Salt-Dependent Inhibition of Epithelial Na+ Channel–Mediated Sodium Reabsorption in the Aldosterone-Sensitive Distal Nephron by Bradykinin
We have documented recently that bradykinin (BK) directly inhibits activity of the epithelial Na channel (ENaC) via the bradykinin B2 receptor (B2R)-Gq/11-phospholipase C pathway. In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R) to probe a physi...
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| Veröffentlicht in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2012-11, Vol.60 (5), p.1234-1241 |
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| creator | Mamenko, Mykola Zaika, Oleg Doris, Peter A Pochynyuk, Oleh |
| description | We have documented recently that bradykinin (BK) directly inhibits activity of the epithelial Na channel (ENaC) via the bradykinin B2 receptor (B2R)-Gq/11-phospholipase C pathway. In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R) to probe a physiological role of BK cascade in regulation of ENaC in native tissue, aldosterone-sensitive distal nephron. Under normal sodium intake (0.32% Na), ENaC open probability (Po) was modestly elevated in B1R, B2R mice compared with wild-type mice. This difference is augmented during elevated Na intake (2.00% Na) and negated during Na restriction ( |
| doi_str_mv | 10.1161/HYPERTENSIONAHA.112.200469 |
| format | Article |
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In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R) to probe a physiological role of BK cascade in regulation of ENaC in native tissue, aldosterone-sensitive distal nephron. Under normal sodium intake (0.32% Na), ENaC open probability (Po) was modestly elevated in B1R, B2R mice compared with wild-type mice. This difference is augmented during elevated Na intake (2.00% Na) and negated during Na restriction (<0.01% Na). Saturation of systemic mineralocorticoid status with deoxycorticosterone acetate similarly increased ENaC activity in both mouse strains, suggesting that the effect of BK on ENaC is independent of aldosterone. It is accepted that angiotensin-converting enzyme represents the major pathway of BK degradation. Systemic inhibition of angiotensin-converting enzyme with captopril (30 mg/kg of body weight for 7 days) significantly decreases ENaC activity and Po in wild-type mice, but this effect is diminished in B1R, B2R mice. At the cellular level, acute captopril (100 μmol/L) treatment sensitized BK signaling cascade and greatly potentiated the inhibitory effect of 100 nmol/L of BK on ENaC. We concluded that BK cascade has its own specific role in blunting ENaC activity, particularly under conditions of elevated sodium intake. Augmentation of BK signaling in the aldosterone-sensitive distal nephron inhibits ENaC-mediated Na reabsorption, contributing to the natriuretic and antihypertensive effects of angiotensin-converting enzyme inhibition.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/HYPERTENSIONAHA.112.200469</identifier><identifier>PMID: 23033373</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Aldosterone - metabolism ; Angiotensin-Converting Enzyme Inhibitors - pharmacology ; Animals ; Arterial hypertension. Arterial hypotension ; Biological and medical sciences ; Blood and lymphatic vessels ; Bradykinin - pharmacology ; Calcium - metabolism ; Captopril - pharmacology ; Cardiology. Vascular system ; Clinical manifestations. Epidemiology. Investigative techniques. Etiology ; Epithelial Sodium Channels - metabolism ; In Vitro Techniques ; Male ; Medical sciences ; Membrane Potentials - drug effects ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Nephrons - cytology ; Nephrons - drug effects ; Nephrons - metabolism ; Patch-Clamp Techniques ; Peptidyl-Dipeptidase A - metabolism ; Receptor, Bradykinin B1 - deficiency ; Receptor, Bradykinin B1 - genetics ; Receptor, Bradykinin B2 - deficiency ; Receptor, Bradykinin B2 - genetics ; Sodium - administration & dosage ; Sodium - metabolism ; Sodium Chloride - metabolism ; Time Factors</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2012-11, Vol.60 (5), p.1234-1241</ispartof><rights>2012 American Heart Association, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5229-2740e2e80abb040b9ae8f3e9c1d2a312bf7c53d6cc9f12b2088190737e3d08853</citedby><cites>FETCH-LOGICAL-c5229-2740e2e80abb040b9ae8f3e9c1d2a312bf7c53d6cc9f12b2088190737e3d08853</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,3674,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26494345$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23033373$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mamenko, Mykola</creatorcontrib><creatorcontrib>Zaika, Oleg</creatorcontrib><creatorcontrib>Doris, Peter