Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “NATRIURESIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed1976

Effects of catecholamines injected into the septal area of the rat brain on natriuresis, kaliuresis and diuresis.

Urinary output of Na+ and K+, and volume of urine have been studied in conscious, unrestrained, water-loaded male rats following the intraseptal injection of catecholamines. Natriuresis and kaliuresis increased after injecting noradrenaline (NA), the intensity being dose related. The dose-response curve suggests that a monomolecular interacting takes place between NA and pharmacological receptors present in the septal area. No change was observed in diuresis. Systematic mapping of the septal area yielded about the same results for all sites except a zone located in the lateral nucleus that was more sensitive. An alpha blocker (dibenamine), injected intraseptally before NA, showed an inhibitory effect while a beta blocker (propranolol) yielded a potentiation effect. These same effects of the blocking agents were observed when adrenaline was used instead of NA. Lidocaine, which inhibits the re-uptake of NA, showed an enhancement of the natriuretic and kaliuretic effect of NA, and the same effect was observed when the enzymatic destruction of NA was prevented by nialamide, an inhibitor of monoaminoxidase. Dopamine showed a natriuretic effect, but no effect was observed on K+ and urine output. Serotonin had no action on natriuresis, kaliuresis and diuresis.

Adrenergic alpha-Agonists↗
PubMed1991

Chronic hydralazine treatment alters the acute pressure-natriuresis curve in young spontaneously hypertensive rats.

The pressure-natriuresis relationship was studied in anesthetized, 7- to 9-week-old control spontaneously hypertensive rats (SHR) and in SHR that had been treated with hydralazine (20 mg.kg-1.day-1 in drinking water) starting at 4-5 weeks of age. To minimize reflex changes in kidney function during changes in renal artery pressure, neural and hormonal influences on the kidney were fixed by surgical renal denervation, adrenalectomy, and infusion of a hormone cocktail (330 microL.kg-1.mikn-1) containing high levels of aldosterone, arginine vasopressin, hydrocortisone, and norepinephrine dissolved in 0.9% NaCl containing 1% albumin. Changes in renal function were measured using standard clearance techniques, while renal artery pressure was varied between 136 +/- 1 and 186 +/- 2 mmHg (1 mmHg = 133.32 Pa) in control SHR (n = 10) and between 113 +/- 1 and 162 +/- 2 mmHg in treated SHR (n = 11). Mean arterial pressure (+/- SE) under Inactin anesthesia was 172 +/- 3 mmHg in control SHR and 146 +/- 3 mmHg in treated SHR (p less than 0.05). Where renal artery pressure overlapped between groups, there were no significant differences in glomerular filtration rate. Renal blood flow was also similar in both groups, although at 160 mmHg blood flow was slightly but significantly reduced in treated SHR. Urine flow and total and fractional sodium excretion increased similarly with increases in renal artery pressure in both groups, but the pressure-natriuresis curve in hydralazine-treated SHR was displaced to the left along the pressure axis. The data indicate that chronic administration of hydralazine in young SHR enhances fractional sodium excretion, suggesting that tubular reabsorption of sodium is decreased by hydralazine.

Animals↗
PubMed1991

Enhanced responsiveness to CNS-induced natriuresis in anesthetized nonascitic cirrhotic rats.

Central nervous system (CNS)-induced natriuresis was investigated in nonascitic rats with CCl4-induced cirrhosis (CTC rats) under pentobarbital anesthesia. At baseline, urine sodium output (UNa+V, in mumol.min-1.100 g body wt-1) (-30%, P less than 0.01) and mean arterial pressure (MAP, in mmHg) (-12%, P less than 0.001) were significantly reduced in CTC rats (n = 32) compared with matched controls (n = 34). In response to intracerebroventricular infusion of sodium-rich (349 mM) artificial cerebrospinal fluid (Na(+)-CSF infusion), UNa+V was significantly higher in CTC rats (2.8 +/- 0.3; n = 15) than in controls (1.7 +/- 0.2; n = 17; P less than 0.01); no differences were found in pressor changes (24 +/- 3 vs. 19 +/- 2). A similar but normal sodium CSF (150 mM) infusion did not influence UNa+V or MAP in any group (n = 12, both). In contrast, CTC rats (n = 5) showed, compared with controls (n = 5), significantly reduced natriuretic (UNa+V, 6.9 +/- 0.5 vs. 12.4 +/- 0.9; P less than 0.001) and pressor (+16 +/- 3 vs. +31 +/- 2; P less than 0.01) responses to an intravenous hypertonic sodium overload. Natriuresis induced by Na(+)-CSF infusion was related to increases in creatinine clearance (similar in both groups) and in fractional sodium excretion, which was significantly higher in CTC rats (5.90 +/- 0.15%) than in controls (3.65 +/- 0.14%; P less than 0.01). In summary, CNS-dependent efferent natriuretic mechanisms were preserved in CTC rats and were able to reverse renal tubular sodium retention in these animals. It is proposed that Na(+)-CSF infusion may be a useful tool for the study of renal sodium retention in experimental liver cirrhosis.

