Altered pressure natriuresis in chronic angiotensin II hypertension in rats
J. van der Mark and R. L. Kline Department of Physiology, University of Western Ontario, London, Canada. Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats drinking 1% NaCl. The acute pressure-natriuresis rela...
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| Veröffentlicht in: | American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 1994-03, Vol.266 (3), p.739-R748 |
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| container_title | American journal of physiology. Regulatory, integrative and comparative physiology |
| container_volume | 266 |
| creator | van der Mark, J Kline, R. L |
| description | J. van der Mark and R. L. Kline
Department of Physiology, University of Western Ontario, London, Canada.
Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in
unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats
drinking 1% NaCl. The acute pressure-natriuresis relationship was studied
under Inactin anesthesia in volume-expanded rats with fixed neurohumoral
influences on the remaining kidney. Renal interstitial hydrostatic pressure
(RIHP) was measured using a catheter implanted into the renal cortex.
Arterial blood pressure before laparotomy was 149 +/- 3 (SE) mmHg (n = 6)
and 152 +/- 6 mmHg (n = 16) for ANG II-infused rats (10 and 30 ng/min,
respectively) and 123 +/- 5 mmHg (n = 6) and 123 +/- 7 mmHg (n = 16) for
the respective control rats. Compared with values in control rats, ANG
II-infused rats had significantly (P < 0.05) lower urine flow and
absolute and fractional sodium excretion at renal artery pressures of
115-150 mmHg. There were no significant differences between RIHP measured
in control and ANG II-hypertensive rats. The shift in the
pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium
excretion relationships was similar with both doses of ANG II and was
reversed by the acute administration of losartan (10 mg/kg iv). In all
groups of rats, renal blood flow was autoregulated, whereas glomerular
filtration rate was not autoregulated in ANG II-infused rats and was
significantly lower than that in control rats at the lower level of renal
artery pressure. The data indicate that rats with ANG II-induced
hypertension have a rightward shift of the pressure-natriuresis curve
caused primarily by a decrease in fractional excretion of sodium. The lack
of effect of chronic ANG II infusion on filtration fraction and RIHP
suggests that the increased tubular reabsorption was due to a direct action
of ANG II on renal tubules. The reversal of these effects by losartan
suggests that the shift in the pressure-natriuresis curve in ANG II-induced
hypertension is mediated by the AT1-receptor subtype. |
| doi_str_mv | 10.1152/ajpregu.1994.266.3.R739 |
| format | Article |
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Department of Physiology, University of Western Ontario, London, Canada.
Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in
unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats
drinking 1% NaCl. The acute pressure-natriuresis relationship was studied
under Inactin anesthesia in volume-expanded rats with fixed neurohumoral
influences on the remaining kidney. Renal interstitial hydrostatic pressure
(RIHP) was measured using a catheter implanted into the renal cortex.
Arterial blood pressure before laparotomy was 149 +/- 3 (SE) mmHg (n = 6)
and 152 +/- 6 mmHg (n = 16) for ANG II-infused rats (10 and 30 ng/min,
respectively) and 123 +/- 5 mmHg (n = 6) and 123 +/- 7 mmHg (n = 16) for
the respective control rats. Compared with values in control rats, ANG
II-infused rats had significantly (P < 0.05) lower urine flow and
absolute and fractional sodium excretion at renal artery pressures of
115-150 mmHg. There were no significant differences between RIHP measured
in control and ANG II-hypertensive rats. The shift in the
pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium
excretion relationships was similar with both doses of ANG II and was
reversed by the acute administration of losartan (10 mg/kg iv). In all
groups of rats, renal blood flow was autoregulated, whereas glomerular
filtration rate was not autoregulated in ANG II-infused rats and was
significantly lower than that in control rats at the lower level of renal
artery pressure. The data indicate that rats with ANG II-induced
hypertension have a rightward shift of the pressure-natriuresis curve
caused primarily by a decrease in fractional excretion of sodium. The lack
of effect of chronic ANG II infusion on filtration fraction and RIHP
suggests that the increased tubular reabsorption was due to a direct action
of ANG II on renal tubules. The reversal of these effects by losartan
suggests that the shift in the pressure-natriuresis curve in ANG II-induced
hypertension is mediated by the AT1-receptor subtype.</description><identifier>ISSN: 0363-6119</identifier><identifier>ISSN: 0002-9513</identifier><identifier>EISSN: 1522-1490</identifier><identifier>DOI: 10.1152/ajpregu.1994.266.3.R739</identifier><identifier>PMID: 8160866</identifier><language>eng</language><publisher>United States</publisher><subject>Angiotensin II ; Angiotensin Receptor Antagonists ; Animals ; Biphenyl Compounds - pharmacology ; Blood Pressure ; Chronic Disease ; Hypertension - chemically induced ; Hypertension - physiopathology ; Imidazoles - pharmacology ; Losartan ; Male ; Natriuresis ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Tetrazoles - pharmacology</subject><ispartof>American journal of physiology. Regulatory, integrative and comparative physiology, 1994-03, Vol.266 (3), p.739-R748</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c347t-140219b175c1922ffb05b4f973505433967c95955b8fedb59850fef641e7bbe03</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8160866$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van der Mark, J</creatorcontrib><creatorcontrib>Kline, R. L</creatorcontrib><title>Altered pressure natriuresis in chronic angiotensin II hypertension in rats</title><title>American journal of physiology. Regulatory, integrative and comparative physiology</title><addtitle>Am J Physiol</addtitle><description>J. van der Mark and R. L. Kline
Department of Physiology, University of Western Ontario, London, Canada.
Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in
unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats
drinking 1% NaCl. The acute pressure-natriuresis relationship was studied
under Inactin anesthesia in volume-expanded rats with fixed neurohumoral
influences on the remaining kidney. Renal interstitial hydrostatic pressure
(RIHP) was measured using a catheter implanted into the renal cortex.
Arterial blood pressure before laparotomy was 149 +/- 3 (SE) mmHg (n = 6)
and 152 +/- 6 mmHg (n = 16) for ANG II-infused rats (10 and 30 ng/min,
respectively) and 123 +/- 5 mmHg (n = 6) and 123 +/- 7 mmHg (n = 16) for
the respective control rats. Compared with values in control rats, ANG
II-infused rats had significantly (P < 0.05) lower urine flow and
absolute and fractional sodium excretion at renal artery pressures of
115-150 mmHg. There were no significant differences between RIHP measured
in control and ANG II-hypertensive rats. The shift in the
pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium
excretion relationships was similar with both doses of ANG II and was
reversed by the acute administration of losartan (10 mg/kg iv). In all
groups of rats, renal blood flow was autoregulated, whereas glomerular
filtration rate was not autoregulated in ANG II-infused rats and was
significantly lower than that in control rats at the lower level of renal
artery pressure. The data indicate that rats with ANG II-induced
hypertension have a rightward shift of the pressure-natriuresis curve
caused primarily by a decrease in fractional excretion of sodium. The lack
of effect of chronic ANG II infusion on filtration fraction and RIHP
suggests that the increased tubular reabsorption was due to a direct action
of ANG II on renal tubules. The reversal of these effects by losartan
suggests that the shift in the pressure-natriuresis curve in ANG II-induced
hypertension is mediated by the AT1-receptor subtype.</description><subject>Angiotensin II</subject><subject>Angiotensin Receptor Antagonists</subject><subject>Animals</subject><subject>Biphenyl Compounds - pharmacology</subject><subject>Blood Pressure</subject><subject>Chronic Disease</subject><subject>Hypertension - chemically induced</subject><subject>Hypertension - physiopathology</subject><subject>Imidazoles - pharmacology</subject><subject>Losartan</subject><subject>Male</subject><subject>Natriuresis</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reference Values</subject><subject>Tetrazoles - pharmacology</subject><issn>0363-6119</issn><issn>0002-9513</issn><issn>1522-1490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1994</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkF1LwzAUhoMoc05_gtg_0Jo0X83lED-GA0H0OjTdSZuxtSXpkP57UzeGVzk573lfznkQeiA4I4Tnj-W291AfMqIUy3IhMpp9Sqou0DyqeUqYwpdojqmgqSBEXaObELYYY0YZnaFZQQQuhJij9-VuAA-bJMaFcPCQtOXgXSyCC4lrk6rxXeuqpGxr1w3QhthbrZJm7MH_fbt2GvPlEG7RlS13Ae5O7wJ9vzx_Pb2l64_X1dNynVaUySHuhnOiDJG8IirPrTWYG2aVpBxzRqkSslJccW4KCxvDVcGxBSsYAWkMYLpA8phb-S4ED1b33u1LP2qC9URHn-joiY6OdDTVE53ovD86-4PZw-bsO-GIenrUG1c3P86D7psxnrjr6vEc-i_vFwILc-w</recordid><startdate>19940301</startdate><enddate>19940301</enddate><creator>van der Mark, J</creator><creator>Kline, R. L</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>19940301</creationdate><title>Altered pressure natriuresis in chronic angiotensin II hypertension in rats</title><author>van der Mark, J ; Kline, R. L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c347t-140219b175c1922ffb05b4f973505433967c95955b8fedb59850fef641e7bbe03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1994</creationdate><topic>Angiotensin II</topic><topic>Angiotensin Receptor Antagonists</topic><topic>Animals</topic><topic>Biphenyl Compounds - pharmacology</topic><topic>Blood