Changes In Electrolyte Excretion Research Articles

The Protective Effects of Ketodiet in Salt‐Sensitive Hypertension

Two‐thirds of hypertension cases in the United States are positively correlated with excessive weight gain. The ketogenic diet gained popularity through the weight loss community. It’s a low‐carb high‐fat diet triggering the body to burn fat for energy instead of carbohydrates. Dietary manipulation, ketoacid supplementation can potentially exert a cardiovascular protective effect in chronic renal failure. We hypothesized that ketodiet can have beneficial effects during the development of salt‐induced hypertension. The Dahl Salt Sensitive (SS) rats fed a high salt diet develop salt‐induced hypertension accompanied by kidney injury. To test effect of ketodiet, the Dahl SS rats were given either 4% NaCl diet (HS; Dyets Inc, 113756) or 4% NaCl modified ketodiet (KD; Harland Tekland, TD 190564) with free access to water for 4 weeks. Blood pressure was monitored with telemetry throughout the study, and urine samples were collected in metabolic cages on days 0, 7, 14, and 28. At the end of the protocol animals were sacrificed and blood and kidney tissues were harvested for following analyses. Urine and plasma samples were analyzed to estimate electrolyte and glucose homeostasis. Dahl SS rats fed a KD had a lower blood pressure compared to control rats fed a HS diet. By the end of the experiment mean arterial pressure was 143 ± 4 mmHg vs 156 ± 4 mmHg for Dahl SS rats fed a KD and HS diets, respectively (p<0.05). The KD group has gained less weight (70 ± 8 vs 85 ± 12 g, p<0.05 compared to HS). Furthermore, we observed reduced renal hypertrophy with decreased kidney to body weight ratio (0.94 ± 0.05 vs 1.14 ± 0.06 p<0.05 compared to HS) and smaller kidneys (3.0 ± 0.1 vs 4.0 ± 0.3 g, p<0.05 compared to HS) in the KD animals. The rats on KD experienced hypoglycemia (305 ± 8 vs 364 ± 11 mg/dL, p<0.05 compared to HS) although they had comparably the same as the HS group amount of food consumption (17 ± 2 vs 19 ± 2 g/day, p>0.05). Metabolic cage studies revealed diminished diuresis (0.010 ± 0.001 ml/100g/h vs 0.020 ± 0.002 ml/100g/hr, p<0.05) in KD compared to HS group with no significant changes in electrolyte excretion. Glucose excretion has been reduced in a KD group (1.2 ± 0.5 vs 12.8 ± 4.8, glucose to creatinine ratio, p<0.05 compared to HS). Therefore, we can conclude that prolonged KD provide protective effect on the development of hypertension during HS challenge. Our data revealed that KD during HS challenge resulted in decreased blood pressure, reduced kidney hypertrophy and diminished levels of plasma glucose.

Structure of Rhythms of Blood Pressure, Heart Rate, Excretion of Electrolytes, and Secretion of Melatonin in Normotensive and Spontaneously Hypertensive Rats Maintained under Conditions of Prolonged Daylight Duration.

We studied the structure of rhythms of BP, HR (by telemetric monitoring), electrolyte excretion (by capillary electrophoresis), and products of epiphyseal melatonin (by the urinary concentration of 6-sulfatoxymelatonin measured by ELISA) in normotensive Wistar-Kyoto rats and spontaneously hypertensive SHR rats maintained at 16/8 h and 20/4 h light-dark regimes. In Wister-Kyoto rats exposed to prolonged daylight, we observed changes in the amplitude, rhythm power (% of rhythm), and range of oscillations of systolic BP; HR mezor decreased. In SHR rats, mezor of HR also decreased, but other parameters of rhythms remained unchanged. Changes in electrolyte excretion were opposite in normo- and hypertensive rats. Under conditions of 20/4 h light-dark regime, daytime melatonin production tended to increase in normotensive rats and significantly increased in SHR rats. At the same time, nighttime melatonin production did not change in both normotensive and hypertensive animals. As the secretion of melatonin has similar features in animals of both lines, we can say that the epiphyseal component of the "biological clock" is not the only component of the functional system that determines the response of the studied rhythms to an increase in the duration of light exposure.

Urea channel inhibitors: a new functional class of aquaretics

Using large-scale small molecule screening techniques, Li et al. have identified a compound that inhibits the UT-B urea channel. They propose that this or similar compounds could be used as aquaretic agents to increase water excretion without changes in electrolyte excretion. Such compounds would potentially be useful in treatment of hyponatremic disorders. Here we review the physiological basis for the action of urea channel inhibitors in the kidney and assess their clinical potential.

