Source:http://linkedlifedata.com/resource/pubmed/id/19073901
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2009-1-27
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| pubmed:abstractText |
Saline administration may change renin-angiotensin-aldosterone system (RAAS) activity and sodium excretion at constant mean arterial pressure (MAP). We hypothesized that such responses are elicited mainly by renal sympathetic nerve activity by beta1-receptors (beta1-RSNA), and tested the hypothesis by studying RAAS and renal excretion during slow saline loading at constant plasma sodium concentration (Na+ loading; 12 micromol Na+.kg(-1).min(-1) for 4 h). Normal subjects were studied on low-sodium intake with and without beta1-adrenergic blockade by metoprolol. Metoprolol per se reduced RAAS activity as expected. Na+ loading decreased plasma renin concentration (PRC) by one-third, plasma ANG II by one-half, and plasma aldosterone by two-thirds (all P < 0.05); surprisingly, these changes were found without, as well as during, acute metoprolol administration. Concomitantly, sodium excretion increased indistinguishably with and without metoprolol (16 +/- 2 to 71 +/- 14 micromol/min; 13 +/- 2 to 55 +/- 13 micromol/min, respectively). Na+ loading did not increase plasma atrial natriuretic peptide, glomerular filtration rate (GFR by 51Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by approximately 2.0 mmHg (P < 0.05). During Na+ loading, sodium excretion increased with CVP at an average slope of 7 micromol.min(-1).mmHg(-1). Concomitantly, plasma vasopressin decreased by 30-40% (P < 0.05). In conclusion, beta1-adrenoceptor blockade affects neither the acute saline-mediated deactivation of RAAS nor the associated natriuretic response, and the RAAS response to modest saline loading seems independent of changes in MAP, CO, GFR, beta1-mediated effects of norepinephrine, and ANP. Unexpectedly, the results do not allow assessment of the relative importance of RAAS-dependent and -independent regulation of renal sodium excretion. The results are compatible with the notion that at constant arterial pressure, a volume receptor elicited reduction in RSNA via receptors other than beta1-adrenoceptors, decreases renal tubular sodium reabsorption proximal to the macula densa leading to increased NaCl concentration at the macula densa, and subsequent inhibition of renin secretion.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/AVP protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Adrenergic beta-Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Aldosterone,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Atrial Natriuretic Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Metoprolol,
http://linkedlifedata.com/resource/pubmed/chemical/Neurophysins,
http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Precursors,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vasopressin,
http://linkedlifedata.com/resource/pubmed/chemical/Renin,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Vasopressins
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0363-6119
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
296
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
R436-45
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:19073901-Adrenergic beta-1 Receptor Antagonists,
pubmed-meshheading:19073901-Adrenergic beta-Antagonists,
pubmed-meshheading:19073901-Adult,
pubmed-meshheading:19073901-Aldosterone,
pubmed-meshheading:19073901-Angiotensin II,
pubmed-meshheading:19073901-Atrial Natriuretic Factor,
pubmed-meshheading:19073901-Blood Pressure,
pubmed-meshheading:19073901-Diet, Sodium-Restricted,
pubmed-meshheading:19073901-Glomerular Filtration Rate,
pubmed-meshheading:19073901-Heart Rate,
pubmed-meshheading:19073901-Humans,
pubmed-meshheading:19073901-Infusions, Intravenous,
pubmed-meshheading:19073901-Kidney,
pubmed-meshheading:19073901-Male,
pubmed-meshheading:19073901-Metoprolol,
pubmed-meshheading:19073901-Natriuresis,
pubmed-meshheading:19073901-Neurophysins,
pubmed-meshheading:19073901-Norepinephrine,
pubmed-meshheading:19073901-Protein Precursors,
pubmed-meshheading:19073901-Receptors, Adrenergic, beta-1,
pubmed-meshheading:19073901-Receptors, Vasopressin,
pubmed-meshheading:19073901-Renin,
pubmed-meshheading:19073901-Renin-Angiotensin System,
pubmed-meshheading:19073901-Sodium,
pubmed-meshheading:19073901-Sodium Chloride,
pubmed-meshheading:19073901-Sympathetic Nervous System,
pubmed-meshheading:19073901-Time Factors,
pubmed-meshheading:19073901-Vasopressins,
pubmed-meshheading:19073901-Young Adult
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| pubmed:year |
2009
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| pubmed:articleTitle |
Normotensive sodium loading in normal man: regulation of renin secretion during beta-receptor blockade.
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| pubmed:affiliation |
Department of Physiology and Pharmacology, Institute of Medical Biology, University of Southern Denmark, 21 Winslowparken, Odense, DK-5000, Denmark.
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| pubmed:publicationType |
Journal Article,
Clinical Trial,
Research Support, Non-U.S. Gov't
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