Normotensive sodium loading in normal man: Regulation of renin secretion during beta-receptor blockade

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Udgivelsesdato: 2008-Dec-10
OriginalsprogEngelsk
TidsskriftAmerican Journal of Physiology: Regulatory, Integrative and Comparative Physiology
Vol/bind296
Udgave nummer2
Sider (fra-til)R436-345
Antal sider9
ISSN0363-6119
DOI
StatusUdgivet - 10. dec. 2008

Fingeraftryk

Renin
Metoprolol
Arterial Pressure
Central Venous Pressure
Aldosterone
Adrenergic Receptors
Kidney
Natriuresis
Atrial Natriuretic Factor
Vasopressins
Glomerular Filtration Rate
Edetic Acid
Adrenergic Agents
Peptides

Citer dette

@article{f9572f70ccf411dd9908000ea68e967b,
title = "Normotensive sodium loading in normal man: Regulation of renin secretion during beta-receptor blockade",
abstract = "Saline administration may change renin 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 con-centration (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 (PRC) by 1/3, AngII by 1/2, and aldosterone (pAldo) by 2/3, (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(-1); 13+/-2 to 55+/-13 micromol min(-1), respectively). Na-loading did not increase plasma atrial natri-uretic peptide (pANP), glomerular filtration rate (GFR by (51)Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by approxi-mately 2.0 mmHg (p<0.05). During Na-loading, sodium excretion increased with CVP at an av-erage slope of 7 micromol/min per mmHg. Concomitantly, plasma vasopressin decreased by 30-40{\%} (p<0.05). In conclusion, beta1-adrenoceptor blockade affects neither the acute saline-mediated deacti-vation 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 norepineph-rine, 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 com-patible 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. Key words: Blood pressure, angiotensin, aldosterone, natriuresis.",
author = "Simon M{\o}lstr{\o}m and Larsen, {Nils Heden} and Simonsen, {Jane Angel} and Remon Washington and Peter Bie",
note = "Paper id:: Epub 2008 Dec 10; PMID:19073901",
year = "2008",
month = "12",
day = "10",
doi = "10.1152/ajpregu.90754.2008",
language = "English",
volume = "296",
pages = "R436--345",
journal = "American Journal of Physiology: Regulatory, Integrative and Comparative Physiology",
issn = "0363-6119",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Normotensive sodium loading in normal man: Regulation of renin secretion during beta-receptor blockade

AU - Mølstrøm, Simon

AU - Larsen, Nils Heden

AU - Simonsen, Jane Angel

AU - Washington, Remon

AU - Bie, Peter

N1 - Paper id:: Epub 2008 Dec 10; PMID:19073901

PY - 2008/12/10

Y1 - 2008/12/10

N2 - Saline administration may change renin 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 con-centration (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 (PRC) by 1/3, AngII by 1/2, and aldosterone (pAldo) by 2/3, (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(-1); 13+/-2 to 55+/-13 micromol min(-1), respectively). Na-loading did not increase plasma atrial natri-uretic peptide (pANP), glomerular filtration rate (GFR by (51)Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by approxi-mately 2.0 mmHg (p<0.05). During Na-loading, sodium excretion increased with CVP at an av-erage slope of 7 micromol/min per mmHg. Concomitantly, plasma vasopressin decreased by 30-40% (p<0.05). In conclusion, beta1-adrenoceptor blockade affects neither the acute saline-mediated deacti-vation 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 norepineph-rine, 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 com-patible 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. Key words: Blood pressure, angiotensin, aldosterone, natriuresis.

AB - Saline administration may change renin 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 con-centration (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 (PRC) by 1/3, AngII by 1/2, and aldosterone (pAldo) by 2/3, (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(-1); 13+/-2 to 55+/-13 micromol min(-1), respectively). Na-loading did not increase plasma atrial natri-uretic peptide (pANP), glomerular filtration rate (GFR by (51)Cr-EDTA), MAP, or cardiac output (CO by impedance cardiography), but increased central venous pressure (CVP) by approxi-mately 2.0 mmHg (p<0.05). During Na-loading, sodium excretion increased with CVP at an av-erage slope of 7 micromol/min per mmHg. Concomitantly, plasma vasopressin decreased by 30-40% (p<0.05). In conclusion, beta1-adrenoceptor blockade affects neither the acute saline-mediated deacti-vation 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 norepineph-rine, 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 com-patible 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. Key words: Blood pressure, angiotensin, aldosterone, natriuresis.

U2 - 10.1152/ajpregu.90754.2008

DO - 10.1152/ajpregu.90754.2008

M3 - Journal article

VL - 296

SP - R436-345

JO - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

JF - American Journal of Physiology: Regulatory, Integrative and Comparative Physiology

SN - 0363-6119

IS - 2

ER -