Autoregulation of renal blood flow in the conscious dog and the contribution of the tubuloglomerular feedback
The aim of this study was to investigate the autoregulation of renal blood flow under physiological conditions, when challenged by the normal pressure fluctuations, and the contribution of the tubuloglomerular feedback (TGF). The transfer function between 0.0018 and 0.5 Hz was calculated from the sp...
Gespeichert in:
| Veröffentlicht in: | The Journal of physiology 1998-01, Vol.506 (1), p.275-290 |
|---|---|
| Hauptverfasser: | , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 290 |
|---|---|
| container_issue | 1 |
| container_start_page | 275 |
| container_title | The Journal of physiology |
| container_volume | 506 |
| creator | Just, Armin Wittmann, Uwe Ehmke, Heimo Kirchheim, Hartmut R. |
| description | The aim of this study was to investigate the autoregulation of renal blood flow under physiological conditions, when challenged
by the normal pressure fluctuations, and the contribution of the tubuloglomerular feedback (TGF).
The transfer function between 0.0018 and 0.5 Hz was calculated from the spontaneous fluctuations in renal arterial blood pressure
(RABP) and renal blood flow (RBF) in conscious resting dogs. The response of RBF to stepwise artificially induced reductions
in RABP was also studied (stepwise autoregulation).
Under control conditions ( n = 12 dogs), the gain of the transfer function started to decrease, indicating improving autoregulation, below 0.06-0.15 Hz
( t = 7-17 s). At 0.027 Hz a prominent peak of high gain was found. Below 0.01 Hz ( t > 100 s), the gain reached a minimum (maximal autoregulation) of -6.3 ± 0.6 dB. The stepwise autoregulation ( n = 4) was much stronger (-19.5 dB). The time delay of the transfer function was remarkably constant from 0.03 to 0.08 Hz (high
frequency (HF) range) at 1.7 s and from 0.0034 to 0.01 Hz (low frequency (LF) range) at 14.3 s, respectively.
Nifedipine, infused into the renal artery, abolished the stepwise autoregulation (-2.0 ± 1.1 dB, n = 3). The gain of the transfer function ( n = 4) remained high down to 0.0034 Hz; in the LF range it was higher than in the control (0.3 ± 1.0 dB, P < 0.05). The time delay in the HF range was reduced to 0.5 s ( P < 0.05).
After ganglionic blockade ( n = 7) no major changes in the transfer function were observed.
Under furosemide (frusemide) (40 mg + 10 mg h â1 or 300 mg + 300 mg h â1 i.v.) the stepwise autoregulation was impaired to -7.8 ± 0.3 or -6.7 ± 1.9 dB, respectively ( n = 4). In the transfer function ( n = 7 or n = 4) the peak at 0.027 Hz was abolished. The delay in the LF range was reduced to -1.1 or -1.6 s, respectively. The transfer
gain in the LF range (-5.5 ± 1.2 or -3.8 ± 0.8 dB, respectively) did not differ from the control but was smaller than that
under nifedipine ( P < 0.05).
It is concluded that the ample capacity for regulation of RBF is only partially employed under physiological conditions. The
abolition by nifedipine and the negligible effect of ganglionic blockade show that above 0.0034 Hz it is almost exclusively
due to autoregulation by the kidney itself. TGF contributes to the maximum autoregulatory capacity, but it is not required
for the level of autoregulation expended under physiological conditions. Around 0.027 Hz, TGF |
| doi_str_mv | 10.1111/j.1469-7793.1998.275bx.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2230714</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>79705475</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5275-d92787087028c029f53c06933d1a4244d04f7b56e620673dd4829c73455283493</originalsourceid><addsrcrecordid>eNqNkV-L1DAUxYso6-zqRxDypE9T87dpQIRlUVdZ0If1OaRJ2mZMmzFpd2a-venO7KBvhkDgnntObvIrCoBgifJ6vykRrcSac0FKJERdYs6afbl_VqzOwvNiBSHGa8IZellcprSBEBEoxEVxIWiNqrpeFcP1PIVou9mryYURhBZEOyoPGh-CAa0PO-BGMPUW6DAm7cKcgAkdUKN5qk7RNfOTe6lNczP70Pkw2JiDI2itNY3Sv14VL1rlk319Oq-Kn58_3d_cru--f_l6c3231iw_ZG0E5jWHeeNaQyxaRjSsBCEGKYopNZC2vGGVrTCsODGG1lhoTihjuCZUkKvi4zF3OzeDNdrmGZWX2-gGFQ8yKCf_VUbXyy48SIwJ5IjmgLengBh-zzZNcnBJW-_VaPMPSC44ZJSz3FgfG3UMKUXbni9BUC6o5EYuRORCRC6o5CMquc_WN38PeTae2GT9w1HfOW8P_50r77_9wI-TvTvae9f1Oxet3PaH5EIK2tnpIBmsJFpM5A_EPLMO</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>79705475</pqid></control><display><type>article</type><title>Autoregulation of renal blood flow in the conscious dog and the contribution of the tubuloglomerular feedback</title><source>MEDLINE</source><source>PMC (PubMed Central)</source><source>Wiley Journals</source><source>IngentaConnect Free/Open Access Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Wiley Online Library (Open Access Collection)</source><creator>Just, Armin ; Wittmann, Uwe ; Ehmke, Heimo ; Kirchheim, Hartmut R.</creator><creatorcontrib>Just, Armin ; Wittmann, Uwe ; Ehmke, Heimo ; Kirchheim, Hartmut R.</creatorcontrib><description>The aim of this study was to investigate the autoregulation of renal blood flow under physiological conditions, when challenged
by the normal pressure fluctuations, and the contribution of the tubuloglomerular feedback (TGF).
