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F Praddaude

Publications and source records attributed to F Praddaude.

At least 19 recordsLinked to original sources
PubMed2001

Bradykinin attenuates the [Ca(2+)](i) response to angiotensin II of renal juxtamedullary efferent arterioles via an EDHF.

1. Bradykinin (BK) effect on the [Ca(2+)](i) response to 1 nM angiotensin II was examined in muscular juxtamedullary efferent arterioles (EA) of rat kidney. 2. BK (10 nM) applied during the angiotensin II-stimulated [Ca(2+)](i) increase, induced a [Ca(2+)](i) drop (73+/-2%). This drop was prevented by de-endothelialization and suppressed by HOE 140, a B2 receptor antagonist. It was neither affected by L-NAME or indomethacin, nor mimicked by sodium nitroprusside, 8-bromo-cyclic GMP or PGI(2). The BK effect did not occur when the [Ca(2+)](i) increase was caused by 100 mM KCl-induced membrane depolarization and was abolished by 0.1 microM charybdotoxin, a K(+) channel blocker. 3. Although proadifen prevented the BK-caused [Ca(2+)](i) fall, more selective cytochrome P450 inhibitors, 17-octadecynoic acid (50 microM) and 7-ethoxyresorufin (10 microM) were without effect. 4. Increasing extracellular potassium from 5 to 15 mM during angiotensin II stimulation caused a [Ca(2+)](i) decrease (26+/-4%) smaller than BK which was charybdotoxin-insensitive. Inhibition of inward rectifying K(+) channels by 30 microM BaCl(2) and/or of Na(+)/K(+) ATPase by 1 mM ouabain abolished the [Ca(2+)](i) decrease elicited by potassium but not by BK. 5. A voltage-operated calcium channel blocker, nifedipine (1 microM) did not prevent the BK effect but reduced the [Ca(2+)](i) drop. 6. These results indicate that the BK-induced [Ca(2+)](i) decrease in angiotensin II-stimulated muscular EA is mediated by an EDHF which activates charybdotoxin-sensitive K(+) channels. In these vessels, EDHF seems to be neither a cytochrome P450-derived arachidonic acid metabolite nor K(+) itself. The closure of voltage-operated calcium channels is not the only cellular mechanism involved in this EDHF-mediated [Ca(2+)](i) decrease.

Angiotensin II↗
PubMed1999

Dissimilar mechanisms of Ca(2+) response to bradykinin in different types of juxtamedullary glomerular arterioles.

Bradykinin (BK)-induced changes in intracellular calcium level ([Ca(2+)](i)) were studied on fura 2-loaded afferent (AA) and efferent glomerular arterioles (EA) microdissected from juxtamedullary renal cortex. A distinction was made between thin and muscular EA. In AA and both types of EA, BK increased [Ca(2+)](i) through activation of B(2) receptors located only on the endothelium. The responses were not affected by nifedipine (10(-6) M) and were smaller in a Ca(2+)-free medium, providing evidence that BK opens voltage-independent Ca(2+) channels and mobilizes intracellular Ca(2+). Thin EA differed from AA and muscular EA by a lower sensitivity to BK (EC(50) = 6.95 +/- 3.81 vs. 0.21 +/- 0.08 and 0.18 +/- 0.13 nM, respectively; P < 0.05), a higher maximal response (89 +/- 5 vs. 57 +/- 5 and 44 +/- 7 nM; P < 0.001), and a spontaneous return to basal Ca(2+) level, even in the presence of BK. Genistein (10(-4) M) and herbimycin A (25 x 10(-6) M), specific inhibitors of tyrosine kinases, inhibited the [Ca(2+)](i) responses exclusively in AA. Genistein reduced the peak and plateau phases of responses by 69 +/- 9 and 82 +/- 6%, respectively, in a medium with Ca(2+) and the peak by 48 +/- 9% in a Ca(2+)-free medium. Similar reductions were observed with herbimycin A. These results show that dissimilar signal transduction pathways are involved in BK effects on juxtamedullary arterioles and that a tyrosine kinase activity could participate in the regulation of BK effect on AA but not on EA.

Animals↗
PubMed1998

Non-immunoglobulin serum proteins prevent the binding of IgG from normal rats and from rats with Th2-mediated autoimmune glomerulonephritis to various autoantigens including glomerular antigens.

