Natriuretic and diuretic effects of salmon calcitonin in rats

1970 ◽  
Vol 48 (12) ◽  
pp. 838-841 ◽  
Author(s):  
R. Keeler ◽  
Valerie Walker ◽  
D. H. Copp
Keyword(s):  
Linear Relationship ◽  
Salmon Calcitonin ◽  
Sodium Excretion ◽  
Free Water ◽  
Potassium Excretion ◽  
Free Water Clearance ◽  
Saline Loading ◽  
Water Clearance

Injection of salmon calcitonin into rats caused a significant increase in the excretion of sodium and water in a dose as small as 4 × 10−9 g. There appeared to be a linear relationship between sodium excretion and the log dose of calcitonin. Potassium excretion and free-water clearance were not significantly affected. Thyroparathyroidectomized rats showed no impairment in their ability to excrete sodium either before or after saline loading.

Potentiation of the natriuretic effect of clonidine following indomethacin in the rat

1991 ◽  
Vol 69 (8) ◽  
pp. 1196-1203 ◽  
Author(s):  
Dorothea E. Blandford ◽  
Donald D. Smyth
Keyword(s):  
Sodium Excretion ◽  
Infusion Rate ◽  
Urine Volume ◽  
Free Water ◽  
Vehicle Group ◽  
Prostaglandin E ◽  
Free Water Clearance ◽  
Prostaglandin Production ◽  
Natriuretic Effect ◽  
Water Clearance

Previous studies have demonstrated a diuretic effect of clonidine at low intrarenal infusion rates with a natriuretic effect being observed at high infusion rates (≥3 μg∙kg−1∙min−1). The natriuresis at high infusion rates may have been secondary to increased renal prostaglandin production. We therefore evaluated the effects of indomethacin (a cyclooxygenase inhibitor) on the response to cionidine in the anesthetized rat. Intrarenal infusions of saline (vehicle) or clonidine (0.1, 0.3, 1, and 3 μg∙kg−1∙min−1) were examined both in the presence and absence of pretreatment with indomethacin (5 mg/kg, i.p.). Clonidine produced a dose-related increase in urine volume and free water clearance at 0.3, 1, and 3 μg∙kg−1∙min−1 as compared with the vehicle group. Sodium excretion and osmolar excretion were increased only at the highest infusion rate investigated. Following indomethacin pretreatment, clonidine produced a greater increase in urine volume at each infusion rate investigated. The indomethacin pretreatment also resulted in a potentiation of the natriuretic effect of clonidine at all infusion rates. Interestingly, this was associated with an increase in osmolar clearance but not free water clearance. These effects of indomethacin were reversed by infusion of prostaglandin E2. An infusion of prostaglandin E2 attenuated the indomethacin-induced increase in both urine flow rate and sodium excretion, indicating that the effects of indomethacin were mediated by prostaglandin inhibition. These results suggest that endogenous prostaglandin production attenuates the renal effects of clonidine, and as well, that in the presence of α2-adrenoceptor stimulation, prostaglandin E2 mediates an antidiuretic and antinatriuretic effect.Key words: clonidine, indomethacin, prostaglandin E2, diuresis, natriuresis.

Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure

2001 ◽  
Vol 281 (2) ◽  
pp. R459-R467 ◽  
Author(s):  
Anders Gabrielsen ◽  
Peter Bie ◽  
Niels Henrik Holstein-Rathlou ◽  
Niels Juel Christensen ◽  
Jørgen Warberg ◽  
...  
Keyword(s):  
Heart Failure ◽  
Sodium Excretion ◽  
Volume Expansion ◽  
Water Immersion ◽  
Free Water ◽  
Ang Ii ◽  
Free Water Clearance ◽  
Fractional Sodium Excretion ◽  
Control Subjects ◽  
Water Clearance

To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 ± 0.03 (mean ± SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis ( P < 0.05 for all) compared with seated control. Compared with control subjects ( n = 9), ANG II, Aldo, and ANP concentrations were increased ( P < 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 ± 16 vs. 88 ± 15 μmol/min and 0.42 ± 0.18 vs. 0.68 ± 0.12% (mean ± SE), respectively, both P < 0.05]. When ANG II and Aldo concentrations were further suppressed ( P < 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased ( P < 0.05) to the level of control subjects (108 ± 34 μmol/min and 0.70 ± 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations.

