Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “DIURESIS”

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 145 records · Page 8Linked to original sources
PubMed2000

State-dependent expression of pressure diuresis in conscious rats.

In 1967, Guyton and Coleman modeled pressure diuresis as the underlying, essential, long-term mechanism that regulates arterial pressure when sodium intake changes. Other mechanisms that influence renal function interact with pressure diuresis to achieve sodium balance and determine the blood pressure. Increases in sodium intake suppress sodium conserving mechanisms and activate natriuretic mechanisms; decreases in sodium intake have the opposite effect. If the Guyton-Coleman model is correct, then pressure diuresis should be more readily detected in animals on a high-salt diet than in animals on a low-salt diet. We measured spontaneous changes in arterial pressure and urine flow in conscious rats fed low-salt (0. 4% NaCl) and high-salt (8.0% NaCl) chow. For 10 rats fed a high-salt diet, arterial pressure and urine flow were positively correlated in 19 of 32 (59%) trials. In 10 rats fed a low-salt diet, a positive correlation was observed in 10 of 33 (30%) trials. Chi-square analysis revealed that differences in Na+ content of the diet were significantly associated with the probability of a positive relationship between blood pressure and urine flow. These results support the hypothesis that the expression of pressure diuresis across time is dependent on the state of sodium balance.

Animals↗
PubMed1979

[Renal blood flow, diuresis and isotope nephrogram in experimental stenosis of the renal artery (author's transl)].

After experimental stenosis of the renal artery of the dog, the isotope nephrogram shows a prolongation of the transit-time, when the renal blood flow is reduced to 40--70%. This finding was most significant in low diuresis (0,05--0,2 ml/min), sporadic in moderate diuresis (0,2--2,0 ml/min), no longer demonstrable in forced diuresis (greater than 2,0 ml/min). The diuretic effect of X-ray contrast medium (70% Na-Meglumin-Jotalamat, 0,5 ml/kg i.v.) normalizes a pathologic ING in low diuresis.

Animals↗
PubMed1989

Physiological evaluation of diuresis in commercial broiler breeders.

A physiological investigation on an outbreak of diuresis syndrome in commercial broiler breeder hens was carried out. Daily water consumption increased 4-fold and daily manure wet weight increased two-fold in affected hens. 2. The syndrome did not have a genetic basis. It was associated with kidney dysfunction which, once acquired, was not alleviated by changing the diet, the drinking water, or the environment. Diuresis ceased when water intake was restricted and returned when water was again made freely available. 3. The syndrome was not caused by nephrogenic diabetes insipidus or diabetes mellitus. Key changes in kidney function associated with diuresis included: increased urine flow, decreased urine osmolality, reduced glomerular filtration rates, increased fraction of the glomerular filtration rate excreted as urine and decreased urinary hydrogen ion concentrations. 4. Preliminary histopathological findings and the physiological patterns of kidney dysfunction indicated that the diuresis syndrome was associated with permanent kidney damage, probably caused by the Arkansas strain of infectious bronchitis virus.

Animals↗
PubMed1988

Dose-dependent effects of felodipine on diuresis and natriuresis in healthy subjects.

We compared the effects of various acute doses of felodipine and placebo on diuresis and natriuresis in healthy men. The subjects were given felodipine, 1 and 3 mg as an intravenous infusion, and 5, 15, and 40 mg as an oral solution on 5 separate days. On each day blood pressure and heart rate were recorded and urine was collected for analysis of volume and sodium for 24 h. Felodipine induced a dose-dependent increase in heart rate and a dose-dependent decrease in diastolic blood pressure. These effects were maximal within 30 min of drug administration. Felodipine induced a maximal increase in diuresis of about 150% compared with placebo and a maximal increase in natriuresis of about 240%. The renal effects were most pronounced during the first 4 h after dose intake. During the 8-24 h interval, diuresis and natriuresis were lower than after placebo, but when the whole 24-h period was considered, no significant differences were found between felodipine and placebo in regard to sodium and water excretion. The most pronounced effects on diuresis and natriuresis were seen after moderate doses (3 mg i.v. and 15 mg orally). The response to the highest dose (40 mg orally) was somewhat less probably due to the excessive drop in diastolic blood pressure.

Adult↗
PubMed1978

Diuresis renography in equivocal urinary tract obstruction.

