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 631 records · Page 35Linked to original sources
PubMed1991

Relationship between baroreflex sensitivity, renin suppression and natriuresis in salt-sensitive rabbits.

This study determined the influence of baroreflex sensitivity (BRS) on the rate of urinary sodium excretion and plasma renin activity (PRA) in response to a saline infusion in conscious male rabbits specifically bred for high (Group I; n = 7) and low (Group II; n = 10) BRS and in seven control animals. Only Group II showed significant increases in blood pressure on a chronic high-salt intake. After ensuring that each animal was in sodium balance, a (0.7-0.9%) saline infusion of 3-4 ml/kg per h for 90 min (25% daily sodium intake for each rabbit) was given and urine collected at 15-min intervals via a bladder catheter. No differences were found in control urine volumes, urinary sodium or PRA. Group I excreted over 50% of the sodium load and Group II less than 20% within 90 min. PRA fell by more than 30% within 30 min in six Group I rabbits but decreased by less than 30% or increased in Group II. In the control animals, sodium excretion rates and PRA suppression were also much greater in those with high BRS. A highly significant correlation (r = 0.808, P less than 0.01) was found between the per cent of the sodium load excreted and BRS. It is suggested that the delayed sodium excretion and blood pressure elevation in salt-sensitive subjects may be due to a genetic impairment in baroreflex control of renal sympathetic nerve activity.

Animals↗
PubMedDate not supplied

Obesity modifies the relationship between ambulatory blood pressure and natriuresis in children.

BACKGROUND: The objective in the present study was to evaluate if obesity beginning in the first two decades of life influences the relationship between ambulatory blood pressure and urinary sodium excretion. DESIGN AND METHODS: Eighty-five obese and 88 non-obese children aged 3-19 years were included in the study. For each subject, a 24h ambulatory blood pressure monitoring and a complete urine collection were simultaneously performed according to the protocols designed. The averages of ambulatory blood pressure and of the urinary excretion rates for sodium, potassium and creatinine were calculated separately for 24-h, awake and sleep periods as defined by a mini-diary. RESULTS: Weight and sodium excretion are directly associated with systolic blood pressure; however, the relationship between blood pressure and sodium excretion seems to be modified in obese children as compared to controls. The interaction between sodium excretion and weight was negative indicating that the rate of change of systolic blood pressure by sodium unit is smaller for the obese than for the non-obese, even though at the same urinary sodium excretion level the obese children had higher ambulatory systolic blood pressure. CONCLUSIONS: Obesity during the first two decades of life seems to restrict sodium excretion, leading to higher blood pressure values. The capacity to excrete sodium seems to be heterogeneous, the lowest capacity being at the highest blood pressure values. Subsets of the obese, those with the lowest ability to excrete sodium, may be further protected by low sodium intake in order to prevent a rise in blood pressure.

Adolescent↗
PubMed1985

Angiotensin II natriuresis and antinatriuresis: role of renal artery pressure, renal hemodynamics, and tubular reabsorption.

The aim of this study was to determine the role of changes in renal artery pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (AII). In anesthetized dogs, endogenous AII formation was blocked with SQ-14225 and AII was infused i.v. at rates of 5-1215 ng/kg/min while RAP was either servo-controlled at the normal level or permitted to increase. When RAP was servo-controlled to prevent a rise i RAP, AII infusion at all rates from 5-1215 ng/kg/min decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa), while increasing fractional reabsorption of lithium (FRLi), an index of proximal tubule fractional sodium reabsorption and distal fractional sodium reabsorption (FRDNa): When RAP was permitted to increase, AII infusion rates up to 45 ng/kg/min decreased UNaV, and FENa, while increasing FRLi and FRDNa. However, at 135 ng/kg/min and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though RBF and FF were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during AII infusion, compared to the dogs in which RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of AII cause antinatriuresis when RAP was prevented from increasing. The natriuretic effect of high dose of AII is caused by increased RAP which decreases fractional sodium reabsorption in proximal and distal tubules and causes slight increases in sodium delivery to the tubules.

