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Mobilization of ascites in cirrhotic dogs following furosemide or mannitol diuresis.

Mobilization of ascites was studied in 20 anesthetized dogs with experimental cirrhosis following a mannitol- or furosemide-induced diuresis. Observations were made at 2 h following the drug, at which time the diuresis was invariably completed, and repeated at 4 h following a 2-h recovery period, during which the ureters were clamped to prevent further urinary losses. In the furosemide group the mean urinary loss was 459 +/- 6 ml and was accompanied by a decline in central venous pressure and hemoconcentration. At 2 h plasma volume had declined by 14% from control values, but at 4 h plasma replenishment was 99% complete. At this time ascites volume had decreased by 467 ml, acting as the major source for vascular replenishment. In the mannitol group, the average urinary loss was 190 +/- 10 ml and was accompanied by maintenance of venous pressure, lack of hemoconcentration, and hyponatremia. At 2 h plasma volume had expanded from control values by 22%, but at 4 h vascular replenishment was only 78% complete. The average ascites volume had decreased by only 55% of the diuretic loss, and was mobilized by a complex sequence of events involving movement of intracellular water.

Animals↗

Mechanism of diuresis following acute modest hyperglycemia in the rat.

In paired micropuncture studies in the Munich-Wistar rat we examined the mechanism of diuresis after acute induction of modest hyperglycemia (430-460 mg/dl) in the absence of an increase in total body water. The major reasons for the diuresis were an increase in nephron filtration rate (SNGFR) (from 30.3 +/- 1.8 to 35.3 +/- 1.6 nl/min) and a reduction in absolute proximal reabsorption (APR) (from 14.0 +/- 0.6 to 9.8 +/- 1.2 nl/min). All determinants of SNGFR were measured and a reduction in systemic oncotic pressure was the sole reason for the increase in SNGFR; vascular resistances did not change. Late proximal tubular fluid-to-plasma glucose concentration ratio was 0.96 +/- 0.04; therefore, the osmotic effects of unreabsorbed glucose could not account for the reduction in APR. Directly measured net renal interstitial pressure increased by 5 mmHg and the peritubular capillary effective reabsorptive pressure decreased (from 15.5 to 10.9 mmHg) in direct proportion to the reduction in APR, changes that could contribute to the reduction in APR. Equal elevations in glucose concentration in tubule and plasma may have also eliminated effective osmotic pressure gradients for water movement and influenced APR. As a result of increases in late proximal tubular flow rate, loop of Henle tubular reabsorption and absolute tubular reabsorption beyond the distal tubule both increased with hyperglycemia. The major reduction in APR was secondary to altered "physical factors" and osmotic effects of glucose that are not dependent on creation of unfavorable chemical gradients for Na+ reabsorption.

Acute Disease↗

Renal escape from vasopressin: role of pressure diuresis.

This study was designed to examine the role of increased renal artery pressure (RAP) in mediating escape from the antidiuretic action of vasopressin (AVP). In six conscious dogs in which RAP was permitted to increase, AVP infusion, at a rate (0.2 mU X kg-1 X mm-1 iv) that was acutely subpressor, gradually raised mean arterial pressure (MAP) from 97 +/- 2 to 126 +/- 4 mmHg after 5 days while decreasing urine volume and increasing urine osmolality. However, after 4-5 days of AVP infusion, urine volume and osmolality returned to control, and the hypertensive effect of AVP waned so that after 9 days of AVP, MAP averaged only 113 +/- 5 mmHg. In contrast, when RAP was prevented from increasing in seven dogs with a servo-controlled aortic occluder, AVP caused sustained decreases in urine volume and elevated urine osmolality from 609 +/- 27 to 1,160-1,711 mosmol/kg H2O throughout 8 days of infusion. The hypertensive effect of AVP did not wane when RAP was servo-controlled, and after 8 days of AVP infusion, MAP averaged 152 +/- 7 mmHg, compared with a control of 96 +/- 2 mmHg. Servo-controlling RAP also prevented the marked sodium and chloride losses seen with chronic AVP infusion in normal dogs. These findings indicate that escape from the antidiuretic action of AVP is mediated by increased RAP, which causes diuresis and natriuresis, thereby diminishing the hypertensive effect of AVP. However, when pressure diuresis and natriuresis are prevented, AVP causes severe chronic hypertensive, suggesting that AVP could be an important hypertensive mechanism when renal function is impaired.