A Role for Sodium-Retaining Steroids in the Regulation of Proximal Tubular Sodium Reabsorption in Man

1972 ◽  
Vol 42 (4) ◽  
pp. 423-432 ◽  
Author(s):  
John R. Gill ◽  
Catherine S. Delea ◽  
F. C. Bartter
Keyword(s):  
Flow Rate ◽  
Sodium Excretion ◽  
Free Water ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Diluting Segment ◽  
Free Water Clearance ◽  
Urinary Osmolality ◽  
Glomerular Filtrate ◽  
Water Clearance

1. The response to an infusion of 4% (w/v) fructose in water was determined in fifteen women on a daily sodium intake of 100 mEq/day. The results were compared with those obtained during a similar infusion on another day after treatment with deoxycorticosterone (20 mg/day; seven subjects), or spironolactone (200 mg/day; eight subjects), for 1 day before the day of study. 2. Treatment with deoxycorticosterone significantly (P < 0·01) decreased sodium excretion (from a mean value of 391 to 192 μEq/min) and urine flow rate (from 14·3 to 12·4 ml min−1 100 ml−1 of glomerular filtrate) without a change in urinary osmolality or the clearance of inulin. The steroid also increased the fractional reabsorption of sodium at the diluting segment of the nephron, but this increase in reabsorption was not sufficient to compensate for the decrease in delivery of sodium to the site, so that absolute free-water clearance decreased. 3. Treatment with spironolactone significantly (P < 0·01) increased sodium excretion (from 349 to 437 μEq/min) and urine flow rate (from 12·5 to 14·4 ml min−1 100 ml−1 of glomerular filtrate) with essentially no change in urinary osmolality or in inulin clearance. Spironolactone also decreased the fractional reabsorption of sodium at the diluting segment of the nephron, but the degree of inhibition of reabsorption was not sufficient to prevent an increase in free-water clearance as a result of increased delivery of sodium to the site. 4. The findings support the concept that changes in circulating aldosterone can alter the renal excretion of sodium in man by affecting its reabsorption in the proximal tubule as well as in the distal tubule.

THE ACUTE EFFECTS OF INFUSED ADRENAL STEROIDS ON RENAL FUNCTION IN ADRENALECTOMIZED DOGS

1961 ◽  
Vol 37 (2) ◽  
pp. 263-278 ◽  
Author(s):  
J. D. H. Slater ◽  
Paul Mestitz ◽  
Geoffrey Walker ◽  
J. D. N. Nabarro
Keyword(s):  
Urine Volume ◽  
Free Water ◽  
Potassium Excretion ◽  
Adrenal Steroids ◽  
Acute Effects ◽  
Filtration Fraction ◽  
Free Water Clearance ◽  
Sodium And Potassium ◽  
Slow Absorption ◽  
Water Clearance

ABSTRACT Infusions of cortisol (11β,17,21-trihydroxy-pregn-4-ene-3,20-dione), prednisolone (11β,17,21-trihydroxy-pregna-1,4-diene-3,20-dione), aldosterone (11β,21-dihydroxy-3,20-dione-pregn-4-en-18-al), and adrenal cortical extract have been given to four adrenalectomized dogs. The changes of inulin, creatinine, para-aminohippuric acid clearances, urine volume, and sodium and potassium excretion have been measured. Between experiments oral replacement therapy was given to obviate the effect of slow absorption of previously injected steroids. The effects of steroid-free control infusions have been studied. Varying the rate of infusion from 1.0–2.6 ml/min, and sodium from 0–170 μeq/min has little effect on glomerular filtration rates (G. F. R.). Infusions of cortisol (1.5 and 10 mg/h), prednisolone (2 mg/h) and adrenal cortical extract (10 ml/h) raised the G. F. R. and lowered the filtration fraction. As the G. F. R. increased the ratio creatinine: inulin clearance fell. The different dogs varied in their responses. Infusions of prednisolone and cortisol (1.5 mg/h) usually increased sodium output as G. F. R. rose. With aldosterone, adrenal cortical extract and cortisol (10 mg/h) there was sodium retention in three of the four dogs, the fourth was resistant to the sodium retaining action of these steroids while the plasma level was high. All steroid infusions increased potassium excretion. Cortisol increased free water clearance independent of G. F. R. provided the infusion rate exceeded 2 ml/min, prednisolone increased both osmolar and free water clearance, aldosterone increased osmolar clearance and reduced free water clearance.