Animals↗
PubMed1995

Role of nitric oxide in regulation of long-term pressure-natriuresis relationship in Dahl rats.

The aim of this study was to determine the role of nitric oxide (NO) in the development of salt-induced hypertension in the Brookhaven strain of Dahl rats. Six- to seven-week-old conscious salt-sensitive (S) and salt-resistant (R) rats with indwelling arterial and venous catheters received low-, normal-, and high-sodium intakes sequentially over a 16-day period, and L-arginine was infused intravenously at 2 or 4 mg.kg-1.min-1 over this time. The S rats had an impaired NO production as evidenced by a decreased urinary nitrate plus nitrite excretion. The administration of the low or high dose of L-arginine increased the whole body NO production of the S rats to that of the control R rats, and the high dose of L-arginine prevented the shift of long-term pressure-natriuresis relationship, the elevation of arterial pressure, and the increase in salt sensitivity of arterial pressure in the S rats. The sodium and water balances were not different between the age-matched R and S rats. In conclusion, a continuous infusion of L-arginine prevented both the changes in the pressure-natriuresis relationship and the development of salt-induced hypertension in Dahl S rats.

Animals↗
PubMed1976

Sodium balance and the natriuresis of hypertonic saline infusion in dogs.

Recently, a paradoxical effect of dietary salt intake on the natriuresis following hypertonic saline infusion was observed in rats. In these experiments the effects of alterations in dietary sodium on the natriuretic response to a hypertonic saline load was studied in dogs. Dogs maintained on a high-sodium diet did not have a significantly different natriuresis than those on a low-sodium diet. When differences in sodium balance were amplified by the use of deoxycorticosterone, furosemide, and manipulation of dietary sodium, dogs in positive sodium balance showed a significantly enhanced initial excretion of sodium followed by a reversal of the pattern. Consequently, the cumulative sodium excretion was not different between low- and high-sodium groups. Since the cumulative natriuretic response to isotonic saline infusion was larger in dogs in positive sodium balance compared to those in negative sodium balance, the failure to detect a difference following hypertonic saline infusion was probably because of the increased plasma sodium concentration.

Animals↗
PubMed2004

Inhibition of the formation of EETs and 20-HETE with 1-aminobenzotriazole attenuates pressure natriuresis.

This study examined the effects of chronic blockade of the renal formation of epoxyeicosatrienoic acids and 20-hydroxyeicosatetraenoic acid with 1-aminobenzotriazole (ABT; 50 mg.kg(-1). day(-1) ip for 5 days) on pressure natriuresis and the inhibitory effects of elevations in renal perfusion pressure (RPP) on Na(+)-K(+)-ATPase activity and the distribution of the sodium/hydrogen exchanger (NHE)-3 in the proximal tubule of rats. In control rats (n = 15), sodium excretion rose from 2.3 +/- 0.4 to 19.4 +/- 1.8 microeq.min(-1).g kidney weight(-1) when RPP was increased from 114 +/- 1 to 156 +/- 2 mmHg. Fractional excretion of lithium rose from 28 +/- 3 to 43 +/- 3% of the filtered load. Chronic treatment of the rats with ABT for 5 days (n = 8) blunted the natriuretic response to elevations in RPP by 75% and attenuated the increase in fractional excretion of lithium by 45%. In vehicle-treated rats, renal Na(+)-K(+)-ATPase activity fell from 31 +/- 5 to 19 +/- 2 micromol P(i).mg protein(-1).h(-1) and NHE-3 protein was internalized from the brush border of the proximal tubule after an elevation in RPP. In contrast, Na(+)-K(+)-ATPase activity and the distribution of NHE-3 protein remained unaltered in rats treated with ABT. These results suggest that cytochrome P-450 metabolites of arachidonic acid contribute to pressure natriuresis by inhibiting Na(+)-K(+)-ATPase activity and promoting internalization of NHE-3 protein from the brush border of the proximal tubule.