Animals↗

Immersion diuresis without expected suppression of vasopressin.

To investigate fluid, electrolyte, and plasma vasopressin (PVP) and renin activity (PRA) responses, six men (20-35 yr) were immersed to the neck (NI) in water at 34.5 degrees C for six h after overnight food and fluid restriction. Diuresis was 1,061 +/- 160 (SE) ml/6 h during immersion and water balance was -1,285 +/- 104 ml/6 h. Preimmersion PVP was 0.7 +/- 0.2 pg/ml and increased to 3.0 +/- 0.6 pg/ml (P less than 0.05) at 6 h. PVP was unchanged at 1.2 +/- 0.1 pg/ml in the 6-h seated nonimmersion experiment at 25 degrees C. Plasma volume increased by 7.8 +/- 1.6% (P less than 0.05) at 60 min of NI and decreased thereafter. Serum osmolality was constant (292 +/- 1 mosmol/kg) throughout NI, whereas PRA decreased progressively from 1.9 to 0.5 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at the end of immersion. In spite of moderate thirst just before NI, thirst sensations were attenuated and no water was consumed ad libitum during immersion. These data indicate that PVP is not suppressed when there is no fluid intake during immersion and suggest that the action of factors other than PVP suppression are necessary to explain the mechanism of immersion diuresis.

Adult↗

Effect of water temperature on diuresis-natriuresis: AVP, ANP, and urodilatin during immersion in men.

Effects of water temperature on diuresis, natriuresis, and associated endocrine responses during head-out immersion were studied in eight men (23.4 +/- 0.3 yr) during four 5-h experimental conditions: air control at 28 degrees C and immersion at 34.5 degrees C [thermoneutral (Tnt)], 36 degrees C [above Tnt (aTnt)], and 32 degrees C [below Tnt (bTnt)]. Esophageal temperature decreased by approximately 0.4 degrees C in bTnt and increased by approximately 0.5 degrees C in aTnt. Cardiac output increased by approximately 80% in aTnt and approximately 40% in bTnt while thoracic impedance, an index of central blood pooling, decreased by 7.5 omega in bTnt (NS vs. Tnt) and 8.8 omega in aTnt (P < 0.05 vs. Tnt and bTnt). Total peripheral resistance decreased at all temperatures (50% in aTnt, 20% in bTnt). Urine flow and Na+ excretion increased by sixfold in bTnt and Tnt but by only threefold in aTnt. Creatinine clearance was unchanged while osmolal clearance (but not free water clearance) increased two-fold with all immersions. Plasma atrial natriuretic peptide (ANP), urinary urodilatin, and urinary guanosine 3',5'-cyclic monophosphate increased while plasma renin activity, aldosterone, and arginine vasopressin (AVP) decreased similarly at all temperatures. bTnt did not potentiate diuresis by selective attenuation of AVP. The overall natriuretic response exhibited a higher correlation with urodilatin (r = 0.45, P < 0.001) than with ANP (r = 0.26, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Influence of water and sodium diuresis and furosemide on urinary excretion of vitamin B(6), oxalic acid and vitamin C in chronic renal failure.

Urinary excretion of vitamin B(6), oxalic acid and vitamin C was investigated in 15 healthy subjects during maximal water diuresis and in the group of 12 patients in polyuric stage of chronic renal failure without dialysis treatment receiving a diet containing high sodium chloride (15g/day). Urinary excretions of the same parameters were investigated in another group of 15 patients in polyuric stage of chronic renal failure without dialysis treatment after i.v. administration of 20 mg furosemide. Urinary excretion of vitamin B(6), oxalic acid and vitamin C significantly increased during maximal water diuresis while during high intake of sodium chloride the urinary excretions of these substances were not affected. The results suggest that urinary excretion of vitamin B(6), oxalic acid and vitamin C depends on the urinary excretion of water. Intravenous administration of 20 mg furosemide led to an increase of urinary excretion of vitamin B(6), oxalic acid and vitamin C in patients with chronic renal failure. The increased urinary excretion of vitamin B(6) and vitamin C is a new negative side effect of furosemide and increased urinary excretion of oxalic acid is a new positive side effect in patients with chronic renal failure.

Adult↗

Morphological changes in the renal macula densa during natriuresis and diuresis.