It is now well established in normal humans and mice that purification of IgG from serum unmasks their autoantibody activity. Mercuric chloride (HgCl2) induces in Brown-Norway (BN) rats a Th2-dependent polyclonal B cell activation, a huge increase in serum IgE and IgG1 concentrations, the production of numerous autoantibodies and an autoantibody-mediated glomerulonephritis. In the present study we have compared the IgG autoantibody activity in the serum and in the purified IgG fraction from normal and HgCl2-injected BN rats. IgG autoantibodies were found to be masked in normal serum by non-immunoglobulin (nonIg) serum proteins and, provided these IgG did not encounter normal serum proteins, they could bind to glomerular antigens as assessed by immunofluorescence in a unilateral perfused kidney model. As a consequence of HgCl2-induced polyclonal activation of B cells, IgG autoantibodies were no longer complexed to non-Ig serum proteins, they were easily detected in the serum and could therefore reach their glomerular target. However, these autoantibodies could still be blocked by normal non-Ig serum proteins not only in vitro but also in a unilateral perfused kidney model so that their binding to glomerular antigens could be prevented. These findings indicate that the ratio between autoantibody level and the amount of non-Ig serum proteins may be crucial in autoantibody-mediated autoimmune diseases.

Animals↗
PubMed1998

Differential induction of functional B1-bradykinin receptors along the rat nephron in endotoxin induced inflammation.

BACKGROUND: Under physiological conditions, the effects of kinins in the kidney are mainly mediated by the bradykinin B2-receptor, whereas the kinin B1-receptor is strongly induced under inflammatory conditions in a variety of tissues. Knowledge of the distribution of the B1-receptor along the nephron is of importance since the B1-receptor might replace B2-receptors under these conditions. METHODS: Using a RT-PCR/Southern blot approach allowing relative quantification of mRNA levels, ten different microdissected rat nephron segments were analyzed for the presence of the B1- and B2-receptor before and after endotoxin treatment to induce experimental inflammation. The functionality of the expressed receptors was assessed by kinin-induced intracellular calcium ([Ca2+]i) mobilization in microdissected nephron segments. RESULTS: While under physiological conditions no B1-receptor mRNA could be detected, after 18 hours of treatment with bacterial lipopolysaccharide (LPS) the expression of B1-receptor mRNA was strongly induced in the efferent arteriole, the medullary and inner medullary thin limb, and in the distal tubule. Moderate expression was found in the glomerulus, proximal convoluted and straight tubules, and in the medullary thick ascending limb. Small but detectable expression was observed in the cortical collecting duct. The induction of B1-receptor mRNA expression resulted in functional receptor expression, since increases in [Ca2+]i were observed upon B1-agonist stimulation. LPS treatment also increased the expression of B2-receptor mRNA in all nephron segments except in the glomerulus, the inner medullary thin limb and the outer medullary collecting duct. However, no related changes in B2-agonist induced rises in [Ca2+]i were found. CONCLUSIONS: These studies show a functional induction of the B1-kinin receptor along the rat nephron, which should be taken in account to address the effects of kinins under inflammatory conditions in the kidney.

Animals↗
PubMed1997

Activation of Flk-1/KDR mediates angiogenesis but not hypotension.

OBJECTIVE: The concept of therapeutic angiogenesis with vascular endothelial growth factor (VEGF) has been validated in peripheral arterial disease. Its use in myocardial ischemia may be delayed as the result of the description in a porcine model of peripheral vasodilation after intraluminal injections of VEGF resulting in a 50% fatality rate by hypotension. We carried out this study to test whether VEGF-induced hypotension (1) is species specific, (2) is mediated by the receptor mediating angiogenesis, (3) is prevented by inhibition of nitric oxide synthase. METHODS: In the rabbit corneal pocket assay we tested whether a previously published anti-idiotypic antibody (AIA) agonist of the VEGF receptor Flk-1/KDR could elicit angiogenesis. Various doses of recombinant VEGF or AIA were injected into anesthetized normotensive Wistar-Kyoto rats and the mean arterial blood pressure (MABP) was recorded. To test the implication of nitric oxide in VEGF-induced hypotension we treated the animals with a competitive inhibitor of nitric oxide synthase prior to the injection of VEGF. RESULTS: Both VEGF and AIA induce angiogenesis but only intravenous injections of VEGF induced a rapid, transient and dose-dependent decrease in MABP. The ED50 was 0.5 micrograms. The interval between two VEGF injections required to lead to a decrease of MABP was 40 minutes. Nitric oxide synthesis inhibitor prevented, in a reversible fashion, the effect of VEGF. CONCLUSION: VEGF-induced hypotension is not species specific. It is prevented by nitric oxide inhibition. VEGF-induced angiogenesis and hypotension are not mediated in vivo by the same VEGF receptor.