Absorption↗
PubMed1985

The natriuresis following oral administration of the calcium antagonists--nifedipine and nitrendipine.

Ten healthy individuals received in random order placebo, nifedipine 10 mg, nifedipine 20 mg, nitrendipine 10 mg and nitrendipine 20 mg as single oral administrations at weekly intervals. On the day before each treatment placebo was administered. Urine was collected for 6 h and then for 18 h after each administration. There was a significant increase in urine volume and sodium excretion after the drugs, but no change in potassium excretion. The effect was most evident in the 6 h after drug administration. The effect was no greater at the higher doses of either drug. A natriuretic-diuretic action of nifedipine and nitrendipine has been confirmed in man. The mechanism of the effect remains unclear.

Administration, Oral↗
PubMed1988

Role of the adrenal cortex in the natriuresis associated with vasopressin infusion.

We have compared the effects of a 48-h continuous infusion of arginine vasopressin (AVP) given to four subjects (one subject studied twice) with that given to four patients lacking adrenocortical function and maintained on fixed doses of mineralocorticoid and glucocorticoid replacement therapy. Both patients and normal subjects were subjected to dietary salt and water restriction during the period of the infusion, and all participants were in balance on a low sodium diet at the start of the infusion period. Infusion of vasopressin in normal subjects was associated with an increase in fractional excretion of sodium by the kidney, which continued during the day after the infusion was stopped. The infusion was also associated with a fall in plasma aldosterone as well as falls in whole blood packed cell volume, plasma renin activity and plasma noradrenaline. Infusion of vasopressin in patients lacking adrenocortical function was associated with a smaller increase in fractional excretion of sodium by the kidney in comparison with that seen in normal subjects, and the increase in sodium excretion was confined to the period of the infusion. Mineralocorticoid activity was maintained constant during the infusion, although a fall in whole blood packed cell volume, plasma renin activity and plasma noradrenaline were noted, in similarity to the study made in normal subjects. We conclude that changes in mineralocorticoid activity are the main factors contributing to the increase in renal sodium excretion seen during, and after, the continuous infusion of vasopressin in salt- and water-restricted man.

Adrenal Cortex↗
PubMed1988

Arginine vasopressin dissociates the diuresis and natriuresis due to atrial natriuretic factor in man.

The possible interaction between arginine vasopressin (AVP) and atrial natriuretic factor (ANF) in the control of urinary sodium and water excretion was investigated in man. Nine healthy male volunteers undergoing stable maximal water diuresis were studied on four separate occasions. Atrial natriuretic factor 15 pmol kg-1 min-1 or placebo (P) was concomitantly administered against a background infusion of either AVP 0.003 pmol kg-1 min-1 or P; thus the combinations P + P, AVP + P, P + ANF and AVP + ANF were studied. Atrial natriuretic factor caused a significant increase in sodium excretion (UNaV) [+56%], urinary flow rate (V) [+17%] and free water clearance (CH2O) [+23%]; creatinine clearance (Ccr) did not change. Arginine vasopressin reduced V (-58%) and CH2O (-68%) but did not alter UNaV or Ccr. On the AVP + ANF study day, UNaV increased (+64%) as with P + ANF, but V (-44%) and CH2O (-52%) continued to decrease below baseline levels; analysis of variance showed this antidiuresis reflected the prevalent effect of AVP rather than any specific interaction. These results show that AVP is able to dissociate the natriuretic and diuretic effects of ANF.

Adult↗
PubMedDate not supplied

Effect of beta-adrenoreceptor blockade on the renin response to acute natriuresis.