Morphological changes in the macula densa have been studied during the infusion of diuretic agents into the renal artery of anesthetized dogs. The kidneys were fixed by rapid high pressure perfusion with glutaraldehyde. Large basolateral intercellular spaces were seen between macula densa cells in control kidneys, but the number and extent of these spaces were strikingly reduced during the natriuresis and diuresis induced by the infusion of frusemide, ethacrynic acid or mannitol. Natriuresis and diuresis produced by the intravenous infusion of large volumes of 0.9% NaCl solution also resulted in closure of these spaces. No simple relationship existed between changes in plasma renin activity and closure of the spaces between macula densa cells during these procedures. A distinctive, membrane-bound, vesicle-containing structure was identified between the basolateral processes of the cells of each macula densa; the function of this structure awaits elucidation. We suggest that changes in the size of the basolateral intercellular spaces of the macula densa reflect changes in fluid flux between the distal tubule and the interstitium of the juxtaglomerular apparatus.

Animals↗

Enalapril and pressure-diuresis in hypertensive rats transgenic for mouse renin gene.

The recent development of a transgenic rat strain bearing the mouse ren-2 renin gene [TGR(mRen2)27] has provided a new monogenetic model of hypertension. Other hypertensive rat strains are characterized by a blunted pressure-diuresis-natriuresis response such that higher renal perfusion pressures are required to excrete normal amounts of water and sodium. Dysfunction of the renin-angiotensin and nitric oxide systems may cause in this abnormality. This study examined the effect of enalapril on the pressure-natriuresis response and urinary nitric oxide metabolite excretion in 6-month-old TGR(mRen2)27 rats. The slope of the line relating renal perfusion pressure and urine flow rate in TGR (0.08+/-0.01 microl x min(-1) x g kidney weight(-1) mm Hg[-1]) was significantly lower than that in control rats (0.15+/-0.01 microl x min(-1) x g kidney weight(-1) mm Hg[-1]). Pressure-natriuresis responses were also shifted to higher pressure levels in TGR. Treatment with enalapril for 3 months lowered the mean arterial pressure from 94+/-2 to 84+/-4 mm Hg in control rats and from 146+/-3 to 89+/-3 mm Hg in TGR. The slopes of lines relating renal perfusion pressure and urine flow rate as well as sodium excretion were significantly increased by enalapril in control and transgenic animals. Urinary nitric oxide metabolite excretion rose similarly with increasing renal perfusion pressure in both control and TGR rats and was not affected by enalapril. These results confirm that older TGR rats have a blunted pressure-diuresis-natriuresis response that can be corrected by inhibition of the renin-angiotensin system and suggest that their production of nitric oxide is normal.

Angiotensin-Converting Enzyme Inhibitors↗

Hypomagnesemia following the diuresis of post-renal obstruction and renal transplant.

Three unusual cases are described which demonstrated hypomagnesemia and symptoms resembling magnesium deficiency syndrome. The hypomagnesemia was most likely secondary to urinary losses from diuresis following release of post-renal obstruction and renal homotransplantation. Heretofore, this association has not been described. Case 1 was unique because of the post-obstructive diuresis in the face of marked renal impairment. Case 2 is noteworthy because of the profound hypomagnesemia, 0.4 mEq/1, and because of the development of congestive heart failure. The rapid improvement noted in cardiac function with magnesium replacement suggests a relationship to magnesium deficiency.

Adult↗

Ultrasound diagnosis of suspected urinary tract obstruction using a stimulated diuresis test.

The aim of this study was to evaluate whether a stimulated diuresis test associated with ultrasound is able to differentiate pelvic dilation due to atonicity from pelviureteric junction obstruction (PUO). 42 patients (25 f, 17 m) with minimal or moderate renal pelvis dilation revealed by sonography were selected for the test. Three different measurements of the anteroposterior diameter (APD) of the renal pelvis were done at the renal hilus level, by using a transversal ultrasound scan: the first under spontaneous diuresis conditions, the second after hydration with 1.5 liters of water, and the third with a full bladder 15 min after intravenous injection of 20 mg frusemide. All the patients underwent pyelography. Baseline APD (bAPD) linearly correlated with the PAD both after hydration and frusemide (r = 0.89 and r = 0.84, respectively). A descriptive evaluation of the frequency distribution of the bAPD suggested the possibility that the data samples could belong to three populations with different underlying pathophysiological conditions. Correspondence analysis between bAPD distribution and PUO suggested that the best grouping of data was: group 1 (11 patients) bAPD < 13 mm, group 2 (14 patients) 13 > or = bAPD < or = 20 mm, group 3 (17 patients) bAPD > 20 mm (likelihood ratio chi 2 46.36; d.f. = 2). Standard intravenous pyelography showed an increase in pelvis size compatible with PUO in 2 patients from group 2 and in all patients from group 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Interrelationships between the renal kallikrein-kinin and prostaglandin systems in furosemide-induced diuresis.

