Effect of Inhibition of Prostaglandin Synthesis on the Natriuresis Induced by Saline Infusion in Man

1978 ◽  
Vol 54 (1) ◽  
pp. 47-50 ◽  
Author(s):  
Th. Mountokalakis ◽  
Th. Karambasis ◽  
D. Mayopoulousymvoulidou ◽  
G. Merikas
Keyword(s):  
Free Water ◽  
Prostaglandin Synthesis ◽  
Saline Infusion ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Prostaglandin Synthetase ◽  
Water Reabsorption ◽  
Post Infusion ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Natriuretic Effect

1. The effect of oral administration of an inhibitor of prostaglandin synthetase, indomethacin, on the natriuresis induced by the infusion of sodium chloride (saline) was studied in 11 healthy volunteers. 2. The administration of indomethacin did not alter sodium excretion before saline infusion, but it resulted in a significant increase of the natriuresis after saline infusion. This increase was not accompanied by any change in post-infusion urine flow rate or free water reabsorption. 3. It is suggested that intrarenal prostaglandins might suppress the natriuretic effect of saline infusion, probably by increasing sodium reabsorption in the distal nephron.

Natriuresis in Rats Acutely Depleted of Chloride

1977 ◽  
Vol 52 (1) ◽  
pp. 23-31
Author(s):  
R. G. Luke ◽  
B. T. Khanh ◽  
R. D. Schmidt ◽  
J. H. Galla
Keyword(s):  
Sodium Bicarbonate Solution ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Variable Degree ◽  
Water Reabsorption ◽  
Chloride Depletion ◽  
Sodium Load ◽  
Clearance Studies ◽  
And Control

1. Acute chloride depletion, without sodium depletion, was produced in rats by a single exchange peritoneal dialysis against sodium bicarbonate solution. Blood volume was restored after dialysis by infusion of salt-free albumin, and exogenous deoxycorticosterone and antidiuretic hormone were given. 2. Clearance studies in the period (3 h) after dialysis revealed no difference in the glomerular filtration rate or in the filtered sodium load between experimental and control rats but urinary sodium concentrations and absolute and fractional sodium excretion were significantly higher in the chloride-depleted group. 3. There was also a significant kaliuresis, increased urinary flow rate and diminished free water reabsorption. Urinary bicarbonate excretion increased to a variable degree but the major rise in anion excretion was ‘unmeasured’ (Na+ + K+ — [Cl− +HCO3− +PO43-]). 4. It is postulated that chloride depletion imposes limitations on sodium reabsorption in the ascending limb of the loop of Henle.

Renal effects of endogenous prostaglandin synthesis promoter ONO-3122

1992 ◽  
Vol 262 (6) ◽  
pp. F1047-F1054
Author(s):  
T. Takabatake ◽  
H. Hara ◽  
Y. Ishida ◽  
H. Ohta ◽  
K. Kobayashi
Keyword(s):  
Proximal Tubule ◽  
Prostaglandin Synthesis ◽  
Fluid Replacement ◽  
Tubuloglomerular Feedback ◽  
Loop Of Henle ◽  
Distal Nephron ◽  
Water Reabsorption ◽  
Renal Vasculature ◽  
Renal Effects ◽  
Collecting Tubules

The renal effects of a prostaglandin synthesis agonist, 1-iodo-3-aminomethyl-5,6,7,8-tetrahydro-2-naphthol (ONO-3122), were investigated in anesthetized rats. ONO-3122 (0.3 mg/kg + 0.3 mg.kg-1.h-1 iv) doubled the urinary excretion of the main metabolites of prostaglandin F, and induced transient increases in renal blood flow and glomerular filtration rate (GFR) with a marked, stable natriuresis. Indomethacin suppressed the natriuresis. When the diuretic fluid losses were replaced, micropuncture showed an unaltered reabsorption of sodium in the proximal tubule but reductions in the loop of Henle (86 +/- 1 vs. 76 +/- 1%) and in the more distal segments (98 +/- 1 vs. 83 +/- 3%) with comparable reductions in water reabsorption. Potassium secretion was seen in the distal and collecting tubules. Without fluid replacement, sodium reabsorption was reduced in the loop and more distal nephron but increased in the proximal tubule. Differences between proximal and distal nephron GFR were unaffected by systemic ONO-3122. Loop perfusion with ONO-3122 did not change tubuloglomerular feedback responses, which were, however, completely suppressed by furosemide. It is concluded that ONO-3122 stimulates renal prostaglandin biosynthesis, transiently dilates renal vasculature, and induces natriuresis mainly by suppressing sodium and water reabsorption in the loop of Henle and the more distal nephron. Luminal ONO-3122 does not affect the tubuloglomerular feedback.