Protective role of NHE-3 inhibition in rat renal transplantation undergoing acute rejection

Acute rejection in renal transplantation disturbs solute and volume maintenance in humans accompanied by delayed graft function and poor prognosis. We recently reported that decreased expression and function of Na+/H+ exchanger type 3 (NHE-3) in proximal tubules and epithelial Na+ channels and aquaporin 2 in collecting ducts are major mechanisms involved in Na+ and water imbalances shortly after transplantation in rat undergoing acute rejection. We performed kidney transplantations in rats with bilaterally nephrectomized recipients with acute rejection and, in addition, systemically administered a specific inhibitor of NHE-3 (NHE-I). NHE inhibition in acute renal failure was shown to improve tubular function and recovery. The aim of this therapy was to reduce energy consumption of the graft and preserve NHE-3 function. Imbalances in electrolyte excretion declined in NHE-I-treated animals and NHE-3 activity was preserved. Observed NHE-I-dependent changes in electrolyte excretion, polyuria, and reduced protein reabsorption in the acute postoperative phase are predictors of favorable graft outcome in humans.

Regulation of 11?? -hydroxylase cytochrome P450 expression by cholesterol in spontaneously hypertensive rats

To investigate whether hypercholesterolaemia interferes with the expression of the enzymes involved in steroid biosynthesis in the adrenal cortex. Twenty-four 5-week-old male spontaneously hypertensive rats (SHR) were randomly assigned to a high (1%) cholesterol diet (n = 8) or to a matched cholesterol-free diet (n = 8) for 6 weeks. A third group (n = 8) was studied after 2 weeks of washout from the high-cholesterol intake. A cohort of age- and sex-matched normotensive Wistar-Kyoto (WKY) rats (n = 24) underwent the same treatments and was used as a control. In SHR cholesterol feeding reduced urinary sodium excretion (0.8 +/- 0.1 versus 1.4 +/- 0.1 mmol/24 h in the cholesterol-free group), increased plasma aldosterone levels (299 +/- 60 versus 154 +/- 24) and reduced plasma corticosterone levels (142 +/- 21 versus 278 +/- 35 ng/ml). Those responses were associated with a reduction of 11 beta-hydroxylase cytochrome P450 messenger RNA (mRNA) in the adrenal cortex (-52.3 +/- 3.4%) whereas aldosterone synthase mRNA remained unchanged. That effect and the changes in electrolyte excretion and steroid levels were no longer detectable after withdrawal of the diet. In WKY rats high-cholesterol diet induced no significant changes in urinary electrolyte excretion, steroid levels and expression of 11 beta-hydroxylase cytochrome P450 and aldosterone synthase in the adrenals. The present results indicate that in SHR hypercholesterolaemia selectively interferes with the adrenal steroid biosynthetic pathway by reducing the expression of 11 beta-hydroxylase, leading to accumulation of mineralocorticoids and sodium retention.

Effects of cilazapril on renal function and hormones in hypertensive patients with renal disease

The effects of cilazapril 2.5 to 5.0 mg every 24 hours orally for one month on blood pressure, renal hemodynamics, and plasma and urinary hormones were investigated in 11 patients with renal disease and hypertension. Six patients had renal failure (pretreatment creatinine clearance of less than 1 ml/second). Both systolic and diastolic blood pressures were significantly decreased in all patients and seven of the 11 required 5.0 mg daily. There was no significant change in the effective renal plasma flow, glomerular filtration rate, or creatinine clearance, although the renal vascular resistance was significantly reduced. Albuminuria was reduced in most patients but the mean change was not significant. The mean plasma potassium concentration rose significantly, but no changes in electrolyte excretion or weight were noted. Mean ambulant plasma renin activity was normal before treatment and rose significantly. Mean ambulant angiotensin II concentrations did not change. Mean ambulant plasma aldosterone concentration and mean urinary aldosterone excretion decreased significantly. Plasma arginine vasopressin and cortisol concentrations did not change. No changes were noted in plasma glucose concentrations, liver function tests, hemoglobin concentrations, or white blood cell or platelet counts. A slight looseness of bowel motions occurred in two patients and was the only side effect recorded. Cilazapril appears to be an effective and safe antihypertensive drug in patients with hypertension and renal disease.