The relationships between the renal kallikrein-kinin (K-K) and prostaglandin (PG) systems under conditions of furosemide-induced diuresis were studied in normal rats. Urinary PGE and PGF2 alpha were measured by radioimmunoassay, and urinary kallikrein by enzymatic activity. The diuretic and natriuretic effects of furosemide were accompanied by a concomitant increase in the urinary excretion of kallikrein and PGE. The urinary excretion of kallikrein and PGE was closely related to the urinary excretion of sodium, potassium and chloride. The urinary excretion of kallikrein also showed a highly significant correlation with the urinary excretion of PGE. Pretreatment of the animal with indomethacin or aprotinin inhibited furosemide-induced diuresis and natriuresis. Aprotinin inhibited the urinary excretion of PGE, while indomethacin did not exert any inhibitory action on the urinary excretion of kallikrein. Although the urinary excretion of kallikrein was closely related to the urinary excretion of potassium, both indomethacin and aprotinin had no effect on the urinary excretion of potassium. The results indicate that the potassium-sodium exchange caused by furosemide in the distal nephron might stimulate the renal K-K system to result in increasing synthesis of PGE, which would, at least in part, participate in the diuretic and natriuretic effects of furosemide.

Animals↗

Diuresis and natriuresis caused by activation of VR1-positive sensory nerves in renal pelvis of rats.

To test the hypothesis that activation of the vanilloid receptor 1 (VR1) expressed in sensory nerves innervating the renal pelvis leads to diuresis and natriuresis, a selective VR1 receptor agonist, capsaicin (2.4 nmol), or vehicle was perfused intravenously or into the left renal pelvis of anesthetized rats at a rate without changing renal perfusion pressure. Mean arterial pressure was not altered by capsaicin administered intravenously or into the renal pelvis. Capsaicin perfusion into the left renal pelvis but not intravenously caused significant increases in urine flow rate and urinary sodium excretion bilaterally in a dose-dependent manner, which were abolished by capsazepine, a selective VR1 receptor antagonist, given ipsilaterally to the renal pelvis or by ipsilateral renal denervation. Capsaicin given intravenously or into the left renal pelvis increased plasma calcitonin gene-related peptide levels to the same extent. Increased plasma calcitonin gene-related peptide levels induced by capsaicin (68.9+/-2.8 pg/mL) perfusion into the renal pelvis was prevented either by capsazepine (22.5+/-10.1 pg/mL) given ipsilaterally into the renal pelvis or by ipsilateral renal denervation (25.9+/-2.3 pg/mL). Taken together, our data show that unilateral activation of VR1-positive sensory nerves innervating the renal pelvis leads to bilateral diuresis and natriuresis via a mechanism that is independent of plasma calcitonin gene-related peptide levels. These data suggest that VR1-positive sensory nerves in the kidney enhance renal excretory function, a mechanism that may be critically involved in sodium and fluid homeostasis.

Animals↗

Activation of the humoral antihypertensive system of the kidney increases diuresis.

Isolated kidneys taken from normotensive Wistar-Kyoto rats were cross-perfused extracorporeally by normotensive strain-matched donor rats. The extracorporeal perfusion circuit was arranged so that the perfusion pressure to the normotensive recipient kidney could be varied from 90 to 200 mm Hg without any change in total flow through this circuit. This setup avoided hemodynamic or mechanical interferences with reflexogenic circulatory control in the normotensive donor rat when the recipient kidney was manipulated. Diuresis and natriuresis were measured in the normotensive donor rat and the normotensive recipient kidney. A few minutes after normotensive recipient kidney perfusion pressure had been raised, mean arterial pressure (MAP) and heart rate started to decline rapidly in the normotensive donor rat, and circulatory collapse ensued within 15 to 100 minutes. During the control period at 90 mm Hg normotensive recipient kidney perfusion pressure, urinary flow, MAP and heart rate were stable in the normotensive donor rat and the normotensive recipient kidney. When perfusion pressure was raised to 200 mm Hg in the recipient kidney, the urinary flow in the donor rat increased 62% on average in the first 10 minutes over values recorded before the pressure rise (p less than 0.05) while MAP simultaneously fell by 16% and HR remained unchanged. During the subsequent period, the urinary flow of the donor rat declined together with MAP and heart rate. In the extracorporeally high-pressure perfused recipient kidneys, an eightfold to ninefold increase in diuresis and natriuresis occurred during the first 45 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Role of nitric oxide in the development of vascular alpha 1-adrenoreceptor desensitization and pressure diuresis in conscious rats.