Animals↗
PubMed1983

Preoptic-hypothalamic periventricular lesions reduce natriuresis to volume expansion.

The present experiment was designed to determine if electrolytic ablation of the periventricular tissue surrounding the anteroventral third ventricle (AV3V) altered the natriuresis typically seen during isotonic volume expansion. Control and AV3V-lesioned rats received intravenous infusions of 0.9% NaCl at 0.5 ml/min until 10% body weight was given. Arterial blood pressure was monitored, and urine was collected throughout the experiment. Following expansion, blood was processed for analysis of natriuretic hormonelike activity by chromatographic separation of plasma extracts followed by measuring antinatriferic activity across the isolated toad bladder. Urinary sodium excretion and urine volume during expansion were significantly less in rats with lesions surrounding the AV3V region than in control rats. Toad bladder bioassay showed a high level of natriuretic hormonelike activity in control animals following volume expansion, but no natriuretic hormonelike activity in plasma from volume-expanded rats with AV3V lesions. These data demonstrate that AV3V periventricular ablation attenuates the natriuresis induced by isotonic-volume expansion. In addition, preliminary results indicate the AV3V region may be a central site critical for natriuretic hormonelike activity and control of extracellular fluid volume.

Animals↗
PubMed1986

Role of atrial natriuretic peptide in volume-expansion natriuresis.

Studies were performed to investigate the role of circulating atrial natriuretic peptide (ANP) in acute volume-expansion natriuresis. Sham-operated (SHAM, n = 6) and right atrial appendectomized (ATRX, n = 12) anesthetized rats underwent acute volume expansion with isoncotic albumin. After equilibration and control periods, volume expansion increased urine flow rate, urinary sodium excretion, fractional excretion of sodium, and circulating ANP. Absolute increases in urine flow rate (delta 46 +/- 4 SHAM; delta 25 +/- 5 microliter/min ATRX), urinary sodium excretion (delta 9.48 +/- 1.01 SHAM; delta 4.77 +/- 1.03 mueq/min ATRX), fractional excretion of sodium (delta 3.16 +/- 0.53 SHAM; delta 1.65 +/- 0.32% ATRX), and ANP (delta 303.3 +/- 35.9 SHAM; delta 156.6 +/- 26.0 pg/ml ATRX) were significantly reduced by right atrial appendectomy. No significant differences in mean arterial pressure, central venous pressure, or glomerular filtration rate during volume expansion were observed between groups. These studies support the hypothesis that right atrial appendectomy in the rat attenuates acute volume expansion-induced increases in circulating ANP and urinary sodium excretion and that the natriuresis of acute volume expansion is mediated in part by an increase in circulating ANP.

Animals↗
PubMed1987

Role of atrial natriuretic factor in the natriuresis of acute volume expansion.

The quantitative role of atrial natriuretic factor (ANF) in mediating the natriuresis induced by acute volume loading was determined in these studies. Plasma level of ANF (PANF), glomerular filtration rate (GFR), and renal excretory responses were measured in three groups of anesthetized Sprague-Dawley rats. In one group of rats (n = 8), acute volume expansion was established by intravenous infusion of saline (5% body wt) over a period of 30 min. A second group of rats (n = 13) was infused with synthetic ANF (2 micrograms X kg-1 X h-1 iv) to mimic the high PANF observed during acute volume loading. A third group (n = 13) served as control. PANF was similar and significantly elevated (P less than 0.05) in volume-expanded and ANF-infused groups compared with control. In control rats, PANF measured 122.0 +/- 12.1 pg/ml, whereas it averaged 389.4 +/- 30.3 pg/ml for volume-expanded and 368.1 +/- 22.3 pg/ml for ANF-infused rats. GFR was also comparable and significantly increased (P less than 0.05) in volume-expanded and ANF-infused groups compared with control rats. Infusion of ANF at a dose to mimic PANF obtained during acute volume expansion resulted in a fourfold increase in the fractional excretion of sodium. The results of these studies suggest that ANF may play an important quantitative role in promoting natriuresis during acute volume expansion.

Animals↗
PubMed1987

Role of atrial natriuretic peptide in natriuresis in volume-expanded rats.

