Affiliation:
1. Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark
2. Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark
3. Clinical Epidemiology, Institute of Medical Biometry and Medical Informatics, University Medical Center Freiburg, Freiburg, Germany
Abstract
NO (nitric oxide) may be involved in fluid homoeostasis. We hypothesized that increases in NO synthesis contribute to acute, saline-induced natriuresis, which, therefore, should be blunted when NO availability is stabilized. Young men were studied during simultaneous infusions of L-NAME [NG-nitro-L-arginine methyl ester; bolus of 750 μg·kg−1 of body weight and 8.3 μg·min−1·kg−1 of body weight] and SNP (sodium nitroprusside), the latter at a rate preventing L-NAME from increasing total peripheral resistance (‘NO-clamping’). Slow volume expansion (saline, 20 μmol of NaCl·min−1·kg−1 of body weight for 3 h) was performed with and without concomitant NO-clamping. NO-clamping itself decreased RPF (renal plasma flow; P~0.02) and tended to decrease arterial blood pressure [MABP (mean arterial blood pressure)]. Volume expansion markedly decreased the plasma levels of renin, AngII (angiotensin II) and aldosterone (all P<0.001), while MABP (oscillometry), heart rate, cardiac output (impedance cardiography), RPF (by p-aminohippurate), GFR [glomerular filtration rate; by using 51Cr-labelled EDTA] and plasma [Na+] and [K+] remained constant. Volume expansion increased sodium excretion (P<0.02) at constant filtered load, but more so during NO-clamping than during control (+184% compared with 52%; P<0.0001). Urinary nitrate/nitrite excretion increased during volume expansion; plasma cGMP and plasma vasopressin were unchanged. The results demonstrate that NO-clamping augments sodium excretion in response to volume expansion at constant MABP and GFR, reduced RPF and decreased renin system activity, a response termed hypernatriuresis. The results indicate that mediator(s) other than MABP, RPF, GFR and renin system activity contribute significantly to the homoeostatic response to saline loading, but the specific mechanisms of hypernatriuresis remain obscure.
Reference52 articles.
1. Blood volume, blood pressure and total body sodium: internal signalling and output control;Bie;Acta Physiol.,2009
2. Subpressor angiotensin infusion, renal sodium handling, and salt-induced hypertension in the dog;DeClue;Circ. Res.,1978
3. Blood pressure and renal function during chronic changes in sodium intake: role of angiotensin;Hall;Am. J. Physiol.,1980
4. The renin-angiotensin system;Le,2008
5. Volume natriuresis vs. pressure natriuresis;Bie;Acta Physiol. Scand.,2004
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