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At least 595 records · Page 33Linked to original sources
PubMed1992

Failure of atrial natriuretic peptide to induce natriuresis in aortocaval fistula dogs.

Creation of an aortocaval fistula (ACF) in dogs induces salt and water retention, activation of the renin-angiotensin and adrenergic nervous systems and renal papillary ischemia associated with high levels of circulating atrial natriuretic peptide (ANP). The effects of intrarenal ANP (1.2 micrograms/min) infusion on systemic and renal hemodynamics, renal excretory function, renal output of renin and norepinephrine (NE) and papillary plasma flow (PPF) were studied in both normal and ACF dogs. ANP did not alter systemic hemodynamics in either group, but led to a significant increase in renal blood flow (RBF), glomerular filtration rate (GFR), urine flow rate (V), sodium excretion (UNaV) and fractional excretion of sodium (FENa), and a significant decrease in renal vascular resistance (RVR) and urine osmolality (UOsm) in normal dogs. GFR, RBF, RVR, V, UNaV, FENa and UOsm remained unchanged, however, in ACF dogs. In ACF dogs, both renal renin and NE output were significantly greater during baseline and remained significantly greater following ANP infusion, associated with a significantly lower PPF compared with normal dogs. These data suggest that ACF dogs are resistant to the renal effects of ANP, which can neither mitigate the hormonal mediators of sodium retention nor reverse the papillary ischemia observed in this model.

Animals↗
PubMed1997

Inhibition of COMT induces dopamine-dependent natriuresis and inhibition of proximal tubular Na+,K+-ATPase.

The enzyme catechol-O-methyltransferase (COMT), which plays an important role for dopamine metabolism, is abundantly expressed in the kidney. To test whether the natriuretic effects of dopamine may be related to the rate of dopamine metabolism, rats were treated with nitecapone, a peripheral inhibitor of COMT. Nitecapone, given by gavage, induced a highly significant (5.6-fold) increase in sodium excretion, which was associated with an inhibition of the Na+,K+-ATPase activity in both the proximal convoluted and proximal straight tubules (PCT and PST, respectively). These effects were completely abolished if the rats were also treated with a specific dopamine 1 antagonist, SCH 23390. Furthermore, the natriuretic effect of nitecapone was also observed in rats on a high salt diet. The kidney-specific pro-drug to dopamine, glu-dopa, induced a significant, but less pronounced increase in urinary sodium excretion, associated with a dopamine-dependent inhibition of the Na+,K+-ATPase activity in the PCT but not in the PST. Nitecapone and glu-dopa had an additive natriuretic effect. It is concluded that COMT plays an important role in determining the natriuretic effects of the renal dopamine system.

Animals↗
PubMed2003

Impaired pressure natriuresis in obese youths.

OBJECTIVE: To compare the response and recovery of blood pressure (BP) and sodium excretion (U(Na)V) in response to a behavioral stressor in overweight/obese and lean adolescents. RESEARCH METHODS AND PROCEDURES: Twenty-five lean (12% to 20% body fat) and 59 overweight/obese (>25% body fat) normotensive adolescents were provided all meals for 3 days (average sodium intake, 4000 +/- 200 mg/d), before performing the stressor on the third day. There was a 2-hour pre-stress rest, followed by a 1-hour stress (involving a video game task), and a 2-hour recovery. Percentage of body fat was obtained from DXA. U(Na)V was measured hourly, whereas systolic BP and diastolic BP measurements were obtained at 15-minute intervals, and averaged for each 1-hour period. RESULTS: There was no significant difference between the lean and overweight/obese group for the response of systolic BP and diastolic BP (group by time interaction, p = 0.60 and p = 0.64, respectively). However, the lean group had a significantly greater increase in U(Na)V in response to the stressor compared with the overweight/obese group (p = 0.02). U(Na)V remained elevated compared with baseline in both groups at the 1-hour (p <or= 0.0001) and 2-hour (p <or= 0.0001) post-time points. Furthermore, there was a tendency for a larger number of sodium retainers in the overweight/obese group compared with the lean group (39.0% vs. 20.0%; chi(2) = 2.85, df = 1, p = 0.09). DISCUSSION: This study provided evidence that sodium regulation was impaired during a behavioral stress in overweight/obese individuals compared with lean individuals.

Absorptiometry, Photon↗
PubMed1975

A comparison of natriuresis after oral and intravenous sodium loading in sodium-depleted man: evidence for a gastrointestinal or portal monitor of sodium intake.

1. Dietary sodium reduction in man is followed by rapid conservation of sodium by the kidneys. The rapidity of this response suggests that the gastrointestinal tract is involved in early recognition of changes in sodium intake or in mediation of the compensatory response. 2. In order to test the hypothesis, 100 mmol of sodium was given to normal volunteers in balance on a low-sodium diet (5 mmol/24 h): the dose was given either orally or intravenously. 3. Those who received their sodium orally excreted it more rapidly than those who received it intravenously and the difference was most marked in the first 8 h after the dose. 4. This finding is consistent with the presence of an input receptor for sodium in the gastrointestinal tract.