Animals↗
PubMed1997

Endothelin increases NO-dependent cGMP production in isolated glomeruli but not in mesangial cells.

The ability of endothelins (ETs) to modulate nitric oxide-dependent glomerular guanosine 3'-5'-cyclic monophosphate (cGMP) production has recently been reported. The aim of this study was to directly confirm, using an antagonist, the involvement of the ETB receptor subtype and to investigate the potential role of mesangial cells (MC) in this ET-induced cGMP production. In glomeruli freshly isolated from rats, endothelin-3 (ET-3) induced a dose-dependent increase in cGMP content. This increase was inhibited by NG-monomethyl-L-arginine (L-NMMA) and methylene blue and was calcium dependent. Moreover, the effect of ET-3 was prevented by two ETB-selective receptor antagonists, BQ-788 and IRL-1038, but not by BQ-123, an ETA-selective receptor antagonist. It therefore appeared that ET-3 stimulates the glomerular constitutive NO pathway through activation of the ETB receptor subtype. In contrast, ET-3 and calcium ionophore had no effect on cGMP formation in cultured MC, whereas incubation with sodium nitroprusside resulted in an approximately 50-fold increase in the intracellular content of cGMP. However, ET-3 induced a dose-dependent rise in free MC cytosolic calcium that was abolished by an ETB antagonist. Moreover, both ETA and ETB receptors mRNA were expressed in primary cultures of MC. Finally, we failed to detect the presence of constitutive NO synthase (NOS), as demonstrated by the absence of L-citrulline forming activity and of the mRNA encoding for endothelial NOS, whereas they were present in isolated glomeruli. These data indicate that MC, despite the fact that they express ETB receptors, are not involved in glomerular NO production induced by exposure to ET-3, because they do not express constitutive NO synthase.

Animals↗
PubMed1996

RT-PCR microlocalization of bradykinin B2 receptor mRNA in microdissected rat nephron segments.

Microlocalization of mRNA coding for the bradykinin 2 (BK2) receptor was carried out in the rat kidney. We combined reverse transcription and polymerase chain reaction (RT-PCR) with microdissection of individual renal tubule segments. Relative quantitation of the resulting amplified cDNA utilized densitometry of autoradiograms from Southern blots probed with a specific 32P labeled probe. The largest signals for BK2 receptor PCR product were detected in the cortical collecting tubule (CCT) and the proximal straight tubule (PST). BK2 receptor mRNA expression was also detected in the glomerulus, inner medullary thin limb (IMTL) and in the distal tubule (DT). Small but detectable signals were founded in the medullary thick ascending limb (MTAL). This distribution is consistent with multiple sites of BK action to account for different renal effects such as hemodynamics, water and electrolytic balance regulations.

Acid-Base Equilibrium↗
PubMed1996

Amino acid loading disrupts whole kidney proximal glomerular-tubular balance in humans.

The effect of amino acid infusion on proximal glomerular-tubular balance (PG-TB) was studied in twelve healthy two-kidney volunteers (2K) and eight uninephrectomized subjects (1K) in similar sodium and protein balance, to provide an extended range of values for renal function. Amino acid infusion induced a reversible significant increase in GFR: +23 +/- 4 and +18 +/- 3 ml/min/1.73 m2 in 2K and 1K respectively (p < 0.001), but not in absolute proximal reabsorption (APR, calculated as inulin clearance--lithium clearance): +8 +/- 3 and +6 +/- 3 ml/min/1.73 m2 respectively, NS. Consequently, the fractional increases in APR for both two kidney- and one kidney-subjects (+11 +/- 4 and +14 +/- 6%) were less than the fractional increases in GFR (+20 +/- 3 and 25 +/- 4%), and the effectiveness of PG-TB was significantly decreased to 53.2 and 55.9% (p < 0.001). Urinary sodium excretion also increased by 116 +/- 24 and 95 +/- 29 mumol/min/1.73 m2 in 2K (p < 0.001) and 1K (p < 0.01) respectively. Urinary excretion of guanosine 3',5'-cyclic monophosphate (cGMP) simultaneously increased (p < 0.001) by 223 +/- 77 and 350 +/- 135 pmol/min/1.73 m2 during infusion of amino acids in 1K and 2K respectively. In the whole group of subjects, impairment of the PG-TB was inversely related to the increase in urinary cGMP (p < 0.05). The results demonstrate that amino acid infusion disrupts proximal glomerular-tubular balance in humans due to non-proportional alterations in glomerular filtration rate and proximal reabsorption, and they suggest that a NO-dependent mechanism may be involved in the disruption.