Continuous intravenous infusion of rat atrial natriuretic peptide (rANP) was carried out for 60 min in urethan-anesthetized rats. Plasma rANP (PANP) levels during 0, 12.5, and 50 ng/min rANP infusion reached 20.9 +/- 3.4, 61.2 +/- 12.3, and 228 +/- 30.6 pg/ml, respectively. Urinary sodium excretion (UNaV) remained unchanged during the 0 and 12.5 ng/min rANP infusion. In contrast, the 50 ng/min rANP infusion resulted in a 5.6-fold increase in UNaV without significant changes in plasma aldosterone levels and glomerular filtration rate. Isotonic saline infusion (116 microliter/min for 60 or 120 min) caused a significant increase in UNaV. UNaV in an experimental model of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was 5.0 times greater than in control animals. PANP levels in 60- or 120-min saline-infused and SIADH rats were 46.3 +/- 6.7, 39.0 +/- 9.0, and 35.6 +/- 3.2 pg/ml, respectively. These values were significantly higher than control values but failed to achieve a level at which natriuresis occurred during the infusion of rANP. These results suggest that endogenous ANP may not play a critical role in the induction of acute natriuresis in volume-expanded states, although it could be partially involved in such a natriuretic response.

Aldosterone↗
PubMed1988

Renal interstitial hydrostatic pressure during pressure natriuresis in hypertension.

The objective of this study was to test the hypothesis that changes in renal perfusion pressure (RPP) are not fully transmitted to the renal interstitium in spontaneous hypertension in comparison with normotensive states. Okamoto spontaneously hypertensive and normotensive Wistar-Kyoto rats were used in this study. Renal interstitial hydrostatic pressure (RIHP) was measured directly and continuously via a polyethylene matrix that was implanted chronically in the left kidney 3 wk before RIHP measurement. When RPP was allowed to increase from 136 +/- 0.5 to 162 +/- 1.3 mmHg in male spontaneously hypertensive rats, RIHP was not significantly changed from 3.7 +/- 0.9 to 4.6 +/- 1.1 mmHg, and fractional excretion of sodium (FENa) increased significantly from 0.26 +/- 0.12 to 0.65 +/- 0.15% (P less than 0.05). When RPP was allowed to change from 104 +/- 0.9 to 127 +/- 1.3 mmHg in male Wistar-Kyoto rats, RIHP increased markedly from 4.0 +/- 0.3 to 7.2 +/- 0.4 mmHg (P less than 0.05), and FENa was significantly elevated from 0.27 +/- 0.08 to 2.02 +/- 0.55% (P less than 0.05). In conclusion, spontaneously hypertensive rats have a blunted increase in RIHP and pressure natriuresis response in comparison with Wistar-Kyoto rats. Thus, in Okamoto spontaneously hypertensive rats, the effect of RPP on RIHP is attenuated, leading to a blunted pressure natriuresis response.

Animals↗
PubMed1988

Control of sodium excretion in NE-ACTH hypertension: role of pressure natriuresis.

The purpose of this study was to test the hypothesis that, in the presence of high circulating catecholamines, ACTH decreases renal excretory capability and that its natriuretic effects are caused by increased renal arterial pressure (RAP). In six conscious dogs, norepinephrine (NE, 0.4 micrograms.kg-1.min-1) alone for 5 days caused a small but significant rise in arterial pressure (AP) from 102 +/- 6 to 115 +/- 8 mmHg. An infusion of ACTH (600 micrograms/day) for 7 days, superimposed upon the NE, caused a further rise in AP to a plateau of 143 +/- 9 mmHg after 5 days while cumulative sodium balance fell to -149 +/- 41 meq by the 7th day. Cumulative water balance fell to -660 +/- 232 ml by the 3rd day and then increased slightly. In contrast, when ACTH infusion was repeated during NE infusion while RAP was prevented from increasing using a servo-controlled aortic occluder, cumulative sodium balance increased to 197 +/- 35 meq and AP rose from 108 +/- 5 to 168 +/- 5 mmHg after 7 days and did not plateau. Cumulative water balance rose to 2,325 +/- 445 ml. Thus, in dogs receiving a background infusion of NE, ACTH causes moderate hypertension and natriuresis. However, when RAP is not allowed to rise, ACTH is associated with sodium retention and severe systemic hypertension, suggesting that the natriuretic effects of ACTH are caused by increased RAP and that the natriuresis blunts the chronic hypertensive effects of ACTH.

Adrenocorticotropic Hormone↗
PubMed1989

Renal sympathetic nerve activity and natriuresis during water immersion in conscious dogs.