Effect of acute unilateral renal denervation on tubular sodium reabsorption in the dog

1977 ◽  
Vol 232 (1) ◽  
pp. F16-F19
Author(s):  
G. Nomura ◽  
T. Takabatake ◽  
S. Arai ◽  
D. Uno ◽  
M. Shimao ◽  
...  
Keyword(s):  
Renal Denervation ◽  
Renal Plasma Flow ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Tubular Sodium Reabsorption ◽  
Renal Tubular

The effects of acute denervation of the kidney on renal tubular sodium and water excretion were studied in anesthetized, hypophysectomized, and cortisone-treated mongrel dogs during stable water diuresis produced by the infusion of 2.5% dextrose. In all experiments, denervation natriuresis, and diuresis were observed without significant change in glomerular filtration rate (GRF) and renal plasma flow (RPF). Fractional sodium delivery to the distal nephron (CNa + CH2O/100 ml GFR) and fractional free water clearance (CH23/100 ml GFR) was significantly greater in the denervated kidney compared with the innervated kidney (9.6+/-1.2 vs. 6.7+/-0.9% and 8.8+/-1.2 vs. 6.5+/-0.8%, respectively). Distal tubular sodium reabsorption (CH2O/(CNa + CH2O)) was not significantly different. We conclude that renal denervation primarily affects the proximal tubule as manifested by a decrease in the reabsorption of sodium and water. A small effect of denervation on the distal nephron is not completely ruled out.

Mechanisms of the antinatriuretic action of physiological doses of angiotensin II in man

1989 ◽  
Vol 76 (6) ◽  
pp. 653-658 ◽  
Author(s):  
Peter H. Seidelin ◽  
John J. McMurray ◽  
Allan D. Struthers
Keyword(s):  
Creatinine Clearance ◽  
Sodium Excretion ◽  
Free Water ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Distal Nephron ◽  
Aldosterone Secretion ◽  
Significant Fall ◽  
Parallel Change ◽  
Proximal Tubular

1. Angiotensin 11 (ANG II; 1 ng min−1 kg−1) or 5% (w/v) d-glucose (placebo) was infused in six normal male volunteers, pretreated with 500 mg of lithium carbonate, who were undergoing maximal water diuresis. 2. This dose of ANG II caused a circulating increment within the physiological range (27 ± 4 to 48 ± 9 pmol/l). 3. Compared with placebo, ANG II caused a significant fall in urinary sodium excretion (113 ± 13 to 82 ± 10 μmol/min). This antinatriuretic effect occurred without a fall in creatinine clearance (107 ± 3 versus 113 ± 3 ml/min). 4. ANG II caused a significant fall in fractional lithium clearance (28 ± 2 to 23 ± 2%). This may indicate a proximal tubular effect of ANG II. 5. ANG II also reduced fractional distal delivery [(sodium clearance plus free water clearance) divided by creatinine clearance], another measure of proximal tubular outflow. A parallel change in these two separate markers of proximal function supports an action of ANG II at this nephron segment. 6. Furthermore, the antinatriuretic effect of ANG II was unlikely to be due to stimulation of aldosterone secretion because (a) the fall in sodium excretion was temporally dissociated from the rise in aldosterone secretion, (b) potassium excretion also tended to fall during ANG II infusion and (c) aldosterone has a distal nephron effect, while, in this study, proximal nephron fractional reabsorption of sodium increased and distal nephron fractional reabsorption of sodium was unchanged. 7. These observations suggest that physiological increments in ANG II can have an antinatriuretic effect in man, which, at least initially, results from increased proximal tubular sodium reabsorption and is independent of the effect of aldosterone.

Furosemide action on collecting ducts: effect of prostaglandin synthesis inhibition

1983 ◽  
Vol 244 (6) ◽  
pp. F666-F673 ◽  
Author(s):  
D. R. Wilson ◽  
U. Honrath ◽  
H. Sonnenberg
Keyword(s):  
Collecting Duct ◽  
Prostaglandin Synthesis ◽  
Water Reabsorption ◽  
Inner Medullary Collecting Duct ◽  
Nephron Segments ◽  
Inhibit Prostaglandin Synthesis ◽  
Collecting Ducts ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Medullary Collecting Duct ◽  
Furosemide Administration