Pressure</topic><topic>Chronic Disease</topic><topic>Hypertension - chemically induced</topic><topic>Hypertension - physiopathology</topic><topic>Imidazoles - pharmacology</topic><topic>Losartan</topic><topic>Male</topic><topic>Natriuresis</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reference Values</topic><topic>Tetrazoles - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van der Mark, J</creatorcontrib><creatorcontrib>Kline, R. L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van der Mark, J</au><au>Kline, R. L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Altered pressure natriuresis in chronic angiotensin II hypertension in rats</atitle><jtitle>American journal of physiology. Regulatory, integrative and comparative physiology</jtitle><addtitle>Am J Physiol</addtitle><date>1994-03-01</date><risdate>1994</risdate><volume>266</volume><issue>3</issue><spage>739</spage><epage>R748</epage><pages>739-R748</pages><issn>0363-6119</issn><issn>0002-9513</issn><eissn>1522-1490</eissn><abstract>J. van der Mark and R. L. Kline
Department of Physiology, University of Western Ontario, London, Canada.
Angiotensin II (ANG II; 10 or 30 ng/min iv) was infused for 7-10 days in
unilaterally adrenalectomized and nephrectomized Sprague-Dawley rats
drinking 1% NaCl. The acute pressure-natriuresis relationship was studied
under Inactin anesthesia in volume-expanded rats with fixed neurohumoral
influences on the remaining kidney. Renal interstitial hydrostatic pressure
(RIHP) was measured using a catheter implanted into the renal cortex.
Arterial blood pressure before laparotomy was 149 +/- 3 (SE) mmHg (n = 6)
and 152 +/- 6 mmHg (n = 16) for ANG II-infused rats (10 and 30 ng/min,
respectively) and 123 +/- 5 mmHg (n = 6) and 123 +/- 7 mmHg (n = 16) for
the respective control rats. Compared with values in control rats, ANG
II-infused rats had significantly (P < 0.05) lower urine flow and
absolute and fractional sodium excretion at renal artery pressures of
115-150 mmHg. There were no significant differences between RIHP measured
in control and ANG II-hypertensive rats. The shift in the
pressure-diuresis, pressure-natriuresis, and pressure-fractional sodium
excretion relationships was similar with both doses of ANG II and was
reversed by the acute administration of losartan (10 mg/kg iv). In all
groups of rats, renal blood flow was autoregulated, whereas glomerular
filtration rate was not autoregulated in ANG II-infused rats and was
significantly lower than that in control rats at the lower level of renal
artery pressure. The data indicate that rats with ANG II-induced
hypertension have a rightward shift of the pressure-natriuresis curve
caused primarily by a decrease in fractional excretion of sodium. The lack
of effect of chronic ANG II infusion on filtration fraction and RIHP
suggests that the increased tubular reabsorption was due to a direct action
of ANG II on renal tubules. The reversal of these effects by losartan
suggests that the shift in the pressure-natriuresis curve in ANG II-induced
hypertension is mediated by the AT1-receptor subtype.</abstract><cop>United States</cop><pmid>8160866</pmid><doi>10.1152/ajpregu.1994.266.3.R739</doi></addata></record> |
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| source | MEDLINE; Alma/SFX Local Collection |
| subjects | Angiotensin II Angiotensin Receptor Antagonists Animals Biphenyl Compounds - pharmacology Blood Pressure Chronic Disease Hypertension - chemically induced Hypertension - physiopathology Imidazoles - pharmacology Losartan Male Natriuresis Rats Rats, Sprague-Dawley Reference Values Tetrazoles - pharmacology |
| title | Altered pressure natriuresis in chronic angiotensin II hypertension in rats |
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