The transfer function between 0.0018 and 0.5 Hz was calculated from the spontaneous fluctuations in renal arterial blood pressure
(RABP) and renal blood flow (RBF) in conscious resting dogs. The response of RBF to stepwise artificially induced reductions
in RABP was also studied (stepwise autoregulation).
Under control conditions ( n = 12 dogs), the gain of the transfer function started to decrease, indicating improving autoregulation, below 0.06-0.15 Hz
( t = 7-17 s). At 0.027 Hz a prominent peak of high gain was found. Below 0.01 Hz ( t > 100 s), the gain reached a minimum (maximal autoregulation) of -6.3 ± 0.6 dB. The stepwise autoregulation ( n = 4) was much stronger (-19.5 dB). The time delay of the transfer function was remarkably constant from 0.03 to 0.08 Hz (high
frequency (HF) range) at 1.7 s and from 0.0034 to 0.01 Hz (low frequency (LF) range) at 14.3 s, respectively.
Nifedipine, infused into the renal artery, abolished the stepwise autoregulation (-2.0 ± 1.1 dB, n = 3). The gain of the transfer function ( n = 4) remained high down to 0.0034 Hz; in the LF range it was higher than in the control (0.3 ± 1.0 dB, P < 0.05). The time delay in the HF range was reduced to 0.5 s ( P < 0.05).
After ganglionic blockade ( n = 7) no major changes in the transfer function were observed.
Under furosemide (frusemide) (40 mg + 10 mg h â1 or 300 mg + 300 mg h â1 i.v.) the stepwise autoregulation was impaired to -7.8 ± 0.3 or -6.7 ± 1.9 dB, respectively ( n = 4). In the transfer function ( n = 7 or n = 4) the peak at 0.027 Hz was abolished. The delay in the LF range was reduced to -1.1 or -1.6 s, respectively. The transfer
gain in the LF range (-5.5 ± 1.2 or -3.8 ± 0.8 dB, respectively) did not differ from the control but was smaller than that
under nifedipine ( P < 0.05).
It is concluded that the ample capacity for regulation of RBF is only partially employed under physiological conditions. The
abolition by nifedipine and the negligible effect of ganglionic blockade show that above 0.0034 Hz it is almost exclusively
due to autoregulation by the kidney itself. TGF contributes to the maximum autoregulatory capacity, but it is not required
for the level of autoregulation expended under physiological conditions. Around 0.027 Hz, TGF even reduces the degree of autoregulation.</description><identifier>ISSN: 0022-3751</identifier><identifier>EISSN: 1469-7793</identifier><identifier>DOI: 10.1111/j.1469-7793.1998.275bx.x</identifier><identifier>PMID: 9481688</identifier><language>eng</language><publisher>Oxford, UK: The Physiological Society</publisher><subject>Animals ; Autonomic Nervous System - drug effects ; Autonomic Nervous System - physiology ; Blood Pressure - drug effects ; Blood Pressure - physiology ; Calcium Channel Blockers - pharmacology ; Cholinergic Antagonists - pharmacology ; Diuretics - pharmacology ; Diuretics - urine ; Dogs ; Furosemide - pharmacology ; Furosemide - urine ; Heart Rate - physiology ; Hexamethonium - pharmacology ; Homeostasis - drug effects ; Homeostasis - physiology ; Kidney - drug effects ; Kidney - innervation ; Kidney - physiology ; Kidney Glomerulus - drug effects ; Kidney Glomerulus - physiology ; Kidney Tubules - drug effects ; Kidney Tubules - physiology ; Nifedipine - pharmacology ; Original ; Renal Circulation - drug effects ; Renal Circulation - physiology ; Vascular Resistance - drug effects ; Vascular Resistance - physiology</subject><ispartof>The Journal of physiology, 1998-01, Vol.506 (1), p.275-290</ispartof><rights>1998 The Journal of Physiology © 1998 The Physiological Society</rights><rights>The Physiological Society 1998 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5275-d92787087028c029f53c06933d1a4244d04f7b56e620673dd4829c73455283493</citedby><cites>FETCH-LOGICAL-c5275-d92787087028c029f53c06933d1a4244d04f7b56e620673dd4829c73455283493</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2230714/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2230714/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,1417,1433,27924,27925,45574,45575,46409,46833,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9481688$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Just, Armin</creatorcontrib><creatorcontrib>Wittmann, Uwe</creatorcontrib><creatorcontrib>Ehmke, Heimo</creatorcontrib><creatorcontrib>Kirchheim, Hartmut R.</creatorcontrib><title>Autoregulation of renal blood flow in the conscious dog and the contribution of the tubuloglomerular feedback</title><title>The Journal of physiology</title><addtitle>J Physiol</addtitle><description>The aim of this study was to investigate the autoregulation of renal blood flow under physiological conditions, when challenged
by the normal pressure fluctuations, and the contribution of the tubuloglomerular feedback (TGF).