The effect of furosemide on inner medullary collecting duct chloride reabsorption has not been determined, and the blunting of furosemide action by drugs that inhibit prostaglandin synthesis, while known to occur, has not been examined in detail. The effect of indomethacin and meclofenamate on furosemide diuresis was studied in the rat using clearance and collecting duct microcatheterization methods. Furosemide-treated control animals showed complete inhibition of chloride, sodium, and water reabsorption in the inner medullary collecting duct. Rats given indomethacin or meclofenamate before and during furosemide administration showed marked reduction of the chloriuresis, natriuresis, and diuresis. Reduced delivery of sodium and chloride to the beginning of the inner medullary collecting duct, associated with a decrease in glomerular filtration rate and increased reabsorption in more proximal nephron segments, was largely responsible for the reduced natriuresis and chloriuresis during inhibition of prostaglandin synthesis. In addition, indomethacin increased collecting duct NaCl reabsorption toward normal, but meclofenamate showed no such effect. The results indicate that furosemide inhibits medullary collecting duct reabsorption of chloride, sodium, and water in the rat. The blunting of diuretic action seen with inhibition of prostaglandin synthesis is largely, although not entirely, due to effects of indomethacin and meclofenamate on furosemide action at nephron sites proximal to the collecting duct.

Different Effects of Frusemide Administered during Hypertonic Saline Infusion in Healthy Subjects and Hypertensive Patients

1970 ◽  
Vol 39 (6) ◽  
pp. 833-845 ◽  
Author(s):  
J. P. Radó ◽  
L. Szende ◽  
L. Borbély ◽  
Cs. Báanos ◽  
J. Takó ◽  
...  
Keyword(s):  
Hypertonic Saline ◽  
Healthy Subjects ◽  
Free Water ◽  
Normal Subjects ◽  
Saline Infusion ◽  
Water Reabsorption ◽  
Salt Loading ◽  
Hypertensive Patients ◽  
Healthy Persons ◽  
Hypertonic Saline Infusion

1. The effects of hypertonic saline and frusemide administered during hypertonic saline infusion were studied during antidiuresis and infusion of lysine-vasopressin in fifteen healthy subjects and seventeen patients with hypertension. 2. Rates of excretion of water and sodium were higher during salt loading in the hypertensive patients as compared to the healthy persons. On the other hand, frusemide administered during saline infusion had a greater effect in the normal subjects. 3. Free water reabsorption increased markedly in the first 10-min clearance period after frusemide injection in the healthy subjects, while in the hypertensive group there was no significant change. This suggested that the diuretic may have a more marked proximal tubular effect in the healthy persons and/or a more intensive Henle's loop action in the hypertensives. However, the latter possibility was not supported by data concerning the correlation between solute excretion and free water reabsorption. 4. It is suggested that sodium transport is competitively inhibited in the same segment(s) of the nephron by frusemide and hypertonic saline and that this may explain the decreased effect of frusemide in the hypertensives.

Inhibition of Frusemide-Induced Natriuresis by Indomethacin in Patients with the Nephrotic Syndrome

1977 ◽  
Vol 52 (2) ◽  
pp. 149-151 ◽  
Author(s):  
R. G. W. L. Tiggeler ◽  
R. A. P. Koene ◽  
P. G. A. B. Wijdeveld
Keyword(s):  
Nephrotic Syndrome ◽  
Renin Angiotensin System ◽  
Prostaglandin Synthesis ◽  
Sodium Retention ◽  
Angiotensin System ◽  
Combined Use ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Natriuretic Effect ◽  
High Doses ◽  
Indomethacin Treatment

1. In four patients with nephrotic syndrome indomethacin not only reduced proteinuria but also inhibited the natriuretic effect of high doses of frusemide. 2. The inhibition of natriuresis by indomethacin could not be antagonized by albumin infusions. 3. Only the combined use of spironolactone and frusemide induced a natriuresis during indomethacin treatment. Spironolactone alone was ineffective. 4. It is suggested that inhibition of prostaglandin synthesis by indomethacin, in the presence of a stimulated renin-angiotensin system and hyperaldosteronism, may cause this strong tendency to sodium retention.