Effects of cilazapril on renal function and hormones in hypertensive patients with renal disease*1

The effects of cilazapril 2.5 to 5.0 mg every 24 hours orally for one month on blood pressure, renal hemodynamics, and plasma and urinary hormones were investigated in 11 patients with renal disease and hypertension. Six patients had renal failure (pretreatment creatinine clearance of less than 1 ml/second). Both systolic and diastolic blood pressures were significantly decreased in all patients and seven of the 11 required 5.0 mg daily. There was no significant change in the effective renal plasma flow, glomerular filtration rate, or creatinine clearance, although the renal vascular resistance was significantly reduced. Albuminuria was reduced in most patients but the mean change was not significant. The mean plasma potassium concentration rose significantly, but no changes in electrolyte excretion or weight were noted. Mean ambulant plasma renin activity was normal before treatment and rose significantly. Mean ambulant angiotensin II concentrations did not change. Mean ambulant plasma aldosterone concentration and mean urinary aldosterone excretion decreased significantly. Plasma arginine vasopressin and cortisol concentrations did not change. No changes were noted in plasma glucose concentrations, liver function tests, hemoglobin concentrations, or white blood cell or platelet counts. A slight looseness of bowel motions occurred in two patients and was the only side effect recorded. Cilazapril appears to be an effective and safe antihypertensive drug in patients with hypertension and renal disease.

Nephrotoxic drugs.

The nephrotoxic effects of cyclosporine, aminoglycoside antibiotics, cisplatin, amphotericin B, beta-lactam antibiotics and indomethacin are reviewed. These drugs were chosen because they are among the most frequent causes of renal injury in children. In addition, their nephrotoxicity is caused by different mechanisms. Several generalizations can be made, however. First, agents which cause tubular damage tend to be synergistic in their toxic effects. This synergism is seen when several nephrotoxic drugs are given simultaneously. In addition, the use of a nephrotoxic agent in a patient with pre-existing renal disease can result in severe tubular injury. Second, serum levels of the drug frequently fail to correlate with the degree of nephrotoxicity in individual patients. Third, early signs of renal injury can be subtle (e.g., minor changes in electrolyte excretion) or dramatic (e.g., acute renal failure). The subtle changes are particularly important, since they can be useful predictors of serious nephrotoxicity.

Effects of prostaglandin inhibition on renal function in deoxycorticosterone-acetate hypertensive Yucatan miniature swine

This study evaluated the effect of prostaglandin (PG) on renal function in normal and deoxycorticosterone-acetate (DOCA) hypertensive Yucatan miniature swine. Eight animals were implanted with DOCA impregnated silicone strips. MAP increased in the conscious DOCA animals from a normal pressure of 110–115 mmHg, to 148 ± 4 mmHg.After 3–4 weeks, the DOCA hypertensive and eight normal (sham or non-implanted) animals were anesthetized with sodium pentobarbital which reduced MAP in the DOCA pigs to normotensive levels. Under anesthesia, PG inhibition (indomethacin or meclofenamate, 2 mg/kg i.v.) increased MAP only in the normal group (P < .05). PG inhibition caused a significant reduction in renal blood flow in both groups, but only decreased glomerular filtration rate in the DOCA animals (P < .05). Radioactive microsphere distribution to the outer cortex of the normal animals was significantly decreased with PG inhibition, (P < .05). No consistant changes in electrolyte excretion or urine flow rate was seen in either group following PG inhibition. These data indicate that PG may influence renal hemodynamics in both normal and DOCA hypertensive Yucatan miniature swine. The finding that PG inhibition selectively decreases GFR in the DOCA animals suggests a possible protective role of these hormones in this hypertensive animal model.

Effects of prostaglandin E2, I2 and F2 alpha on systemic and renal hemodynamics, renal function and renin secretion in anesthetized dogs.

Effects of intrarenal-arterial (i.r.a.) and intravenous (i.v.) infusions of PGE2, I2 and F2 alpha on systemic blood pressure (BP), heart rate (HR), renal blood flow (RBF), urine volume (UV), renal function and plasma renin activity (PRA) of the renal venous blood (RVPRA) were investigated. A dose-dependent fall in BP was observed with PGE2 and I2 and was accompanied by a tachycardia (PGE2 < I2, i.r.a. < i.v.). PGE2 and I2 induced increases in RBF and UV in a roughly dose-dependent manner (PGE2 > I2, i.r.a. > i.v.), however, antidiuresis was observed with the highest intravenously given dose of PGI2 (300 ng/kg/min) such being ascribed to a pronounced hypotension. Changes in electrolyte excretion induced by PGE2 and I2 were similar to the pattern of those in RBF or UV. Neither PGE2 or I2 produced any significant changes in the glomerular filtration rate (GFR). The diuretic effect of PGE2 and F2 alpha correlated with osmolar clearance (Cosm) (r = 0.89, p < 0.01; r = 0.55, p < 0.01) and free water clearance (CH2O) (r = 0.52, p < 0.01; r = 0.83, p < 0.01), whereas that of PGI2, only with Cosm (r = 0.74, p < 0.01). PGF2 alpha produced the weakest changes in the parameters described above. PGE2 and I2 (30 ng/kg/min, i.r.a.), but not PGF2 alpha, produced a significant elevation of RVPRA without any significant change in BP. These findings suggest that PGE2 plays a primary role in the kidney, whereas PGI2 is important in the regulation of the systemic circulation, and that PGE2, I2 and F2 alpha all have different modes of action in producing diuresis. Both PGE2 and I2 may participate in the control of renin secretion.