The role of renal sympathetic nerve activity (RSNA) in the natriuresis and diuresis induced by head-out water immersion (WI) was studied in eight conscious female dogs. The dog was instrumented chronically with a stainless steel electrode for the measurement of RSNA and two catheters for the measurements of systemic arterial (Pa) and central venous (Pv) pressures. The WI caused an immediate reduction of RSNA by 43 +/- 7% (P less than 0.05), and this low level was sustained throughout a 120-min WI under thermoneutral conditions (37 degrees C). Urine flow and sodium excretion increased by 211 +/- 54 (P less than 0.05) and 240 +/- 122% (P less than 0.05), respectively, but creatinine clearance did not change significantly during WI. A step increase in Pa (by 10 +/- 4 mmHg, P less than 0.05) and Pv (by 10.0 +/- 0.8 mmHg, P less than 0.05) was observed also during WI. In another series of studies, renal denervations were performed 2-4 wk before the experiment in six of the same dogs. Dogs with renal denervation showed no significant changes in urine flow and sodium excretion in response to WI, whereas Pa and Pv increased by 10 +/- 7 and 10.0 +/- 2.0 mmHg relative to the control level, respectively. It is concluded that the reduction of RSNA observed during WI plays a major role in the natriuresis in the dog.

Animals↗
PubMed1990

Atrial natriuretic peptide induces sustained natriuresis in conscious dogs.

Although acute infusions of atrial natriuretic peptide (ANP) often cause natriuresis, these effects are not sustained, possibly because of reductions in arterial pressure or other compensatory adaptations. The aim of this study was to determine whether physiological increases in intrarenal ANP levels cause sustained natriuresis if changes in arterial pressure and other neurohumoral influences that might obscure the renal responses are controlled. Changes in renal function were quantitated during chronic unilateral renal arterial infusion of ANP at rates of 1, 2, and 4 ng.kg-1.min-1 in conscious dogs (n = 7) with the urinary bladder split to allow continuous measurement of renal excretion in the ANP-infused and contralateral, vehicle-infused kidneys. There was no change in mean arterial pressure at any infusion rate. During 1 ng.kg-1.min-1 infusion of ANP for 5 days, the renal excretory responses were small and variable. However, during 2 and 4 ng.kg-1.min-1 ANP infusion for 7 days, sodium excretion averaged 37.2 +/- 10.0 and 134.8 +/- 19.0% greater, respectively, in the ANP-infused kidneys compared with the vehicle-infused kidneys but there were no changes in glomerular filtration rate or effective renal plasma flow. These results demonstrate that when compensatory changes in arterial pressure and neurohumoral factors are controlled, ANP, at physiological concentrations, causes marked increases in renal excretion. This study supports the concept that ANP's effects to increase renal excretory capability could play a role in long-term control of arterial pressure and body fluid homeostasis.

Aldosterone↗
PubMed1993

Endothelin-induced natriuresis and diuresis are pressure-dependent events in the rat.

The goal of the current study was to determine the mechanism by which doses of endothelin (ET) that do not markedly affect the glomerular filtration rate (GFR) cause a natriuresis and diuresis. ET was infused into pentobarbital-anesthetized female rats at 50 ng.kg-1.min-1 iv for 30 min. In controls (n = 6 rats; n = 5 in all other groups), ET increased mean arterial blood pressure (MAP) from 95 +/- 2 to 131 +/- 2 (SE) mmHg, Na excretion (UNa V) from 0.34 +/- 0.07 to 1.83 +/- 0.2 meq/min, and urine flow rate (V) from 13 +/- 1 to 24 +/- 3 ml/min (all P < 0.01 vs. baseline). At 15 min during infusion of ET, the GFR was not affected (2.1 +/- 0.1 to 2.2 +/- 0.1 ml/min) but modestly decreased to 1.8 +/- 0.1 ml/min at 30 min (P < 0.05 vs. baseline). Either removing the capsule from both kidneys during surgery or maintaining renal arterial pressure at baseline values with an adjustable clamp on the aorta above the right renal artery abolished the ET-induced increase in UNa V and V. Meclofenamate also did not alter the ET-induced increase in MAP, V, or UNa V. To determine the intrarenal site of action of ET, experiments were conducted with ET plus amiloride or with a combination of amiloride plus furosemide; there was a larger ET-induced diuresis and natriuresis in amiloride-treated rats and an even larger response with amiloride plus furosemide compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiloride↗
PubMed1997

Age-related changes in the pressure diuresis and natriuresis response.