Administration, Oral↗
PubMed1977

Natriuresis in rats acutely depleted of chloride.

1. Acute chloride depletion, without sodium depletion, was produced in rats by a single exchange peritoneal dialysis against sodium bicarbonate solution. Blood volume was restored after dialysis by infusion of salt-free albumin, and exogenous deoxycorticosterone and antidiuretic hormone were given. 2. Clearance studies in the period (3 h) after dialysis revealed no difference in the glomerular filtration rate or in the filtered sodium load between experimental and control rats but urinary sodium concentrations and absolute and fractional sodium excretion were significantly higher in the chloride-depleted group. 3. There was also a significant kaliuresis, increased urinary flow rate and diminished free water reabsorption. Urinary bicarbonate excretion increased to a variable degree but the major rise in anion excretion was 'unmeasured' (Na+ + K+ - [Cl- + HCO3- + PO4(3-)]). 4. It is postulated that chloride depletion imposes limitations on sodium reabsorption in the ascending limb of the loop of Henle.

Animals↗
PubMed1984

Intracerebroventricular infusion of sodium chloride-rich artificial cerebrospinal fluid in rats induces natriuresis and releases an inhibitor of prostaglandin synthesis.

Urinary sodium excretion in anaesthetized rats subjected to high-sodium artificial cerebrospinal fluid (CSF) infusion into the lateral brain ventricle, was significantly higher than in rats infused with normal-sodium CSF. Urinary immunoreactive 6-ketoprostaglandin F1 alpha, the stable derivative of prostacyclin, was significantly reduced in the high-sodium CSF group, as compared with the normal-sodium CSF group. When dog aortic endothelium was incubated in the presence of plasma, endothelial prostacyclin production was found to be inhibited by plasma from rats infused with high-sodium CSF compared with the effect of plasma from the rats infused with normal-sodium CSF. Our results indicate that intracerebroventricular infusion of high-sodium CSF induces a natriuretic response and is associated with the appearance of a humoral factor which blocks prostacyclin biosynthesis.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Atrial natriuretic peptide: physiological release associated with natriuresis during water immersion in man.

Thermoneutral water immersion produces a physiological increase of thoracic blood volume, raises central venous pressure and increases urinary sodium excretion by a hitherto ill-understood mechanism. We have investigated whether this enhanced sodium excretion could be mediated by the recently discovered natriuretic factor, atrial natriuretic peptide (ANP). During water immersion there was a highly significant (P less than 0.001) twofold increase of the mean plasma ANP concentration and a doubling of the mean urinary sodium excretion. Both were unchanged during the control experiments. These results are consistent with the hypotheses that ANP is released into plasma in response to central blood volume expansion and that it functions as a natriuretic hormone in normal man under physiological conditions.

Adult↗
PubMed1999

Pretreatment renal vascular tone predicts the effect of specific renin inhibition on natriuresis in essential hypertension.

BACKGROUND: In essential hypertension an elevated renal vascular resistance (RVR) may be a marker of renin-angiotensin-aldosterone system-mediated impairment of renal sodium excretion. This hypothesis was tested by investigating whether, in subjects with essential hypertension, the natriuretic response to specific renin-angiotensin-aldosterone system (RAAS) blockade by renin-inhibitor remikiren could be predicted from pretreatment renal vascular tone. MATERIALS AND METHODS: Renal hemodynamics, and the effects of single (n = 17) and multiple doses (n = 8, 8 days) of remikiren (600 mg day-1) on sodium excretion were studied under conditions of carefully controlled sodium balance. RESULTS: Pretreatment renal vascular tone showed considerable individual differences: filtration fraction (FF) ranged from 21.2 to 30.3% and RVR from 18.8 to 33.5 10-2 mmHg min mL-1 in the single dose study, and FF from 20.8 to 24.9% and RVR from 14.8 to 28.8 10-2 mmHg min mL-1 in the multiple dose study. Remikiren induced a fall in blood pressure, FF and RVR, with considerable interindividual variability in natriuretic response. During single dose, cumulative sodium loss was 5.1 mmol per 5 h (-8.8 to +24.6), whereas after 8 days treatment cumulative sodium loss was 72 +/- 30 mmol (-46 to +187). The natriuretic response to remikiren during single as well as multiple dose significantly correlated with pretreatment renal vascular tone (estimated from FF and RVR) but not with remikiren-induced changes in renal hemodynamics or in hormonal parameters. Cumulative sodium loss was largest in patients with a higher pretreatment FF and RVR (r = 0.74, P < 0.001 and r = 0.52, P < 0.05, respectively, single dose; and r = 0.75, P < 0.05 and r = 0.73, P < 0.05, respectively, multiple dose). CONCLUSION: These data support the hypothesis that in essential hypertension an elevated renal vascular tone is a marker of RAAS-mediated impairment of sodium excretion.

Adult↗