The transfer function between 0.0018 and 0.5 Hz was calculated from the spontaneous fluctuations in renal arterial blood pressure
(RABP) and renal blood flow (RBF) in conscious resting dogs. The response of RBF to stepwise artificially induced reductions
in RABP was also studied (stepwise autoregulation).
Under control conditions ( n = 12 dogs), the gain of the transfer function started to decrease, indicating improving autoregulation, below 0.06-0.15 Hz
( t = 7-17 s). At 0.027 Hz a prominent peak of high gain was found. Below 0.01 Hz ( t > 100 s), the gain reached a minimum (maximal autoregulation) of -6.3 ± 0.6 dB. The stepwise autoregulation ( n = 4) was much stronger (-19.5 dB). The time delay of the transfer function was remarkably constant from 0.03 to 0.08 Hz (high
frequency (HF) range) at 1.7 s and from 0.0034 to 0.01 Hz (low frequency (LF) range) at 14.3 s, respectively.
Nifedipine, infused into the renal artery, abolished the stepwise autoregulation (-2.0 ± 1.1 dB, n = 3). The gain of the transfer function ( n = 4) remained high down to 0.0034 Hz; in the LF range it was higher than in the control (0.3 ± 1.0 dB, P < 0.05). The time delay in the HF range was reduced to 0.5 s ( P < 0.05).
After ganglionic blockade ( n = 7) no major changes in the transfer function were observed.
Under furosemide (frusemide) (40 mg + 10 mg h â1 or 300 mg + 300 mg h â1 i.v.) the stepwise autoregulation was impaired to -7.8 ± 0.3 or -6.7 ± 1.9 dB, respectively ( n = 4). In the transfer function ( n = 7 or n = 4) the peak at 0.027 Hz was abolished. The delay in the LF range was reduced to -1.1 or -1.6 s, respectively. The transfer
gain in the LF range (-5.5 ± 1.2 or -3.8 ± 0.8 dB, respectively) did not differ from the control but was smaller than that
under nifedipine ( P < 0.05).
