Effect of Hypertonic and Hypotonic Infusions on Aldosterone in Conscious Sodium-Depleted Dogs

1981 ◽  
Vol 61 (2) ◽  
pp. 191-199 ◽  
Author(s):  
Jennifer W. Childers ◽  
E. G. Schneider
Keyword(s):  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Plasma Aldosterone ◽  
Plasma Sodium ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Plasma Sodium Concentration ◽  
Sodium Load

1. The role of the plasma sodium concentration in the regulation of aldosterone secretion and sodium excretion was investigated by comparing in 13 conscious sodium-depleted dogs the effects of the same sodium load (2.5 mmol/kg) given as either a hypertonic or hypotonic infusion. 2. The plasma sodium concentration was significantly higher and the plasma aldosterone concentration and urinary aldosterone excretion were significantly lower after the hypertonic infusion as compared with the hypotonic infusion. 3. The cumulative urinary sodium excretion during the 22 h after beginning the infusion was significantly greater after the hypertonic infusion, but this difference was not observed in five sodium-depleted dogs who were treated with deoxycorticosterone acetate before the infusions were given. 4. These data suggest that elevations in plasma sodium concentration are effective in decreasing aldosterone secretion and, hence, in increasing sodium excretion in conscious sodium-depleted dogs.

Aldosterone and the enhanced natriuresis of hypertonic infusions in the dog

1982 ◽  
Vol 242 (1) ◽  
pp. F30-F37 ◽  
Author(s):  
J. W. Childers ◽  
E. G. Schneider
Keyword(s):  
Sodium Excretion ◽  
Important Determinant ◽  
Sodium Concentration ◽  
Conscious Dogs ◽  
Plasma Sodium ◽  
Aldosterone Secretion ◽  
Sodium Diet ◽  
Plasma Sodium Concentration ◽  
Sodium Load

The purpose of this study was to determine whether small elevations in plasma sodium concentration (PNa) were effective in decreasing aldosterone secretion and, hence, in increasing sodium excretion in dogs fed normal sodium diets. Ten dogs fed a normal sodium diet, six DOCA-treated dogs, and four adrenalectomized dogs were given the same sodium load (2.5 mmol/kg) either as a hypertonic (1 M NaCl) or hypotonic (0.1 M NaCl) infusion. In all three groups of dogs, PNa was greater after the hypertonic than after the hypotonic infusion during most of the 22-h experiment. The dogs fed a normal sodium diet responded to the elevation in PNa (hypertonic infusion) with decreased aldosterone excretion and an exaggerated natriuresis. When aldosterone levels were maintained constant by either DOCA treatment or adrenalectomy, the exaggerated natriuresis that accompanied the hypertonic infusion was prevented. Therefore, elevation of PNa appears to be an important determinant of aldosterone secretion and, hence, of sodium excretion in conscious dogs fed normal sodium diets.

Dietary Sodium Intake: A Determinant of Postprandial Plasma Sodium Concentration in the Dog

1982 ◽  
Vol 62 (5) ◽  
pp. 471-477 ◽  
Author(s):  
E. G. Schneider ◽  
Sarah D. Gleason ◽  
A. Zucker
Keyword(s):  
Sodium Excretion ◽  
Sodium Intake ◽  
Urinary Sodium Excretion ◽  
Sodium Concentration ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Plasma Sodium ◽  
Free Access ◽  
Potassium Excretion ◽  
Plasma Sodium Concentration

1. The effect of dietary sodium intake on pre-and post-prandial plasma sodium concentrations and on the pattern of sodium and potassium excretion was determined in conscious female dogs, who were allowed free access to water and were fed on commercial low sodium diets supplemented with 0, 50, 100 or 250 mmol of sodium chloride/day for 6 days. 2. The preprandial plasma sodium concentration was not altered by the dietary sodium intake. However, the 4 h postprandial plasma sodium concentration was linearly related to the magnitude of dietary sodium intake, whereas the 8 h postprandial plasma sodium concentration was elevated only in dogs receiving 250 mmol of sodium/day. 3. The (0–8 h/0–24 h) ratio for urinary sodium excretion was significantly correlated with both the dietary sodium intake and the postprandial increase in plasma sodium concentration. 4. The 24 h excretion of potassium was not markedly affected by the dietary sodium intake; however, the (0–8 h/0–24 h) ratio for potassium excretion was significantly correlated with both the dietary sodium intake and the (0–8 h/0–24 h) ratio for sodium excretion. 5. These data indicate that: (a) postprandial increases in plasma sodium concentration need to be considered when evaluating the mechanisms involved in the daily regulation of sodium balance; (b) the daily pattern of potassium excretion is closely linked to the dietary sodium intake.