Effects of Prostaglandin E2, I2 and F2α on Systemic and Renal Hemodynamics, Renal Function and Renin Secretion in Anesthetized Dogs

Effects of intrarenal-arterial (i.r.a.) and intravenous (i.v.) infusions of PGE2, I2 and F2α on systemic blood pressure (BP), heart rate (HR), renal blood flow (RBF), urine volume (UV), renal function and plasma renin activity (PRA) of the renal venous blood (RVPRA) were investigated. A dose-dependent fall in BP was observed with PGE2 and I2 and was accompanied by a tachycardia (PGE2<I2, i.r.a.<i.v.). PGE2 and I2 induced increases in RBF and UV in a roughly dose-dependent manner (PGE2> I2, i.r.a.>i.v.), however, antidiuresis was observed with the highest intravenously given dose of PGI2 (300 ng/kg/min) such being ascribed to a pronounced hypotension. Changes in electrolyte excretion induced by PGE2 and I2 were similar to the pattern of those in RBF or UV. Neither PGE2 or I2 produced any significant changes in the glomerular filtration rate (GFR). The diuretic effect of PGE2 and F2α correlated with osmolar clearance (Cosm) (r=0.89, p<0.01; r=0.55, p<0.01) and free water clearance (Ch2o) (r=0.52, p<0.01; r=0.83, p<0.01), whereas that of PGI2, only with Cosm (r=0.74, p<0.01). PGF2a produced the weakest changes in the parameters described above. PGE2 and I2 (30 ng/kg/min, i.r.a.), but not PGF2a, produced a significant elevation of RVPRA without any significant change in BP. These findings suggest that PGE2 plays a primary role in the kidney, whereas PGI2 is important in the regulation of the systemic circulation, and that PGE2, I2 and F2a all have different modes of action in producing diuresis. Both PGE2 and I2 may participate in the control of renin secretion.

Corticoid effects on angiotensin- and norepinephrine-induced proteinuria in rats.

Adrenalectomy is known to prevent the proteinuria induced by renin or angiotensin, but it is not clear whether the loss of glucocorticoids or mineralocorticoids is responsible. The problem was reinvestigated using dexamethasone and aldosterone, essentially pure glucocorticoid and mineralocorticoid, respectively. Dexamethasone treatment for 2--5 days completely restored the protein-uric response to angiotensin II or norepinephrine, but aldosterone did not, even though the dose and treatment were sufficient to induce changes in electrolyte excretion. Fractional sodium excretion was also increased by angiotensin II and norepinephrine in the dexamethasone-treated rats, but not in the aldosterone-treated rats. Both dexamethasone and aldosterone treatments restored the increase in filtration fraction, but the increase was not associated with proteinuria in some groups, and it is concluded that there is no causal relationship between increased filtration fraction and proteinuria. Reasons for considering binding of norepinephrine and angiotensin to the glomerular basement membrane as causal for the proteinuria and the hormonal requirements for such binding are discussed.

The effects of indanyloxyacetic acid (mk 196) on electrolyte excretion in the rat kidney.