A</creatorcontrib><creatorcontrib>Pochynyuk, Oleh</creatorcontrib><title>Salt-Dependent Inhibition of Epithelial Na+ Channel–Mediated Sodium Reabsorption in the Aldosterone-Sensitive Distal Nephron by Bradykinin</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>We have documented recently that bradykinin (BK) directly inhibits activity of the epithelial Na channel (ENaC) via the bradykinin B2 receptor (B2R)-Gq/11-phospholipase C pathway. In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R) to probe a physiological role of BK cascade in regulation of ENaC in native tissue, aldosterone-sensitive distal nephron. Under normal sodium intake (0.32% Na), ENaC open probability (Po) was modestly elevated in B1R, B2R mice compared with wild-type mice. This difference is augmented during elevated Na intake (2.00% Na) and negated during Na restriction (<0.01% Na). Saturation of systemic mineralocorticoid status with deoxycorticosterone acetate similarly increased ENaC activity in both mouse strains, suggesting that the effect of BK on ENaC is independent of aldosterone. It is accepted that angiotensin-converting enzyme represents the major pathway of BK degradation. Systemic inhibition of angiotensin-converting enzyme with captopril (30 mg/kg of body weight for 7 days) significantly decreases ENaC activity and Po in wild-type mice, but this effect is diminished in B1R, B2R mice. At the cellular level, acute captopril (100 μmol/L) treatment sensitized BK signaling cascade and greatly potentiated the inhibitory effect of 100 nmol/L of BK on ENaC. We concluded that BK cascade has its own specific role in blunting ENaC activity, particularly under conditions of elevated sodium intake. Augmentation of BK signaling in the aldosterone-sensitive distal nephron inhibits ENaC-mediated Na reabsorption, contributing to the natriuretic and antihypertensive effects of angiotensin-converting enzyme inhibition.</description><subject>Aldosterone - metabolism</subject><subject>Angiotensin-Converting Enzyme Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Bradykinin - pharmacology</subject><subject>Calcium - metabolism</subject><subject>Captopril - pharmacology</subject><subject>Cardiology. Vascular system</subject><subject>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</subject><subject>Epithelial Sodium Channels - metabolism</subject><subject>In Vitro Techniques</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Potentials - drug effects</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Nephrons - cytology</subject><subject>Nephrons - drug effects</subject><subject>Nephrons - metabolism</subject><subject>Patch-Clamp Techniques</subject><subject>Peptidyl-Dipeptidase A - metabolism</subject><subject>Receptor, Bradykinin B1 - deficiency</subject><subject>Receptor, Bradykinin B1 - genetics</subject><subject>Receptor, Bradykinin B2 - deficiency</subject><subject>Receptor, Bradykinin B2 - genetics</subject><subject>Sodium - administration & dosage</subject><subject>Sodium - metabolism</subject><subject>Sodium Chloride - metabolism</subject><subject>Time Factors</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1uEzEUhUcIRNPCKyALCQkJTfHf_JhFpZAGEqmkqCkSrEae8R2NqWMP9kyr7HgAdrwhT4JDAkisWNm-_s65V_ckyVOCTwnJycvFp_fzq-v5ar28XE0X01ikpxRjnot7yYRklKc8y9n9ZIKJ4Kkg5ONRchzCZ4wJ57x4mBxRhhljBZsk39bSDOk59GAV2AEtbadrPWhnkWvRvNdDB0ZLg1byBZp10lowP75-fwdKywEUWjulxw26AlkH5_tfQm1RVKGpUS4M4J2FdA02RNdbQOc6DDs76Lv4g-oteu2l2t5oq-2j5EErTYDHh_Mk-fBmfj1bpBeXb5ez6UXaZJSKlBYcA4USy7rGHNdCQtkyEA1RVDJC67ZoMqbyphFtfFFclkTgghXAVLxn7CR5vvftvfsyQhiqjQ4NGCMtuDFUhBAmSkYwj-irPdp4F4KHtuq93ki_rQiudmlU_6QRi7TapxHFTw59xnoD6o_09_oj8OwAyNBI03ppGx3-cjkXnPHdwGd77s6ZuNFwY8Y78FUHMbzufyb5CeBbqxI</recordid><startdate>201211</startdate><enddate>201211</enddate><creator>Mamenko, Mykola</creator><creator>Zaika, Oleg</creator><creator>Doris, Peter A</creator><creator>Pochynyuk, Oleh</creator><general>American Heart Association, Inc</general><general>Lippincott Williams & Wilkins</general><scope>IQODW</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>201211</creationdate><title>Salt-Dependent Inhibition of Epithelial Na+ Channel–Mediated Sodium Reabsorption in the Aldosterone-Sensitive Distal Nephron by Bradykinin</title><author>Mamenko, Mykola ; Zaika, Oleg ; Doris, Peter A ; Pochynyuk, Oleh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5229-2740e2e80abb040b9ae8f3e9c1d2a312bf7c53d6cc9f12b2088190737e3d08853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Aldosterone - metabolism</topic><topic>Angiotensin-Converting Enzyme Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Arterial hypertension. Arterial hypotension</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Bradykinin - pharmacology</topic><topic>Calcium - metabolism</topic><topic>Captopril - pharmacology</topic><topic>Cardiology. Vascular system</topic><topic>Clinical manifestations. Epidemiology. Investigative techniques. Etiology</topic><topic>Epithelial Sodium Channels - metabolism</topic><topic>In Vitro Techniques</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Potentials - drug effects</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Nephrons - cytology</topic><topic>Nephrons - drug effects</topic><topic>Nephrons - metabolism</topic><topic>Patch-Clamp Techniques</topic><topic>Peptidyl-Dipeptidase A - metabolism</topic><topic>Receptor, Bradykinin B1 - deficiency</topic><topic>Receptor, Bradykinin B1 - genetics</topic><topic>Receptor, Bradykinin B2 - deficiency</topic><topic>Receptor, Bradykinin B2 - genetics</topic><topic>Sodium - administration & dosage</topic><topic>Sodium - metabolism</topic><topic>Sodium Chloride - metabolism</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mamenko, Mykola</creatorcontrib><creatorcontrib>Zaika, Oleg</creatorcontrib><creatorcontrib>Doris, Peter A</creatorcontrib><creatorcontrib>Pochynyuk, Oleh</creatorcontrib><collection>Pascal-Francis</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>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mamenko, Mykola</au><au>Zaika, Oleg</au><au>Doris, Peter A</au><au>Pochynyuk, Oleh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Salt-Dependent Inhibition of Epithelial Na+ Channel–Mediated Sodium Reabsorption in the Aldosterone-Sensitive Distal Nephron by Bradykinin</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2012-11</date><risdate>2012</risdate><volume>60</volume><issue>5</issue><spage>1234</spage><epage>1241</epage><pages>1234-1241</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>We have documented recently that bradykinin (BK) directly inhibits activity of the epithelial Na channel (ENaC) via the bradykinin B2 receptor (B2R)-Gq/11-phospholipase C pathway. In this study, we took advantage of mice genetically engineered to lack bradykinin receptors (B1R, B2R) to probe a physiological role of BK cascade in regulation of ENaC in native tissue, aldosterone-sensitive distal nephron. Under normal sodium intake (0.32% Na), ENaC open probability (Po) was modestly elevated in B1R, B2R mice compared with wild-type mice. This difference is augmented during elevated Na intake (2.00% Na) and negated during Na restriction (<0.01% Na). Saturation of systemic mineralocorticoid status with deoxycorticosterone acetate similarly increased ENaC activity in both mouse strains, suggesting that the effect of BK on ENaC is independent of aldosterone. It is accepted that angiotensin-converting enzyme represents the major pathway of BK degradation. Systemic inhibition of angiotensin-converting enzyme with captopril (30 mg/kg of body weight for 7 days) significantly decreases ENaC activity and Po in wild-type mice, but this effect is diminished in B1R, B2R mice. At the cellular level, acute captopril (100 μmol/L) treatment sensitized BK signaling cascade and greatly potentiated the inhibitory effect of 100 nmol/L of BK on ENaC. We concluded that BK cascade has its own specific role in blunting ENaC activity, particularly under conditions of elevated sodium intake. Augmentation of BK signaling in the aldosterone-sensitive distal nephron inhibits ENaC-mediated Na reabsorption, contributing to the natriuretic and antihypertensive effects of angiotensin-converting enzyme inhibition.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>23033373</pmid><doi>10.1161/HYPERTENSIONAHA.112.200469</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Hypertension (Dallas, Tex. 1979), 2012-11, Vol.60 (5), p.1234-1241 |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Ovid Autoload |
| subjects | Aldosterone - metabolism Angiotensin-Converting Enzyme Inhibitors - pharmacology Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Bradykinin - pharmacology Calcium - metabolism Captopril - pharmacology Cardiology. Vascular system Clinical manifestations. Epidemiology. Investigative techniques. Etiology Epithelial Sodium Channels - metabolism In Vitro Techniques Male Medical sciences Membrane Potentials - drug effects Mice Mice, Inbred C57BL Mice, Knockout Nephrons - cytology Nephrons - drug effects Nephrons - metabolism Patch-Clamp Techniques Peptidyl-Dipeptidase A - metabolism Receptor, Bradykinin B1 - deficiency Receptor, Bradykinin B1 - genetics Receptor, Bradykinin B2 - deficiency Receptor, Bradykinin B2 - genetics Sodium - administration & dosage Sodium - metabolism Sodium Chloride - metabolism Time Factors |
| title | Salt-Dependent Inhibition of Epithelial Na+ Channel–Mediated Sodium Reabsorption in the Aldosterone-Sensitive Distal Nephron by Bradykinin |
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