Mechanisms of angiotensin II natriuresis and antinatriuresis

1985 ◽  
Vol 249 (2) ◽  
pp. F299-F307 ◽  
Author(s):  
M. E. Olsen ◽  
J. E. Hall ◽  
J. P. Montani ◽  
A. C. Guyton ◽  
H. G. Langford ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Excretion ◽  
Distal Tubule ◽  
Urinary Sodium Excretion ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Sodium Load ◽  
Proximal Tubular ◽  
Anesthetized Dogs

The aim of this study was to determine the role of changes in renal arterial pressure (RAP), renal hemodynamics, and tubular reabsorption in mediating the natriuretic and antinatriuretic actions of angiotensin II (ANG II). In seven anesthetized dogs, endogenous ANG II formation was blocked with captopril, and ANG II was infused intravenously at rates of 5-1,215 ng X kg-1 X min-1 while RAP was either servo-controlled at the preinfusion level or permitted to increase. When RAP was servo-controlled, ANG II infusion at all rates from 5-1,215 ng X kg-1 X min-1 decreased urinary sodium excretion (UNaV) and fractional sodium excretion (FENa) while increasing fractional reabsorption of lithium (FRLi) (an index of proximal tubular fractional sodium reabsorption) and causing no change in calculated distal tubule fractional sodium reabsorption (FRDNa). When RAP was permitted to increase, ANG II infusion rates up to 45 ng X kg-1. min-1 also decreased UNaV and FENa while increasing FRLi and causing no change in FRDNa. However, at 135 ng X kg-1 X min-1 and above, UNaV and FENa increased while FRLi and FRDNa decreased when RAP was allowed to rise, even though renal blood flow and filtration fraction were not substantially different from the values observed when RAP was servo-controlled. Filtered sodium load was slightly higher when RAP was permitted to increase during ANG II infusion compared with when RAP was servo-controlled, although the differences were not statistically significant. Thus, even very large doses of ANG II cause antinatriuresis when RAP is prevented from increasing.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension in dogs during antidiuretic hormone and hypotonic saline infusion

1979 ◽  
Vol 236 (2) ◽  
pp. H314-H322 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton ◽  
T. G. Coleman ◽  
R. E. McCaa
Keyword(s):  
Arterial Pressure ◽  
Antidiuretic Hormone ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Saline Infusion ◽  
Plasma Sodium ◽  
Experimental Hypertension ◽  
Plasma Aldosterone Concentration ◽  
Plasma Sodium Concentration ◽  
Hypotonic Saline

Experimental hypertension was produced in 7 dogs by continuously infusing suppressor amounts of antidiuretic hormone (ADH) and hypotonic saline after renal mass had been surgically reduced to 30% of normal. Data were collected during 9 days of control measurements, 14 days of ADH and saline infusion, and then 3 days of saline infusion to 1) determine the chronic effects of ADH on arterial pressure and 2) determine whether hypertension could be maintained during hyponatremia. During the period of ADH infusion, arterial pressure increased to hypertensive levels while plasma sodium concentration decreased almost 20 meq/1. Also, during the ADH infusion period, the dogs demonstrated decreases in heart rate, plasm potassium concentration, plasma renin activity, and plasma aldosterone concentration. Fluid volume expansion was evidenced by sustained increases in blood volume and sodium space. We conclude that when renal function is compromised, subpressor amounts of ADH can contribute to the development of hypertension, probably due to its fluid-retaining properties and in spite of the attendant hyponatremia.