Effects of indomethacin on renal response to atrial natriuretic peptide

1987 ◽  
Vol 253 (5) ◽  
pp. F868-F873
Author(s):  
C. A. Gaillard ◽  
H. A. Koomans ◽  
A. J. Rabelink ◽  
E. J. Mees
Keyword(s):  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Free Water ◽  
Fractional Excretion ◽  
Lithium Clearance ◽  
Free Water Clearance ◽  
Fractional Excretion Of Sodium ◽  
Natriuretic Effect ◽  
Water Clearance

We studied the effect of alpha-human natriuretic peptide (ANP, 100 micrograms iv) on renal sodium handling in eight healthy subjects before and after 7 days of indomethacin (50 mg 3 times a day). Sodium intake was 100 mmol/day. Prior to indomethacin, ANP caused a fourfold rise in sodium excretion over the first 20 min and a threefold rise in fractional sodium excretion. The clearance studies, performed during maximal water diuresis, showed increased fractional free water clearance and lithium clearance. Indomethacin caused marked sodium retention. Complete escape did not occur until the sixth day, when cumulative balance was 244 mmol (range 176-337). By this time renin and aldosterone were suppressed and fractional lithium and free water clearance reduced. The natriuretic effect of ANP was not attenuated, and the fractional excretion of sodium and chloride rose even more than without indomethacin. The reduction in lithium and free water clearance under indomethacin tended to be reversed by ANP. These data suggest that the natriuretic effect of ANP is not mediated by or dependent on renal prostaglandins. Indomethacin and ANP appear to have opposite effects on sodium excretion, maximal free water clearance, and lithium clearance.

Effect of sodium nitrate loading on electrolyte transport by the renal tubule

1975 ◽  
Vol 229 (3) ◽  
pp. 746-753 ◽  
Author(s):  
T Kahn ◽  
J Bosch ◽  
MF Levitt ◽  
MH Goldstein
Keyword(s):  
Sodium Nitrate ◽  
Sodium Excretion ◽  
Free Water ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Urine Ph ◽  
Free Water Clearance ◽  
Saline Loading ◽  
Urinary Potassium

Effects of sodium nitrate were compared with sodium chloride loading on transport of electrolytes by the nephron. Maximal levels of free water clearance/clomerular filtration rate (CH2O/GFR) averaged 8.4% with nitrate loading and 14.4% with saline loading. Since ethacrynic acid and chlorothiazide exert their major natriuretic effect in the distal nephron, the increment in Na ad Cl reabsorbed beyond the proximal tubule. The administration of these agents resulted in an increase in fractional sodium excretion (CNa/GFR) of 21.1%, urinary sodium excretion (UNaV) of 1,126 mueq/min, and urinary chloride excretion (UClV) of 848 mueq/min during nitrate loading compared with an increase in CNa/GFR of 37.6%, UNaV of 2,362 mueq/min, and UClV of 2,397 mueq/min during saline loading. The smaller diuretic-induced increment in Na and Cl excretion in the nitrate studies suggests, as do the hydrated studies, that less Cl and Na are reabsorbed in the distal nephron during nitrate than saline loading. At every level of UNaV, fractional bicarbonate reabsorption was higher, urine pH was lower, and urinary potassium excretion (UKV) was higher in the nitrate studies. Thus, compared with saline loading, sodium nitrate decreases chloride and sodium reabsorption in the distal nephron. The higher hydrogen and potassium secretion in the nitrate studies may be consequent to the decreased ability of the distal nephron to reabsorb chloride.

Salt depletion inhibits cerebral-induced natriuresis in the dog

1984 ◽  
Vol 247 (5) ◽  
pp. F725-F728 ◽  
Author(s):  
J. P. Gilmore ◽  
M. N. Nemeh
Keyword(s):  
Sodium Excretion ◽  
Free Water ◽  
Free Water Clearance ◽  
Conscious Dog ◽  
Sensing Mechanism ◽  
Body Sodium ◽  
Salt Depletion ◽  
Total Body ◽  
Renal Responses ◽  
Water Clearance

Experiments were carried out in the conscious dog to determine whether renal responses to intracarotid (IC) infusion of hypertonic NaCl are altered in the sodium-depleted state. In the sodium-replete animal, both IC and IV infusion of hypertonic NaCl produced significant increases in sodium excretion and significant decreases in free water clearance. However, both of these renal responses were more rapid in onset with IC infusion. Both IC and IV infusion decreased free water clearance. In the sodium-deplete animal, IC hypertonic NaCl infusion had no effect on sodium excretion but did decrease free water clearance. It is concluded that total body sodium is a determinant of the gain of the cerebral sodium-sensing mechanism and that this mechanism is different from the osmosensitive mechanism.

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