A trial of the value of diuresis renography in equivocal upper urinary tract obstruction is presented. Fifty-two patients were examined by standard renography and renography under a diuretic provocation. The results indicate that the technique is of considerable value in making the vital distinction between dilatation on the excretion urogram due to atonicity and that caused by a genuine obstruction. A quantitative index of the response to diuresis reflecting the degree of impedance to flow is described--the Diuresis Excretion Index. Diuresis renography is recommended in the evaluation of the patient with equivocal urinary tract obstruction.

Diuresis↗
PubMed1979

Diuresis renography and the results of pyeloplasty for idiopathic hydronephrosis.

Eighty-six kidneys in 82 patients have been assessed by diuresis renography after pyeloplasty. A non-obstructed diuresis renogram was found in 64% of kidneys. Ninety per cent of patients were clinically improved by surgery and 51% of cases studied had improved urographic features. Thirty kidneys (29 patients) were assessed both before and after pyeloplasty. An improvement in the diuresis renogram was found in 89% of cases postoperatively. Standard renography demonstrated improved drainage in only 33% of kidneys. These findings are discussed in relation to the value of diuresis renography after pyeloplasty.

Adolescent↗
PubMed1985

A comparison of diuresis renography, the Whitaker test and renal pelvic morphology in idiopathic hydronephrosis.

Diuresis renography and the Whitaker test are established methods of diagnosing obstruction in dilated renal pelves. These techniques have been compared in 36 patients with radiologically demonstrated idiopathic hydronephrosis and evaluated, where possible, against renal pelvic morphological features. The agreement between the results of the tests was as follows: diuresis renography/Whitaker test 67%; diuresis renography/renal pelvic morphology 74%; Whitaker test/renal pelvic morphology 58%. Both diuresis renography and the Whitaker test are indicated in some cases of idiopathic hydronephrosis.

Diuresis↗
PubMed1993

Desmopressin in elderly women with increased nocturnal diuresis. A short-term study.

We report the changes in the pattern of diuresis in 20 women (average age 71 years) with increased nocturnal diuresis who were treated with 20 micrograms desmopressin (Minirin). Before treatment, antidiuretic hormone levels were measured every 4 h over a 24-h period and 75% of the levels were found to be beneath the lowest detectable limit (< 0.4 pmol/l). Nocturnal diuresis decreased by 355 +/- 208 ml and in 8 cases the decrease exceeded 400 ml. Diurnal diuresis, on the other hand, increased by 226 +/- 331 ml. Side effects were mild and occurred in only 2 women.

Aged↗
PubMed1986

On the mechanisms of kappa-opioid-induced diuresis.

In conscious saline loaded rats, the kappa-opioid agonists tifluadom, U50488, and ethylketocyclazocine, given subcutaneously, induced a characteristic diuresis which could be antagonized by naloxone. Bilateral adrenal demedullation significantly reduced adrenal gland catecholamine content and plasma adrenaline levels, but did not significantly affect plasma corticosterone levels, indicating that the adrenal cortex remained both intact and functional. Seven days following bilateral adrenal demedullation, the subcutaneous administration of the kappa-agonists no longer induced diuresis. However, demedullation did not affect the diuretic response to frusemide or clonidine, nor did it affect the antidiuretic response induced by the mu-opioid agonists morphine and buprenorphine. Adrenal catecholamines do not appear to be involved in kappa-opioid-induced diuresis, since pretreatment with propranolol, prazosin and idazoxan did not affect the diuretic response in intact animals. The results indicate a link between the adrenal medulla and kappa-opioid-induced diuresis and suggest that a peripheral mechanism may also be involved in mediating this effect.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1997

Neurohumoral and hemodynamic mechanisms of diuresis during atrioventricular nodal reentrant tachycardia.