1. The response of plasma renin activity to frusemide 40 mg given intravenously, was examined before and after oral propranolol 160 mg daily for 7 days in normal and hypertensive subjects. 2. Although basal renin levels were often reduced, the increase following frusemide was essentially unaltered by propranolol therapy. 3. These findings indicate that enhanced renin activity associated with diuretic use may not be prevented by concurrent propranolol administration. Limitation of hypotensive action of combined beta-blocker diuretic therapy can therefore be anticipated. 4. Preservation of the renin stimulatory effect of frusemide during beta blockade confirms the value of this procedure in the investigation of mineralocorticoid and renovascular hypertension were discontinuation of treatment may be undesirable.

Adrenergic beta-Antagonists↗
PubMed1985

Diuresis and natriuresis following acute pneumothorax in very low birthweight infants.

Seven tension pneumothoraces developed in six very low birthweight infants receiving assisted ventilation for hyaline membrane disease. Mean values for blood pressure and creatinine clearance (Ccr) tended to increase following pneumothorax decompression, although neither increase was statistically significant. Urine volume, osmolar clearance and urine sodium excretion all increased significantly in the 8 h following diagnosis and decompression of pneumothoraces. However, when expressed as a percentage of Ccr, none of these variables changed significantly. Mean sodium balance changed from positive to negative despite a significant increase in urine aldosterone excretion. It is suggested that the increases in osmolar clearance and sodium excretion were consequences of the increase in Ccr following pneumothorax decompression. Developmental immaturity in the renal tubular response to aldosterone might also have contributed to development of negative sodium balance.

Acute Disease↗
PubMed1995

The role of the peripheral sympathetic nervous system in the natriuresis following central administration of an I1 imidazoline agonist, moxonidine.

1. Central administration of the I1-imidazoline receptor agonist moxonidine increases sodium excretion without alteration of blood pressure. In the present study we determined whether this natriuretic action was mediated through a decrease in activity of the sympathetic nervous system, as has been reported for the antihypertensive action of this compound. Interruption of the sympathetic nervous system was achieved with prazosin (alpha 1-adrenoceptor antagonist) and renal denervation. 2. In pentobarbitone-anaesthetized Sprague-Dawley rats, intracerebroventricular (i.c.v.) injection of moxonidine alone increased urine volume and sodium excretion. Prazosin (0.15 mg kg-1, i.v.) alone decreased urine flow rate and sodium excretion as compared to the vehicle controls. In the presence of prazosin, i.c.v. injection of moxonidine failed to increase sodium excretion or urine volume as compared to animals which received the prazosin alone. 3. The administration of moxonide (i.c.v.) to sham renal-denervated animals caused an increase in urine flow rate, urine sodium excretion, osmolar clearance and free water clearance. The increase in sodium excretion and osmolar clearance were completely attenuated in renal denervated rats, however, urine flow rate was still increased and this was secondary to the increase in free water clearance which remained intact. 4. These results indicate the importance of an intact sympathetic nervous system in the renal response to i.c.v. moxonidine. Moreover, the differential antagonism of these interventions on solute and water excretion indicate that they may be mediated at two separate sites and/or receptors following i.c.v. moxonidine.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1992

Atrial natriuretic peptide in the preterm infant. Lack of correlation with natriuresis and diuresis.

We assessed the relation of atrial natriuretic peptide (ANP) to renal function on postnatal day 2 and day 5 in preterm infants. Plasma ANP concentration was measured by radioimmunoassay in two groups of preterm infants: group 1, gestational age less than 30 weeks, n = 10; and group 2, gestational age 30-34 weeks, n = 11. The identity of the immunoreactivity as ANP-28 was confirmed by HPLC. Plasma ANP was significantly higher in group 1 than in group 2 on day 2 and day 5 (p < 0.01) and ANP concentration decreased by day 5 in both groups (group 1, p < 0.01; group 2, p < 0.02). The results showed no correlation between plasma ANP concentration and urinary sodium excretion or creatinine clearance, which may be due to a blunted renal response to ANP, but other factors may be involved also. We conclude that preterm infants are able to release large amounts of ANP, but a high plasma ANP concentration does not correlate directly with renal regulation of sodium and water balance.

Atrial Natriuretic Factor↗