Adult↗
PubMed1995

In vivo and in vitro homologous desensitization of rat glomerular bradykinin B2 receptors.

We investigated the effects of bradykinin on glomerular bradykinin B2 receptor functions and parameters in vivo, after intrarenal infusion of bradykinin, and in vitro, after incubation of isolated rat glomeruli with bradykinin. Bradykinin transiently increased renal plasma flow whereas a second challenge was ineffective. Scatchard analysis demonstrated the presence of two populations of bradykinin binding sites whose densities were similarly decreased by about 40% after intrarenal bradykinin infusion. This decrease was not altered by an acid wash suggesting internalization of the radiolabelled ligand. The effect of bradykinin was prevented by a bradykinin B2 receptor antagonist. Pre-exposure of isolated rat glomeruli to bradykinin mimicked the in vivo results because there was a reduction in bradykinin-induced prostaglandin E2 and prostaglandin F2 alpha release. Rapid recovery was observed 15 min after washing out the bradykinin. Our results directly demonstrate a negative homologous down-regulation of B2 glomerular bradykinin receptor density under both in vivo and in vitro conditions, an effect which involves a rapid sequestration of the receptor.

Animals↗
PubMed1994

Renal functional reserve in cyclosporin-treated recipients of kidney transplant.

The aims of this study were to determine whether renal functional reserve (RFR) is still present in cyclosporin-treated renal transplant recipients, and to examine the relationship between RFR and proximal reabsorption. A serial study was carried out in 12 renal allograft recipients (R) with good renal graft function at 20 +/- 2.5 days (S1) and at 7.6 +/- 0.4 months (S2) post-transplantation, and the results were compared to those in eight subjects who had undergone unine-phrectomy (one-kidney controls: UNx.C) and in 12 healthy volunteers (two-kidney controls: 2K.C). R and C were in similar sodium and protein balance and with similar plasma renin and aldosterone levels. R had normal serum creatinine level on moderate doses of cyclosporin (whole blood cyclosporin concentration: 212 +/- 20 and 125 +/- 20 ng/ml at S1 and S2, respectively). Eight one-hour clearance periods were performed prior to, during and following a three-hour i.v. infusion of a mixture of 20 l-amino acids (Azonutril 25, 4.5 mg amino acids/kg/min). Baseline glomerular filtration rate (GFR) was lower in recipients at S1 and S2 (55 +/- 5 and 54 +/- 4 ml/min/1.73 m2, respectively) than in UNx.C and 2K.C (72 +/- 4 and 113 +/- 4 ml/min/1.73 m2, respectively, P < 0.05 and 0.001). Amino acid infusion elicited significant GFR increases in controls as well as in recipients in spite of higher renal vascular resistances (RVR). The greater measured increase in GFR, which represented RFR, was 18 +/- 3 and 28 +/- 2 ml/min/1.73 m2 in UNx.C and 2K.C, respectively (P < 0.001), and 17 +/- 3 ml/min/1.73 m2 in R at both S1 and S2 (P < 0.001). Contrary to both UNx and 2K controls, the acute hyperfiltration in R at S1 and S2 occurred with a significant increase in effective renal plasma flow, no alteration in filtration fraction and a large decrease (approximately 20 and 17%) in RVR while no correlation could be detected between the RFR and baseline GFR. Baseline lithium clearance, used as a marker of overall proximal fluid delivery (CLi), was significantly lower, whereas baseline fractional excretion of lithium (FELi) was significantly higher in R at S1 and S2 and in UNx.C (41 +/- 4, 40 +/- 3 and 38 +/- 3%, respectively) than in 2K.C (31 +/- 2%, P < 0.05). Consistent and significant increase in CLi, FELi and absolute proximal reabsorption occurred both in R at S1 and S2 and in UNx and 2K controls during elicitation of RFR.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Direct effects of bradykinin on glomerular filtration and proximal tubule reabsorption in rat kidney.