Thirty-two consecutive patients with paroxysmal supraventricular tachycardias, with previously defined mechanisms of the tachycardias, were interviewed by noninvestigators about whether they experienced symptoms of diuresis during or at the termination of the tachycardias, to test the hypothesis that patients with AV nodal reentrant tachycardia would have a feeling of diuresis, polyuria, or both during or at the termination of the tachycardia. Twelve of the 13 patients with AV nodal reentrant tachycardia (92%), two of the 15 patients with AV reentrant tachycardia (13%), and one of the 4 patients with atrial flutter associated with 2:1 AV conduction (25%) felt diuresis during or at the termination of the tachycardias (AV nodal reentrant tachycardia vs other forms of tachycardia; P < 0.001). In 14 of the 32 patients, the right atrial pressure and plasma atrial natriuretic peptide (ANP) concentration were measured during both the tachycardias and sinus rhythm. The mean right atrial pressure during AV nodal reentrant tachycardia was significantly elevated compared to that during other forms of tachycardia (P < 0.01). The plasma ANP concentration during AV nodal reentrant tachycardia was also elevated significantly compared to that during other forms of tachycardias (P < 0.001). There were no significant differences in the cycle lengths of the tachycardias, age, left atrial dimensions, or the left ventricular ejection fraction between the AV nodal reentrant tachycardia and the other forms of tachycardia. We concluded that the feeling of diuresis during or at the termination of tachycardia was a more common symptom in patients with AV nodal reentrant tachycardia. The higher secretion of plasma ANP from the right atrium might be involved in the mechanism of this symptom.

Atrial Natriuretic Factor↗
PubMedDate not supplied

Evaluation of 99MTC-diethylenetriaminepentaacetic acid renal scintigram curves in normal dogs after induction of diuresis.

The normal 99mTc-diethylenetriaminepentaacetic acid (DTPA) renal scintigram curve has 3 distinct phases; an arterial phase followed by progressive uptake and subsequent excretion from the kidney. In dogs with X-linked hereditary nephritis, a distinct flattening of the renal scintigram curve has been observed prior to any decline in glomerular filtration rate (GFR). The cause of this shape change is not known, however, it coincided with decreased urine-specific gravity and thus might be related to polyuria. To further evaluate this possibility, we assessed whether diuresis without concurrent renal disease could flatten the 99mTc-DTPA renal scintigram curve. GFR scintigraphy was performed in six healthy dogs once as a baseline, and again after induction of diuresis by each of four different methods. Scintigram curves were evaluated subjectively as well as quantitatively by calculation of GFR estimates, mean renal transit times, time to peak activity and half-time clearance. Complete flattening of the renal scintigram curve did not occur with diuresis alone, and therefore, flattening of the scintigram curve may serve as an early indicator of renal dysfunction. However, during diuresis after intravenous saline administration, alterations in time to peak activity and mean renal transit time may create inaccuracies in GFR estimates based on the conventional regression formula that cause a false lowering of the resultant global GFR value.

Animals↗
PubMed1985

Signals from the oropharynx may contribute to the diuresis which occurs in man to drinking isotonic fluids.

The drinking of a variety of isotonic salt solutions provoked a short load-dependent diuretic response in man, similar in latency to that of a water diuresis and reaching its maximum 40-60 min from the start of drinking. Subjects differed in the threshold load at which the response became evident, and also in the magnitude of their responses. Changes in free water clearance matched the increases in urinary minute volume, with no significant change in either urinary sodium or potassium excretion. Changes in urinary pH and in ammonium excretion were similar to those described for a water diuresis. Drinking an isotonic solution of mannitol provoked a diuresis similar to that of the salt solutions. All subjects had diarrhoea after drinking the mannitol. Signals arising from the oropharynx might be partly responsible for eliciting the diuresis. The significantly smaller urinary responses to infusions of isotonic salt solutions directly into the stomach support this view. The absence of a significant response to 'sham drinking' appears inconsistent with this, but oropharyngeal signals may only have a priming role in man and interact with other signals to give the full response.

Adult↗
PubMed1996

Neuropeptide Y-enhanced diuresis and natriuresis in anaesthetized rats is independent of renal blood flow reduction.