Atrial natriuretic hormone effect on renal function and aldosterone secretion in sodium depletion

1988 ◽  
Vol 255 (6) ◽  
pp. R867-R873
Author(s):  
Y. Shenker
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Low Dose ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Urinary Sodium ◽  
Aldosterone Secretion ◽  
Natriuretic Hormone ◽  
Atrial Natriuretic Hormone

The effects of atrial natriuretic hormone (ANH) on aldosterone secretion and renal function have been well documented, but the physiological role of ANH is still unknown. To address this issue, eight normal men were infused for 4 h with low-dose (1.1 pmol.kg-1.min-1) human [Ser-Tyr28]ANH after 3 days of low-salt (LS) diet. The same subjects were also studied with placebo infusion on LS and high-salt (HS) diet. ANH infusion caused doubling of urine flow, a fourfold increase in urinary sodium excretion, and a slight increase in potassium excretion. Immunoreactive ANH levels increased from 3.1 +/- 0.5 to 21.0 +/- 1.9 pmol/l during ANH infusion. ANH infusion suppressed plasma renin activity (PRA) to one-third of the basal value, and plasma aldosterone was suppressed from 46.5 +/- 6.5 to 20.9 +/- 2.6 ng/dl. Low-dose ANH infusion caused a marked increase in urine flow and urinary sodium excretion and prominent suppression of PRA and plasma aldosterone in sodium-depleted subjects. These results suggest a physiological significance of ANH in regulation of kidney function and aldosterone secretion.

Hyponatremia in Patients Undergoing CAPD: Role of Water Gain and/or Malnutrition

2001 ◽  
Vol 21 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Gonzalo Zevallos ◽  
Dimitrios G. Oreopoulos ◽  
Mitchell L. Halperin
Keyword(s):  
Extracellular Fluid ◽  
Free Water ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Fluid Composition ◽  
Major Mechanism ◽  
Plasma Sodium Concentration ◽  
Catabolic State ◽  
Water Gain

Background Hyponatremia has a number of different causes; some may have serious untoward implications for patients undergoing chronic ambulatory peritoneal dialysis (CAPD). Objective To determine the pathophysiology of hyponatremia in patients on CAPD. Methods A retrospective analysis was carried out on 210 patients on CAPD. We selected patients with 2 – 4 consecutive periods when the plasma sodium concentration was ≤130 mmol/L and again when it was > 133 mmol/L. Exclusion criteria included hyperglycemia, orthostatic hypotension, edema, and inadequate records. Results An electrolyte-free water gain appeared to be the main cause of hyponatremia in only 1 of 5 patients because this was the only patient with a significant increase in body weight. In 1 patient, there was weight loss in the hyponatremic period, suggesting tissue catabolism was present. In 3 patients, there was neither weight gain nor evidence for a contracted extracellular fluid volume in the hyponatremic period, suggesting that intracellular potassium and phosphate loss could be the major mechanism for their hyponatremia. Conclusion When hyponatremia is due to a catabolic state, its management should aim to restore intracellular fluid composition ( i.e., to correct malnutrition).

Attenuation of the osmotic release of vasopressin by enkephalins in dogs

1989 ◽  
Vol 256 (2) ◽  
pp. E270-E276
Author(s):  
K. Matsui ◽  
T. Kimura ◽  
K. Ota ◽  
M. Shoji ◽  
M. Inoue ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Levels ◽  
Sodium Concentration ◽  
Conscious Dogs ◽  
Plasma Sodium ◽  
Time Control ◽  
Plasma Vasopressin ◽  
Plasma Sodium Concentration ◽  
Anesthetized Dogs

To assess the possible role of circulating enkephalins in the osmotic release of vasopressin, Met5 (M-Enk)- or Leu5-enkephalin (L-Enk) dissolved in 0.9 or 10% NaCl was infused to either anesthetized or conscious dogs at a dose of 3.5 nM.kg-1.min-1 for 15 min. Intravenous infusion of M-Enk or L-Enk produced 150- to 200-fold increases in their plasma levels, and the elevated levels were maintained during the infusion. Although blood pressure (BP) in anesthetized dogs decreased significantly during L-Enk infusion, BP in conscious dogs was unaffected by both enkephalins. Neither M-Enk nor L-Enk infusion affected plasma vasopressin concentration (PAVP) in these anesthetized and conscious dogs that were not osmotically stimulated. PAVP in conscious time control dogs increased significantly after start of 10% NaCl infusion in spite of an increase in BP. M-Enk or L-Enk significantly blunted the increase in PAVP induced by 10% NaCl infusion. This attenuation was not accompanied by any significant changes in plasma sodium concentration and BP compared with those of time control dogs. Thus increase in plasma enkephalins attenuates the osmotic release of vasopressin.