We evaluated whether a minor impairment of the L-arginine-nitric oxide pathway would affect the desensitization of vascular alpha-adrenoreceptor and pressure diuresis induced by prolonged intravenous infusion of phenylephrine (an alpha-adrenoreceptor agonist) in conscious Wistar-Kyoto rats. We examined dose-pressor-response curves to phenylephrine after an intravenous infusion of phenylephrine (2.5 micrograms.kg-1.min-1) or saline for 9 hours with and without concomitant infusion of N omega-L-arginine methyl ester (L-NAME) given to partially inhibit the L-arginine-nitric oxide pathway. In addition, to evaluate the effect of plasma volume loss on the pressor response to phenylephrine, we evaluated the dose-pressor-response curves to phenylephrine after intravenous injection of furosemide (5 mg/kg) or infusion of phenylephrine (5 micrograms.kg-1.min-1) for 9 hours. The renin-angiotensin, vasopressin and autonomic nervous systems were blocked before the examination of dose-pressor responses. Prolonged infusion of phenylephrine (2.5 micrograms.kg-1.min-1) shifted the dose pressor-response curve to this agent rightward, with significantly increased log ED50 (the dose needed to reach 50% of the maximal response) to a similar extent in both L-NAME-treated (0.51 +/- 0.05 versus 0.93 +/- 0.07 microgram/kg) and -untreated (0.79 +/- 0.06 versus 1.08 +/- 0.03 micrograms/kg) rats. The log ED50 value after phenylephrine infusion (5 micrograms.kg-1.min-1) was significantly higher than that after furosemide injection (1.28 +/- 0.06 versus 1.02 +/- 0.01 micrograms/kg, respectively, P < .01), although the two treatments induced a similar loss of plasma volume. The slope in the linear relationship between the average change in mean arterial pressure during the 9-hour infusion period and the rate of urine excretion was significantly depressed in L-NAME-treated versus control rats (L-NAME: 0.057 mL.kg-1.h-1.mm Hg-1, control: 0.146 mL.kg-1.h-1.mm Hg-1, P < .05). In conclusion, a minor impairment of the L-arginine-nitric oxide pathway does not appear to interfere with the desensitization of vascular alpha-adrenoreceptor but does inhibit the pressure-diuresis response in conscious normotensive rats.

Analysis of Variance↗

Renal handling of sodium in premature and full-term neonates: a study using clearance methods during water diuresis.

A study using fractional clearances during orally induced water diuresis was designed to delineate the mechanism underlying defective tubular reabsorption of sodium in very low-birth-weight neonates. The use of clearance methodology during maximal water diuresis may give an indirect estimate of distal sodium delivery [urine volume (V), CH2O + CNa + K], sodium reabsorption at the diluting segments (CH2O), and proportion of the distal load reabsorbed distally (CH2O/CH2O + CNa + K), when all values are corrected to 100 ml glomerular filtration rate. The study was carried out in 28 healthy newborn infants who were grouped according to conceptual age (CA): 13 infants with mean birth weight of 1370 +/- 330 g and mean CA of 31.8 wk (range, 28-34 wk), and 15 infants with mean birth weight of 2330 +/- 550 g and mean CA of 37.9 wk (range, 35-41 wk). All studies were performed at 6-7 days of age. It was demonstrated that higher urinary osmolality (67.5 +/- 23.2 versus 52.9 +/- 9.4 mOsm/kg, P less than 0.0025) and higher fractional sodium excretion (2.3 +/- 1.8 versus 0.9 +/- 0.5 ml/dl glomerular filtration, P less than 0.01) observed in the group of very preterm infants resulted from significantly decreased proximal (V: 18.7 +/- 6.0 versus 13.3 +/- 3.6 ml/dl glomerular filtration, P less than 0.005; CH2O + CNa + K: 17.1 +/- 5.2 versus 11.9 +/- 3.3 ml/dl glomerular filtration, P less than 0.005) and distal (CH2O/CH2O + CNa + K X 100: 81.9 +/- 8.2 versus 88.2 +/- 4.5%, P less than 0.01) tubular sodium reabsorption.(ABSTRACT TRUNCATED AT 250 WORDS)

Diuresis↗

Is clonidine-induced diuresis mediated by atrial natriuretic factor?