Action of prostaglandin synthetase inhibitors on rostral hypothalamic neurones: thermoregulation and biogenic amines

1976 ◽  
Vol 54 (2) ◽  
pp. 161-166 ◽  
Author(s):  
Ralph M. Jell ◽  
Paul Sweatman
Keyword(s):  
Biogenic Amines ◽  
Neuronal Excitability ◽  
Prostaglandin Synthesis ◽  
Prostaglandin Synthetase ◽  
Depressant Action ◽  
Rostral Hypothalamus ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Induced Changes

Sensitivity of neurones in the rostral hypothalamus of methoxyflurane anesthetized cats to the prostaglandin synthetase inhibitors (PGSIs), salicylate and fenoprofen, has been examined using the technique of microiontophoresis. Results were compared with sensitivity to prostaglandin (PG) E1 and no noradrenaline (NA) and 5-hydroxytryptamine (5HT). Simultaneous applications of PGSIs and NA or 5HT were made to investigate the role of PG in monoamine induced changes in neuronal excitability. PGSIs did not excite these cells, but depressions were common, particularly with fenoprofen. PGE1 did not reverse the depressions. NA and 5HT responses were generally unaffected by simultaneous PGSI application and responsiveness to PGSIs was found to be unrelated to amine sensitivity.The results support the conclusion that PGSIs have a depressant action on neurones in this region, which may not be related to inhibition of prostaglandin synthesis, and that the actions of microiontophoretically applied NA and 5HT are not dependent upon PG.

Effects of growth hormone on renal tubular handling of sodium in healthy humans

2001 ◽  
Vol 281 (6) ◽  
pp. E1326-E1332 ◽  
Author(s):  
Troels Krarup Hansen ◽  
Jens Møller ◽  
Klaus Thomsen ◽  
Erik Frandsen ◽  
Rolf Dall ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Day Treatment ◽  
Extracellular Volume ◽  
Plasma Renin ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Water Reabsorption ◽  
Synthesis Inhibition ◽  
Healthy Humans ◽  
Renal Tubular

To investigate the mechanisms behind the water- and sodium-retaining effects of growth hormone (GH), we studied the effect of GH on 1) water and sodium homeostasis, 2) the renin-angiotensin-aldosterone system (RAAS), and 3) lithium clearance (CLi) with and without concomitant prostaglandin (PG) synthesis inhibition with ibuprofen. GH administration for 6 days induced a significant increase in plasma renin, which was abolished by coadministration of ibuprofen (mU · l−1 · 24 h−1: control: 22.4 ± 4.3; GH: 37.7 ± 8.8; ibuprofen: 15.2 ± 3.0; GH + ibuprofen: 19.7 ± 2.5; ANOVA: P < 0.01). Comparable increments in extracellular volume were seen after 6-day treatment with GH alone and in combination with ibuprofen [liters: control, 19.57 ± 0.92; GH, 20.80 ± 1.00 (ANOVA: P< 0.0005); ibuprofen, 19.38 ± 0.90; GH + ibuprofen, 21.63 ± 1.37 (ANOVA: P < 0.0005)]. Treatment with GH increased CLi and changed the tubular handling of sodium and water. The absolute distal sodium reabsorption was increased, and this was only partially counterbalanced by decreased reabsorption in the proximal tubules. The data demonstrate that GH-induced activation of the RAAS can be blocked by concomitant PG synthesis inhibition and that the tubular effects of GH include increased distal nephron sodium and water reabsorption.

Contribution of renal prostaglandins to the natriuretic action of bradykinin in the dog

1979 ◽  
Vol 237 (3) ◽  
pp. F182-F187
Author(s):  
M. C. Blasingham ◽  
A. Nasjletti
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Urine Volume ◽  
Prostaglandin Synthesis ◽  
Urine Flow ◽  
Prostaglandin Synthetase ◽  
Renal Functions ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Stimulation Of

To study the effects of stimulation of renal prostaglandin biosynthesis by bradykinin, we assessed the changes in renal functions induced by intrarenal infusion of bradykinin (10 ng . min-1 . kg-1) in the dog anesthetized with pentobarbital before and during inhibition of prostaglandin synthesis by sodium meclofenamate (5 mg/kg). Before meclofenamate administration, bradykinin augmented the urinary output of a "PGE"-like substance from 1.00 +/- 0.25 to 3.88 +/- 1.09 ng/min (P less than 0.05) and increased renal blood flow by 65 +/- 9 ml/min (P less than 0.001), urine flow by 0.55 +/- 0.23 ml/min (P less than 0.05), and sodium excretion by 64.8 +/- 18.0 mueq/min (P less than 0.01). Administration of meclofenamate did not affect the bradykinin-induced increase in renal blood flow and urine volume, but suppressed the evoked output of "PGE" and reduced the associated natriuresis, i.e., sodium excretion increased by only 11.1 +/- 4.8 mueq/min (P greater than 0.05). In contrast, meclofenamate did not affect the natriuresis effected by an equidilator dose of PGE2 (5 ng . min-1 . kg-1) infused intrarenally. These observations suggest that a product of prostaglandin synthetase produced by the kidney during intrarenal infusion of bradykinin contributes to the natriuretic action of the peptide.

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