Effect of rapid sodium load on circulating atrial natriuretic polypeptide

1988 ◽  
Vol 254 (4) ◽  
pp. F540-F546
Author(s):  
Y. Nishida ◽  
A. Miyata ◽  
H. Morita ◽  
N. Uemura ◽  
K. Kangawa ◽  
...  
Keyword(s):  
Small Volume ◽  
Control Level ◽  
Sodium Concentration ◽  
Plasma Sodium ◽  
Nacl Solution ◽  
High Concentration ◽  
Atrial Natriuretic Polypeptide ◽  
Plasma Sodium Concentration ◽  
Sodium Load ◽  
Atrial Natriuretic

The hypothesis that an increase in plasma sodium concentration (PNa) causes an increase in circulating atrial natriuretic polypeptide (ANP) was examined in conscious dogs. NaCl solution in small volume (0.3 ml/kg body wt) and at high concentration (20%) was injected intravenously within 2 s to rapidly increase PNa. PNa rapidly increased to 5.1 +/- 0.3 meq/l. Urinary excretion of sodium and water increased to 4.1 and 2.5 times the control levels, respectively. Plasma vasopressin level increased to 3.7 times the control level. Plasma ANP level (PANP) did not change significantly. PANP corrected for sodium-induced hemodilution did not change either. On a different day, a double amount of sodium (0.6 ml/kg body wt of 20% NaCl solution) was intravenously injected into the dogs. PNa increased by 7.3 +/- 0.4 meq/l, which was significantly more than the increase after the 0.3 ml/kg injection. PANP with or without correction for hemodilution again did not change. These results indicate that a rapid increase in PNa within the physiological range does not cause elevation of circulating ANP. This suggests that ANP does not contribute to the regulation of plasma sodium concentration.

Modulation of plasma aldosterone by physiological changes in hydrogen ion concentration

1992 ◽  
Vol 262 (2) ◽  
pp. R269-R275
Author(s):  
G. V. Jones ◽  
B. M. Wall ◽  
H. H. Williams ◽  
D. N. Presley ◽  
D. G. Sapir ◽  
...  
Keyword(s):  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Hydrogen Ion ◽  
Ion Concentration ◽  
Plasma Sodium ◽  
Physiological Changes ◽  
Weight Changes ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Hydrogen Ion Concentration

To assess the effect of extracellular hydrogen ion concentration (PH+) on aldosterone secretion, studies in which other known modulators could be controlled were performed on 13 patients undergoing hemodialysis. High (35 mM) or low (14-17 mM) dialysate bicarbonate concentrations were utilized on separate days to either decrease or increase PH+, while plasma potassium concentrations (PK) were held at constant levels and changes in plasma renin activity (PRA) were minimized by avoiding changes in body weight. Changes in PH+ were associated with concordant changes in plasma aldosterone concentration (Pa) in both high- and low-bicarbonate studies. When these changes in Pa in high- and low-bicarbonate studies were analyzed together as a function of corresponding changes in PH+, a significant correlation could be demonstrated (r = 0.659, P less than 0.001). There was no correlation between changes in Pa and changes in PK, plasma sodium, plasma adrenocorticotropic hormone (ACTH), or PRA. Using the same methods to control PH+ and other variables during hemodialysis, the effects of altered PH+ on ACTH-stimulated aldosterone and cortisol secretion were evaluated in studies on six patients who received incremental infusions of ACTH after pretreatment with dexamethasone. In these studies, there was no demonstrable effect of PH+ on Pa or plasma cortisol concentration. We conclude that physiological changes in PH+ have a weak modulating effect on basal aldosterone secretion that may not be evident in the presence of other acutely applied stimuli.

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