The renal-excretory responses to changes in renal perfusion pressure (RPP) were studied in anesthetized young (3 mo old), adult (12 mo old), and senescent (24 mo old) rats to evaluate whether the pressure diuresis and natriuresis mechanism is altered as a function of age. Experiments were performed in anesthetized animals in which nervous and systemic hormonal influences to the kidney were fixed. Mean arterial pressure was similar in all three groups: 97.6 +/- 2.6, 102.1 +/- 3.7, and 95.2 +/- 5.2 mmHg in young, adult, and senescent rats, respectively. The relationships between RPP and diuresis/natriuresis or fractional excretions of water and sodium were similar in young and adult rats. However, in senescent rats the pressure-diuretic and pressure-natriuretic responses were slightly shifted to the right, so that diuresis and natriuresis were significantly lower at higher levels of RPP. Glomerular filtration rate was well autoregulated, and there were no differences between young and adult rats at each level of RPP. However, a significantly lower glomerular filtration rate was observed in senescent rats. These results indicate an age-related decline in the pressure-dependent sodium and water excretion that appears to be due to a decrease in glomerular filtration and an increase in tubular sodium reabsorption.

Aging↗
PubMed1998

Mechanism of vasopressin natriuresis in the dog: role of vasopressin receptors and prostaglandins.

Renal effects of physiological amounts of vasopressin were studied in conscious dogs during servocontrolled overhydration (2% body wt). During infusion of vasopressin (50 pg . min-1 . kg body wt-1), plasma vasopressin concentration increased to 2.30 +/- 0.20 pg/ml compared with 0.12 +/- 0.03 pg/ml during control (water diuresis). With vasopressin infusion, urine flow was significantly lower (0.30 +/- 0.10 ml/min) and sodium excretion (UNaV) was significantly higher (58.0 +/- 15.8 micromol/min) than without vasopressin (4.6 +/- 0.4 ml/min and 14.4 +/- 4.1 micromol/min, respectively). Deamino-[Cys1,D-Arg8]vasopressin, a V2 receptor agonist (4 pg . min-1 . kg-1), mimicked the antidiuretic response (0.20 +/- 0.03 ml/min) without changing UNaV (9.7 +/- 4.4 micromol/min). Indomethacin given during arginine vasopressin (AVP) infusion suppressed prostaglandin E2 excretion, intensified the antidiuresis (0.10 +/- 0.02 ml/min), and abolished the natriuresis (13.4 +/- 3.7 micromol/min). During AVP infusion, UNaV was highly correlated (r = 0.85) with prostaglandin E2 excretion. Blood pressure, glomerular filtration rate, plasma atrial natriuretic peptide concentration, and the rate of proximal tubule reabsorption (derived from lithium clearance) were similar in all series. The data indicate that, in the dog, physiological amounts of vasopressin can induce natriuresis, probably through activation of non-V2 receptors and the intrarenal synthesis of prostaglandins.

Animals↗
PubMed1998

Preventing hemodilution abolishes natriuresis of water immersion in humans.

The hypothesis was tested that hemodilution is one of the determinants of the water immersion (WI)-induced natriuresis. Eight males were subjected to 3 h of 1) WI to the midchest (Chest), 2) WI to the neck combined with thigh cuff-induced (80 mmHg) venous stasis (Neck + stasis), and 3) a seated time control (n = 6). Central venous pressure and left atrial diameter increased to the same extent during Chest and Neck + stasis (P < 0.05), whereas renal sodium excretion only increased during Chest from 77 +/- 7 to 225 +/- 13 micromol/min (P < 0.05). During Chest, plasma colloid osmotic pressure (COP) decreased from 27.7 +/- 0.7 to 25.1 +/- 0.7 mmHg (P < 0.05), and plasma volume (PV) increased from 3,263 +/- 129 to 3,581 +/- 159 ml (P < 0.05), whereas these variables remained unchanged during Neck + stasis. Plasma norepinephrine concentration decreased similarly during Chest and Neck + stasis by 45 +/- 7 and 34 +/- 4%, respectively (P < 0.05), whereas plasma renin activity decreased only during Chest (P < 0.05). In conclusion, during WI in humans 1) hemodilution (decrease in COP and increase in PV) is a pivotal stimulus for the natriuresis and 2) central blood volume expansion without hemodilution does not augment renal sodium output.

Adult↗