1. Neuropeptide Y (NPY) has been reported to enhance diuresis and natriuresis in anaesthetized rats although it is a potent renal vasoconstrictor in vitro in vivo in several species. Therefore, we have investigated anaesthetized rats to see whether reduction in renal blood flow (RBF) and enhancement of diuresis and natriuresis can occur concomitantly, and how diuresis and natriuresis might be enhanced despite reduced RBF. 2. Systemic or intrarenal NPY infusion (0.03-3 micrograms kg-1 min-1) had only a small effect on mean arterial pressure (maximal increase 15-20 mmHg) and heart rate (maximal decrease 30 beats min-1) but dose-dependently reduced RBF (maximal peak reduction 3 ml min-1) Endogenous creatinine clearance was not significantly altered. 3. In anaesthetized rats systemic infusion of 1 or 3 micrograms kg-1 min-1 NPY enhanced urine formation and sodium and calcium excretion by a maximum of 110, 110 and 45%, respectively, but did not alter potassium excretion. Enhancement of diuresis was also detectable in conscious rats. 4. The diuretic and natriuretic effects of systemically infused NPY were at least partly maintained in rats with decapsulated kidneys and in rats where NPY-induced increase of renal perfusion pressure was excluded mechanically by an adjustable clamp placed on the abdominal aorta. 5. Intrarenal infusion of 0.3 or 1 microgram kg-1 min-1 NPY reduced RBF to a greater extent than systemic infusion (maximal peak reduction 4 ml min-1) but caused a smaller enhancement or even a reduction of urine formation and sodium excretion. 6. We conclude that systemic infusion of NPY reduces RBF by a direct effect on the renal vasculature. Systemic NPY infusion enhances urine formation and sodium and calcium excretion. This occurs independently (at least in part) of pressure natriuresis by formation and/or release of an extrarenal factor which might act on distal tubules and/or collecting ducts.

Anesthesia, General↗
PubMed1991

Atrial natriuretic factor and postnatal diuresis in respiratory distress syndrome.

To find out if atrial natriuretic factor plays a part in the control of urine output during the initiation alone or throughout postnatal diuresis in neonates with respiratory distress syndrome, atrial natriuretic factor concentrations and clinical and renal variables were measured prospectively three times during the first three days of life in 13 premature infants. Atrial natriuretic factor concentrations rose significantly between the first and second sample times as did the urine output and output:input ratio. By the time that the third sample was taken, atrial natriuretic factor concentration had decreased significantly since the second sample had been taken, while urine flow was maintained. All subjects initiated a spontaneous diuresis that was related to the second concentration of atrial natriuretic factor. With partial correlation analysis a significant relationship was shown between the concentration of atrial natriuretic factor and the maintenance of urine output throughout the study period. Individual hormone concentrations did not, however, correlate with simultaneous renal variables. Changes in the concentrations of atrial natriuretic factor coincided with initiation of spontaneous diuresis in babies with respiratory distress syndrome, and may have a role in the complex mechanisms that maintain this diuresis.

Atrial Natriuretic Factor↗
PubMed1989

Kappa-opioid agonist induced diuresis. Is it mediated by a blood-borne factor of adrenomedullary origin?

Intravenous administration of the kappa-opioid agonists U50488H, tifluadom, and ethylketocyclazocine induced a characteristic diuresis in conscious, intact, saline-loaded rats. Naloxone pretreatment antagonized U50488H-induced diuresis. The diuretic response to the kappa-opioid agonists was significantly attenuated in adrenal demedullated rats. However, basal urine output, the diuretic response to furosemide, and the antidiuretic response to the mu-opioid agonist buprenorphine were unaffected. Transfusion studies established that 1 mL of blood, from intact donor rats treated with U50488H, induced a diuretic response when administered to intact or demedullated recipient rats, whether or not the recipients had been pretreated with naloxone. However, blood from demedullated rats treated with U50488H was unable to induce diuresis in intact or demedullated recipients. The results indicate that kappa-opioid agonist induced diuresis appears to be mediated by a nonopioid blood-borne "diuretic factor" of adrenomedullary origin and that this factor might be responsible for the dependence of the diuretic response upon an intact and functional adrenal medulla in conscious rats.

Adrenal Medulla↗
PubMed1986

Prostaglandin blockade impairs denervation diuresis and natriuresis in the rat.

Acute unilateral renal denervation of control rats produced an ipsilateral diuresis (5.5 +/- 0.8 to 10.0 +/- 1.0 microliter/min, P less than 0.01) and natriuresis (579 +/- 202 to 2,668 +/- 225 neq/min, P less than 0.01) without a significant change in glomerular filtration rate or effective renal plasma flow. Inhibition of prostaglandin synthesis with indomethacin or meclofenamate (4 mg/kg iv) after acute unilateral denervation eliminated the diuresis (13.3 +/- 1.6 to 5.0 +/- 0.9 microliter/min, P less than 0.01) and attenuated the natriuresis (3,098 +/- 462 to 1,097 +/- 163 neq/min, P less than 0.01). Denervation diuresis and natriuresis were significantly impaired to the same extent when denervation was performed after inhibition of prostaglandin synthesis (3.2 +/- 0.3 to 4.9 +/- 0.4 microliter/min, NS; and 490 +/- 154 to 1,036 +/- 274 neq/min, P less than 0.05 vs. control, respectively). These results indicate that the natriuresis and diuresis seen after acute unilateral denervation in anesthetized rats are highly dependent upon prostaglandins and cannot be initiated or maintained when prostaglandin synthesis is impaired by indomethacin or meclofenamate.