The effect of intracerebroventricular (ICV) administration of clonidine on urine output, urinary sodium excretion, urinary cGMP, and plasma immunoreactive atrial natriuretic factor (IR-ANF) was studied in conscious, normally hydrated rats. Clonidine treatment evoked a significant dose-dependent increase in urine output. A 20-fold elevation was noted after the highest clonidine dose (2 micrograms/rat). The observed diuresis was accompanied by enhanced sodium excretion, which with the highest dose (2 micrograms) of clonidine increased from 1.6 +/- 0.36 to 39.4 +/- 10.5 meq/liter (P less than 0.001). Plasma IR-ANF rose from 30.7 +/- 8.8 to 113.3 +/- 32.3 pg/ml plasma 5 min after the 0.5 micrograms clonidine dose (P less than 0.05), and urinary cGMP excretion was augmented from 8.49 +/- 4.29 to 27.7 +/- 5.0 pmol/min 1 h after 0.5 micrograms clonidine (P less than 0.05). Pretreatment with peripherally administered anti-ANF serum abolished the diuretic effect of intracerebroventricularly administered clonidine; urine output decreased from 1.49 +/- 0.41 to 0.42 +/- 0.21 ml/h. The urinary cGMP level after anti-ANF serum treatment fell from 25.0 +/- 7.56 to 7.1 +/- 3.5 pmol/min (P less than 0.05). Peripheral pretreatment with the alpha 2-antagonist yohimbine or the opioid antagonist naloxone partially abolished clonidine's diuretic impact: urine output dropped from 1.91 +/- 0.55 to 0.42 +/- 0.18 and 0.46 +/- 0.18 ml/h (P less than 0.05), respectively. At the same time, plasma IR-ANF decreased from 113.3 +/- 32.2 to 30.3 +/- 11.4 after yohimbine and to 24.6 +/- 12.1 pg/ml after naloxone treatment (P less than 0.05). These data suggest that ANF may be involved in the mechanism of diuresis of centrally applied clonidine, which appears to enhance ANF release through its central stimulation of opiate and alpha 2-adrenergic receptors.

Animals↗

Effect of intraventricular administration of noradrenaline on water diuresis in goats.

Duriing water diuresis in conscious goats, noradrenaline (NA), its antagonists phentolamine, phenoxybenzamine and propranolol and also atropine were administered into the 3rd ventricle. The subsequent effects on water diuresis and on the excretion rates of Na+, K+ and Cl- were investigated. Infusion of NA into the 3rd ventricle induced a strong and significant antidiuretic response and a decrease in the Na+ : K+ excretion ratio; these effects were dose-dependent. High doses of NA produced a significant increase in urinary K+ excretion. Similar results were observed after i.v. administration of arginine-vasopressin. Pretreatment with phentolamine injected into the 3rd ventricle produced a dose-dependent inhibition of the NA-induced antidiuretic effects. Phenoxybenzamine also blocked the response to NA but a dose-response relationship was not apparent. Atropine and propranolol did not block the response to NA.

Animals↗

Role of endogenous atrial natriuretic peptide in volume expansion diuresis and natriuresis of the Pekin duck.

Polyclonal antibodies raised in a rabbit against avian atrial natriuretic peptide (ANP) were shown to reduce circulating endogenous ANP levels in Pekin ducks by more than 90%, and were subsequently used to investigate the role of this peptide in volume expansion diuresis and natriuresis. Conscious birds, undergoing a steady-state diuresis and natriuresis maintained by an i.v. infusion of hypotonic saline at a rate of 0.7 ml/min, responded to ANP antiserum (anti-ANP) with an immediate 30% reduction in urine flow rate and sodium excretion which lasted for about 30 min. Plasma arginine vasotocin levels were not changed by anti-ANP whereas circulating angiotensin II concentrations increased immediately following the administration of anti-ANP. Serum from non-immunized normal rabbits produced no changes in the renal and plasma parameters monitored. The results show that the high circulating levels of endogenous ANP associated with volume expansion promote renal salt and fluid excretion and thus have a major physiological role in avian volume homeostasis.

Animals↗