Intrarenal infusion of a low dose of bradykinin devoid of extrarenal action exerts direct vasodilator and diuretic effects on rat kidney. It does not significantly alter glomerular filtration rate and absolute proximal reabsorption but increases the delivery of fluid from the proximal tubule evaluated by the clearance of lithium. None of these effects are observed in kidneys infused with both bradykinin and a specific bradykinin antagonist.

Animals↗
PubMed1991

Glomerular B2-kinin-binding sites in two-kidney, one-clip hypertensive rats.

To extend our recent observations of the possible downregulation of glomerular B2-kinin-binding sites, we investigated density (Bmax) of bradykinin (BK)-binding sites in glomerular membranes of both the clipped (C) and nonclipped (NC) kidneys of two-kidney, one-clip (2K-1C) Goldblatt hypertensive rats, in relation to tissue kallikrein activity and glomerular three-dimensional structure. Compared with the Bmax of sham-operated (SO) kidney (31.8 +/- 7 fmol/mg protein), a significant increase in Bmax was observed in glomeruli of both kidneys in hypertensive rats, the Bmax being higher in glomeruli of NC than in C kidneys (98 +/- 11 vs. 59 +/- 12 fmol/mg protein). NC kidney compensatory hypertrophy was expressed by an increase in glomerular diameter, surface area, and volume. When expressed per unit of area or volume, Bmax in NC kidneys remained significantly higher than in both C and SO kidneys. Increased Bmax in both kidneys of 2K-1C rats was associated with a decreased intrarenal level of kallikrein. We also examined prostaglandin (PG) E2 release by isolated glomeruli from SO, C, and NC kidneys as a possible biological effect induced by BK. Whereas C kidney released more PGE2 than NC kidney under basal conditions, addition of BK (10 nM) induced greater PGE2 production in NC kidney consistent with the difference in Bmax between C and NC kidneys. These results suggest a possible downregulation of glomerular B2-binding sites by bradykinin, which may explain the difference between SO and C kidneys.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

Effects of chronic administration of an angiotensin-converting enzyme inhibitor on angiotensin-converting enzyme activity in the pars recta of rabbits.

1. To determine whether chronic angiotensin-converting enzyme inhibition induces a decrease in proximal tubular angiotensin-converting enzyme activity, urine and blood samples were collected in conscious New Zealand rabbits before and after 16 days administration in drinking water of low doses of captopril (2.6 +/- 0.6 mg 24 h-1 kg-1), high doses of captopril (7.6 +/- 0.9 mg 24 h-1 kg-1) or no captopril (controls). The kidneys were then removed and angiotensin-converting enzyme activity was determined in isolated pars recta of microdissected nephrons as pmol of tritiated hippurylglycylglycine substrate hydrolysed min-1 of incubation and mm-1 of tubule. 2. Both low and high doses of captopril significantly decreased plasma angiotensin-converting enzyme activity and increased plasma renin activity, thus indicating an effective inhibition of circulating angiotensin-converting enzyme. Both low and high doses of captopril also significantly decreased mean arterial pressure and increased water intake and urine flow rate. Neither dose modified creatinine clearance and absolute and fractional sodium excretion. 3. None of the doses altered urinary kallikrein excretion. Urinary excretion of kinins was increased by 98.7% compared with control rabbits by the high dose of captopril (402 +/- 152 vs 251 +/- 104 ng/24 h, P less than 0.01) but was unchanged by the low dose of captopril. 4. Angiotensin-converting enzyme activity in the pars recta was lower in rabbits given the high dose of captopril than in control rabbits (17.6 +/- 7.2 vs 37.3 +/- 9.0 pmol min-1 mm-1, P less than 0.01) but was not decreased in rabbits given the low dose of captopril (40.4 +/- 5.0 pmol min-1 mm-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Nephron sites of the natriuretic effect of intrarenal infusion of atrial natriuretic peptide in the rat.

