages:971-976 extent:6 http://dx.doi.org/10.1007/s004240050093 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 431 1996 6 971-976 6 |
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(DE-627)NLEJ201007886 DE-627 ger DE-627 rakwb eng Role of the native kidney in experimental post-transplantation hypertension 1996 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. Springer Online Journal Archives 1860-2002 Sander, Steffen oth Ehrig, Burghard oth Rettig, R. oth in Pflügers Archiv 1868 431(1996) vom: Juni, Seite 971-976 (DE-627)NLEJ188987363 (DE-600)1463014-x 1432-2013 nnns volume:431 year:1996 month:06 pages:971-976 extent:6 http://dx.doi.org/10.1007/s004240050093 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 431 1996 6 971-976 6 |
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Role of the native kidney in experimental post-transplantation hypertension |
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Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. |
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Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. |
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Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ201007886</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210706064558.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070527s1996 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ201007886</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Role of the native kidney in experimental post-transplantation hypertension</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1996</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract In experimental renal transplantation studies using several animal models of primary hypertension, including stroke-prone spontaneously hypertensive rats (SHRSP) and their normotensive Wistar-Kyoto controls (WKY), single transplanted kidneys from genetically hypertensive but not normotensive donors elicited post-transplantation hypertension in bilaterally nephrectomized genetically normotensive recipients. The underlying mechanisms are presently unclear. The present study was designed to investigate the effects of a remaining native kidney on post-transplantation blood pressure, plasma renin activity and plasma angiotensin II concentration in (WKY×SHRSP) F1 hybrid recipients of a WKY or SHRSP kidney. The presence of a native kidney markedly reduced, but did not prevent, post-transplantation hypertension in recipients of an SHRSP kidney. WKY kidney grafts did not significantly alter blood pressure in bilaterally or unilaterally nephrectomized recipients. Plasma renin activity was lower in bilaterally than in unilaterally nephrectomized recipients, regardless of the source of the graft. The plasma angiotensin II concentration was similar in all groups. Renal graft function as assessed by 99mtechnetium-mercaptoacetyltriglycine scintigraphy was well preserved. These data suggest that post-transplantation hypertension in recipients of an SHRSP kidney may be partly due to the failure of the graft to eliminate a hypertensinogenic substance or to produce a blood pressure lowering agent.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sander, Steffen</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ehrig, Burghard</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rettig, R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Pflügers Archiv</subfield><subfield code="d">1868</subfield><subfield code="g">431(1996) vom: Juni, Seite 971-976</subfield><subfield code="w">(DE-627)NLEJ188987363</subfield><subfield code="w">(DE-600)1463014-x</subfield><subfield code="x">1432-2013</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:431</subfield><subfield code="g">year:1996</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:971-976</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/s004240050093</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">431</subfield><subfield code="j">1996</subfield><subfield code="c">6</subfield><subfield code="h">971-976</subfield><subfield code="g">6</subfield></datafield></record></collection>
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