Animals↗
PubMed1989

Distribution of major organic osmolytes in rabbit kidneys in diuresis and antidiuresis.

Sorbitol, glycerophosphorylcholine (GPC), inositol, and betaine are organic osmolytes that accumulate in renal medullary cells. Two roles have been proposed for them: 1) that all four are "compatible osmolytes" that help regulate cell volume without disturbing function, and 2) that the methylamines (GPC and betaine) are "counteracting osmolytes," i.e., stabilizers that offset the perturbing effects of the high urea concentration. To test these hypotheses we have measured the osmolyte gradients in diuresis and antidiuresis in rabbit kidneys cut in 7 sections along the corticopapillary axis. In both antidiuresis and diuresis, inositol was highest in the outer medulla and decreased toward the tip of the inner medulla. In antidiuresis, contents of sodium, urea, sorbitol, GPC, and betaine increased monotonically toward the tip of the inner medulla. All osmolytes were significantly lower in diuresis compared with antidiuresis in two or more kidney sections. Urea, GPC, and sorbitol had the greatest differences between the two states. The sum of the four (mainly intracellular) compatible osmolytes showed a strong linear correlation with Na (presumably mostly extracellular), with a similar slope in both states, consistent with the compatible osmolytes hypothesis. Considering the osmolytes individually, only two linear correlations were highly significant and had similar slopes in both diuresis and antidiuresis: betaine with Na and GPC with urea. The latter is consistent with the counteracting osmolytes hypothesis, suggesting that GPC is the main agent stabilizing against urea in the renal medulla.

Animals↗
PubMed1995

Restoration of urine concentrating ability and accumulation of medullary osmolytes after chronic diuresis.

Restoration of urine osmolality (Uosm) and medullary osmolyte contents after chronic diuresis was studied in rats infused for 6 days with furosemide and subsequently given the vasopressin analogue, 1-desamino-8-D-arginine vasopressin (DDAVP). Papillary tip intra- and extracellular electrolyte concentrations were measured by electron microprobe analysis, tissue contents of methylamines (glycerophosphorylcholine, betaine), polyols (myo-inositol, sorbitol), and several amino acids in different kidney zones by high-performance liquid chromatography. Administering DDAVP continuously after diuresis increased Uosm from (means +/- SE) 348 +/- 8 to 1,265 +/- 127 after 1 day and 2,485 +/- 186 mosmol/kgH2O after 3 days. The sum of all osmolytes at the papillary tip rose from 309.2 +/- 28.9 to 690.9 +/- 105.8 and 1,282.8 +/- 21.0 mmol/kg protein after days 1 and 3, respectively. Although interstitial tonicity (sum of Na, Cl, and K concentrations) was increased by 116 and 223% after 1 and 3 days DDAVP, intracellular tonicity was similar in chronic diuresis and following 1 or 3 days DDAVP. Coadministration of DDAVP with betaine, myo-inositol, and choline ("osmolyte treatment") did not accelerate the restoration of Uosm but caused significantly higher contents of osmolytes (except myo-inositol) in inner medulla and/or papilla after 3 days. In a minority of animals, restoration of Uosm and reaccumulation of medullary osmolytes were impeded in both DDAVP- and DDAVP/osmolyte-treated rats. These data indicate that, after chronic diuresis, accumulation of organic osmolytes and restoration of Uosm proceed in parallel. Capacity for transport and/or synthesis of organic osmolytes, rather than their availability, appear to limit reaccumulation on the first day of recovery. By the third day, delivery of some osmolytes or their precursors may limit the restoration of medullary osmolyte content. The failure of some rats to attain sufficient concentrating ability within this time period may be related to deficient reaccumulation of medullary osmolytes.

Amino Acids↗