Since renal mechanisms by which ANP induces a natriuresis remain unclear, the effects of the infusion of 0.03 micrograms/min/kg body weight of rANP 1-28 into the right renal artery (via a very thin catheter inserted into the suprarenal artery) were studied in anesthetized rats using lithium clearance to monitor proximal tubular function. Intrarenal ANP did not cause changes in arterial pressure and hematocrit, nor in contralateral kidney handling of sodium. Its natriuretic effect on the right kidney resulted from an increase in the filtered load of sodium and from a decrease in reabsorption in the distal segments of the nephron. Proximal tubule sodium reabsorption increased in proportion to the filtered load.

Animals↗
PubMed1989

Renal kallikrein activity in rats developing spontaneous hypertension.

1. Spontaneously hypertensive rats (SHR) excrete less kallikrein in urine than Wistar-Kyoto rats (WKY) during the developmental phase of hypertension. The present study was designed to examine whether the urinary defect is related to abnormalities in the renal kallikrein content in this hypertensive model. 2. Active and total kallikrein were measured (amidolytic assay) in the renal cortex of newborn and 4-, 8- and 12-week-old SHR and age-matched WKY. Active and total kallikrein were also measured in urine at the same ages, except at birth. 3. Tissue active kallikrein was significantly lower in SHR at birth, representing on average 53% of the values in WKY expressed as content per total cortex weight. Tissue total kallikrein did not differ between newborn SHR and WKY. 4. SHR at 4, 8 and 12 weeks of age had lower urinary active and total kallikrein excretion. Tissue active akllikrein, but not total kallikrein, was higher than in age-matched WKY per g of cortex weight or per mg of protein, whereas both tissue active and total kallikrein were lower in SHR when expressed as content per total cortex weight. At these three ages, active kallikrein represented, on average 86%, while total kallikrein represented 77%, of the values in age-matched WKY. 5. Our results indicate a defect in prokallikrein activation rather than in kallikrein synthesis in the renal cortex of SHR at birth. The reduction in urinary kallikrein excretion during the developmental phase of hypertension in young SHR is similar to the reduction observed in the renal tissue.

Aging↗
PubMed1988

Renal tissue kallikrein in newborn and young SHR.

Since young SHR excrete less urinary kallikrein than WKY, active and total kallikrein (A and T Kall, respectively) was measured (amidolytic assay) in the renal cortex of both strains. Neither at birth nor at age 4 weeks did renal T Kall differ between SHR and WKY. Renal A Kall was significantly lower in newborn SHR and higher in 4-week-old-SHR than in age-matched WKY. Our results indicate that urinary kallikrein does not accurately reflect the renal enzyme activity. They suggest that SHR exhibit an inherited defect in prokallikrein activation and a secondary defect in the release of tissue kallikrein into urine.

Aging↗
PubMed1988

[Arterial hypertension with hyperkalemia, tubular acidosis and normal renal function: Gordon syndrome and/or pseudohypoaldosteronism type II?].

Basic examination of Mr S., 45 years of age, short in stature and overweight (1.60 m, 76 kg), was carried out because of the mild hypertension (mean AP 125 mm Hg) from which he had suffered for 20 years. The results were as follows: (1) variable hyperkalemia: plasma potassium values were 5.3 to 6.9 mmol/l; (2) normal renal function: serum creatinine 91.5 mumol/l, clearance of inulin 136.6 ml/mn; (3) proximal tubular acidosis: plasma bicarbonate and chloride values were 18.4 and 109 mmol/l, respectively; urinary pH was 7.1 with negative H+ ions urinary excretion (-33 mumol/mn); when plasma bicarbonate level was raised to 26 mmol/l by acute loading, fractional excretion of bicarbonate increased to 19,5 p. 100 while plasma potassium value decreased to 4.2 mmol/l; (4) low PRA (0.29 ng/ml/h) and normal plasma aldosterone concentration (63 pg/ml) with a normal intake of sodium and in a recumbent position. Plasma atrial natriuretic factor (ANF) level was normal: 14 fmol/ml. Intravenous infusion of ANF for 2 h (1 microgram/mn) induced the expected increases in urinary flow rate, and sodium and potassium excretions (+226, +307 and +171 p. 100, respectively). Intravenous infusion of isotonic saline (2 l in 2 h) and oral administration of fludrocortisone acetate for 4 weeks (400 micrograms per day) resulted in a normal decrease in PRA and plasma aldosterone concentration, a normal rise in plasma ANF level (22 and 42 fmol/ml) while slightly increasing AP without improving bicarbonaturia and acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