It is concluded that the ample capacity for regulation of RBF is only partially employed under physiological conditions. The
abolition by nifedipine and the negligible effect of ganglionic blockade show that above 0.0034 Hz it is almost exclusively
due to autoregulation by the kidney itself. TGF contributes to the maximum autoregulatory capacity, but it is not required
for the level of autoregulation expended under physiological conditions. Around 0.027 Hz, TGF even reduces the degree of autoregulation.</description><subject>Animals</subject><subject>Autonomic Nervous System - drug effects</subject><subject>Autonomic Nervous System - physiology</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Pressure - physiology</subject><subject>Calcium Channel Blockers - pharmacology</subject><subject>Cholinergic Antagonists - pharmacology</subject><subject>Diuretics - pharmacology</subject><subject>Diuretics - urine</subject><subject>Dogs</subject><subject>Furosemide - pharmacology</subject><subject>Furosemide - urine</subject><subject>Heart Rate - physiology</subject><subject>Hexamethonium - pharmacology</subject><subject>Homeostasis - drug effects</subject><subject>Homeostasis - physiology</subject><subject>Kidney - drug effects</subject><subject>Kidney - innervation</subject><subject>Kidney - physiology</subject><subject>Kidney Glomerulus - drug effects</subject><subject>Kidney Glomerulus - physiology</subject><subject>Kidney Tubules - drug effects</subject><subject>Kidney Tubules - physiology</subject><subject>Nifedipine - pharmacology</subject><subject>Original</subject><subject>Renal Circulation - drug effects</subject><subject>Renal Circulation - physiology</subject><subject>Vascular Resistance - drug effects</subject><subject>Vascular Resistance - physiology</subject><issn>0022-3751</issn><issn>1469-7793</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV-L1DAUxYso6-zqRxDypE9T87dpQIRlUVdZ0If1OaRJ2mZMmzFpd2a-venO7KBvhkDgnntObvIrCoBgifJ6vykRrcSac0FKJERdYs6afbl_VqzOwvNiBSHGa8IZellcprSBEBEoxEVxIWiNqrpeFcP1PIVou9mryYURhBZEOyoPGh-CAa0PO-BGMPUW6DAm7cKcgAkdUKN5qk7RNfOTe6lNczP70Pkw2JiDI2itNY3Sv14VL1rlk319Oq-Kn58_3d_cru--f_l6c3231iw_ZG0E5jWHeeNaQyxaRjSsBCEGKYopNZC2vGGVrTCsODGG1lhoTihjuCZUkKvi4zF3OzeDNdrmGZWX2-gGFQ8yKCf_VUbXyy48SIwJ5IjmgLengBh-zzZNcnBJW-_VaPMPSC44ZJSz3FgfG3UMKUXbni9BUC6o5EYuRORCRC6o5CMquc_WN38PeTae2GT9w1HfOW8P_50r77_9wI-TvTvae9f1Oxet3PaH5EIK2tnpIBmsJFpM5A_EPLMO</recordid><startdate>19980101</startdate><enddate>19980101</enddate><creator>Just, Armin</creator><creator>Wittmann, Uwe</creator><creator>Ehmke, Heimo</creator><creator>Kirchheim, Hartmut R.</creator><general>The Physiological Society</general><general>Blackwell Science Ltd</general><general>Blackwell Science Inc</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><scope>5PM</scope></search><sort><creationdate>19980101</creationdate><title>Autoregulation of renal blood flow in the conscious dog and the contribution of the tubuloglomerular feedback</title><author>Just, Armin ; Wittmann, Uwe ; Ehmke, Heimo ; Kirchheim, Hartmut R.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5275-d92787087028c029f53c06933d1a4244d04f7b56e620673dd4829c73455283493</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Autonomic Nervous System - drug effects</topic><topic>Autonomic Nervous System - physiology</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Pressure - physiology</topic><topic>Calcium Channel Blockers - pharmacology</topic><topic>Cholinergic Antagonists - pharmacology</topic><topic>Diuretics - pharmacology</topic><topic>Diuretics - urine</topic><topic>Dogs</topic><topic>Furosemide - pharmacology</topic><topic>Furosemide - urine</topic><topic>Heart Rate - physiology</topic><topic>Hexamethonium - pharmacology</topic><topic>Homeostasis - drug effects</topic><topic>Homeostasis - physiology</topic><topic>Kidney - drug effects</topic><topic>Kidney - innervation</topic><topic>Kidney - physiology</topic><topic>Kidney Glomerulus - drug effects</topic><topic>Kidney Glomerulus - physiology</topic><topic>Kidney Tubules - drug effects</topic><topic>Kidney Tubules - physiology</topic><topic>Nifedipine - pharmacology</topic><topic>Original</topic><topic>Renal Circulation - drug effects</topic><topic>Renal Circulation - physiology</topic><topic>Vascular Resistance - drug effects</topic><topic>Vascular Resistance - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Just, Armin</creatorcontrib><creatorcontrib>Wittmann, Uwe</creatorcontrib><creatorcontrib>Ehmke, Heimo</creatorcontrib><creatorcontrib>Kirchheim, Hartmut R.</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Just, Armin</au><au>Wittmann, Uwe</au><au>Ehmke, Heimo</au><au>Kirchheim, Hartmut R.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autoregulation of renal blood flow in the conscious dog and the contribution of the tubuloglomerular feedback</atitle><jtitle>The Journal of physiology</jtitle><addtitle>J Physiol</addtitle><date>1998-01-01</date><risdate>1998</risdate><volume>506</volume><issue>1</issue><spage>275</spage><epage>290</epage><pages>275-290</pages><issn>0022-3751</issn><eissn>1469-7793</eissn><abstract>The aim of this study was to investigate the autoregulation of renal blood flow under physiological conditions, when challenged
by the normal pressure fluctuations, and the contribution of the tubuloglomerular feedback (TGF).
The transfer function between 0.0018 and 0.5 Hz was calculated from the spontaneous fluctuations in renal arterial blood pressure
(RABP) and renal blood flow (RBF) in conscious resting dogs. The response of RBF to stepwise artificially induced reductions
in RABP was also studied (stepwise autoregulation).
Under control conditions ( n = 12 dogs), the gain of the transfer function started to decrease, indicating improving autoregulation, below 0.06-0.15 Hz
( t = 7-17 s). At 0.027 Hz a prominent peak of high gain was found. Below 0.01 Hz ( t > 100 s), the gain reached a minimum (maximal autoregulation) of -6.3 ± 0.6 dB. The stepwise autoregulation ( n = 4) was much stronger (-19.5 dB). The time delay of the transfer function was remarkably constant from 0.03 to 0.08 Hz (high
frequency (HF) range) at 1.7 s and from 0.0034 to 0.01 Hz (low frequency (LF) range) at 14.3 s, respectively.
Nifedipine, infused into the renal artery, abolished the stepwise autoregulation (-2.0 ± 1.1 dB, n = 3). The gain of the transfer function ( n = 4) remained high down to 0.0034 Hz; in the LF range it was higher than in the control (0.3 ± 1.0 dB, P < 0.05). The time delay in the HF range was reduced to 0.5 s ( P < 0.05).
After ganglionic blockade ( n = 7) no major changes in the transfer function were observed.
Under furosemide (frusemide) (40 mg + 10 mg h â1 or 300 mg + 300 mg h â1 i.v.) the stepwise autoregulation was impaired to -7.8 ± 0.3 or -6.7 ± 1.9 dB, respectively ( n = 4). In the transfer function ( n = 7 or n = 4) the peak at 0.027 Hz was abolished. The delay in the LF range was reduced to -1.1 or -1.6 s, respectively. The transfer
gain in the LF range (-5.5 ± 1.2 or -3.8 ± 0.8 dB, respectively) did not differ from the control but was smaller than that
under nifedipine ( P < 0.05).
It is concluded that the ample capacity for regulation of RBF is only partially employed under physiological conditions. The
abolition by nifedipine and the negligible effect of ganglionic blockade show that above 0.0034 Hz it is almost exclusively
due to autoregulation by the kidney itself. TGF contributes to the maximum autoregulatory capacity, but it is not required
for the level of autoregulation expended under physiological conditions. Around 0.027 Hz, TGF even reduces the degree of autoregulation.</abstract><cop>Oxford, UK</cop><pub>The Physiological Society</pub><pmid>9481688</pmid><doi>10.1111/j.1469-7793.1998.275bx.x</doi><tpages>16</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0022-3751 |
| ispartof | The Journal of physiology, 1998-01, Vol.506 (1), p.275-290 |
| issn | 0022-3751 1469-7793 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2230714 |
| source | MEDLINE; PMC (PubMed Central); Wiley Journals; IngentaConnect Free/Open Access Journals; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection) |
| subjects | Animals Autonomic Nervous System - drug effects Autonomic Nervous System - physiology Blood Pressure - drug effects Blood Pressure - physiology Calcium Channel Blockers - pharmacology Cholinergic Antagonists - pharmacology Diuretics - pharmacology Diuretics - urine Dogs Furosemide - pharmacology Furosemide - urine Heart Rate - physiology Hexamethonium - pharmacology Homeostasis - drug effects Homeostasis - physiology Kidney - drug effects Kidney - innervation Kidney - physiology Kidney Glomerulus - drug effects Kidney Glomerulus - physiology Kidney Tubules - drug effects Kidney Tubules - physiology Nifedipine - pharmacology Original Renal Circulation - drug effects Renal Circulation - physiology Vascular Resistance - drug effects Vascular Resistance - physiology |
| title | Autoregulation of renal blood flow in the conscious dog and the contribution of the tubuloglomerular feedback |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-27T23%3A20%3A39IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Autoregulation%20of%20renal%20blood%20flow%20in%20the%20conscious%20dog%20and%20the%20contribution%20of%20the%20tubuloglomerular%20feedback&rft.jtitle=The%20Journal%20of%20physiology&rft.au=Just,%20Armin&rft.date=1998-01-01&rft.volume=506&rft.issue=1&rft.spage=275&rft.epage=290&rft.pages=275-290&rft.issn=0022-3751&rft.eissn=1469-7793&rft_id=info:doi/10.1111/j.1469-7793.1998.275bx.x&rft_dat=%3Cproquest_pubme%3E79705475%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=79705475&rft_id=info:pmid/9481688&rfr_iscdi=true |