A substituted derivative of ethacrynic acid, 6,7-dichloro-2-methyl-l-oxo-phenyl-5-indanyloxyacetic acid (MK 196), has been shown in preliminary studies to be a potent uricosuric and diuretic agent in the rat and monkey (1, 2). Prior studies from this laboratory have localized the nephron site of inhibition of urate reabsorption to the proximal convoluted tubule. The reabsorption of sodium in the proximal tubule, however, is not affected by MK 196, and the sodium diuresis results from impaired reabsorption in the ascending limb of the loop of Henle (1). The current studies were undertaken to examine further the changes in electrolyte excretion induced by this agent and to gain additional inferential information on the nephron site of action. Methods. Clearance studies. Male Sprague-Dawley rats weighing 200 to 400 g were used in all studies. Animals were anesthetized with Inactin (Promonta, Hamburg, Germany), 100 mg/kg body wt injected in-traperitoneally, and prepared for clearance studies as previously described (3). A solution of isotonic saline containing [methoxy-3H]inulin (25 μCi/ml) was infused at a rate of 1.2 ml/hr for the duration of the experiment. MK 196 was dissolved in distilled water containing an equal concentration of sodium bicarbonate and infused in a dose of 50 mg/kg body wt/hr in a volume of 1.2 ml/ hr. Control animals received the same solution without the drug. In the experimental animals, urinary losses of sodium and water were replaced with a volume of isotonic saline equal to the urine flow rate. Hematocrits were measured before and after the study to ensure the adequacy of volume replacement. After 60 to 90 min of equilibration, blood and urine samples were obtained. Free water clearance and reabsorption studies. Studies were performed in a separate group of animals that were lightly anesthetized with ether for placement of catheters, placed in restraining cages, and allowed to awaken.

Renal action of cholera toxin: I. Effects on urinary excretion of electrolytes and cyclic AMP

The infusion of cholera toxin (CT), 4 mug/min, into one renal artery of normal and thyroparathyroidectomized (T-PTX) dogs produced ipsilateral increments in the excretion of Na, K, Ca, Mg and Cl. Phosphate excretion increased from both kidneys, but more from the infused kidney in intact dogs. Unilateral phosphaturia occurred in T-PTX dogs studied five or more days after T-PTX. The changes in electrolyte excretion appeared 40 to 80 min after initiation of CT infusion and the maximal effects were noted after 100 to 140 min. The effects of CT on electrolyte excretion could not be accounted for by changes in glomerular filtration rate or renal plasma flow. Urinary cyclic adenosine monophosphate (AMP) increased from both kidneys but slightly more from the infused kidney. Adenylate cyclase activity of cortex and outer medulla of the infused kidney was 109 to 142% higher than that of the control kidney. The results indicate that CT decreases the net transport of various electrolytes by the renal tubule. This effect is probably mediated by the activation of renal adenylate cyclase(s) sensitive to the enterotoxin.

Changes in electrolyte excretion following intraperitoneal injection of dibutyryl cyclic AMP in the brattleboro rat

Intraperitoneal injection of 40 μg of dibutyryl cyclic AMP to homozygous Brattleboro rats fasted for 12 hours but having free access to water resulted in an increase in urine flow and in the rates of excretion of Na, K, PO 4 and urea. Similar results were obtained in Brattleboro rats having free access to food and water which received 200 μg of nucleotide. The injection of 20 μg of dibutyryl cyclic AMP or 40 μg 5′-AMP to homozygous Brattleboro rats with free access to food and water or the administration of 40 μg of 5′-AMP to homozygous rats fasted for 12 hours but with free access to water did not alter renal excretion patterns. These results indicate that dibutyryl cyclic AMP may depress tubular reabsorption of water, Na and PO 4 as has been shown to be the case in the intact dog. In homozygous Brattleboro rats fasted for 24 hours but allowed free access to water, 40 μg of dibutyryl cyclic AMP resulted in a tendency to reduced urine flow and diminished excretion of Na, K and urea. The explanation for these results is not apparent from these data.

The effect of saluretics and spironolactone on aldosterone production and electrolyte excretion in man.

Healthy volunteers received orally the saluretics furosemide (40 mg/day) and thiabutazide (10 mg/day) over a 5-day period, and the aldosterone antagonist spironolactone (5 mg and 10 mg/kg per day) over 7-and 3-day periods, respectively. On the first day of treatment both saluretics induced a marked increase in sodium and water excretion, but only a moderate increase in potassium excretion. On the second day, however, the sodium and water excretion had already returned to almost normal values, reaching a minimum after discontinuation of the saluretics. Under saluretic therapy, a steep increase in plasma aldosterone concentration and in urinary aldosterone was observed. After the saluretics were discontinued, both the markedly elevated plasma aldosterone concentration and the aldosterone excretion returned to normal within two days. Under saluretic therapy potassium excretion appeared to be aldosterone-dependent, since potassium excretion paralleled aldosterone excretion. Spironolactone (5 mg/kg oder a 7-day period) caused a moderate increase in sodium excretion and a moderate decrease in potassium excretion. Spironolactone (10 mg/kg over a 3-day period) caused a distinct increase in sodium excretion and a slight decrease in potassium excretion. Neither of the two spironolactone doses used here produced an increase in aldosterone excretion. After discontinuation of spironolactone, a rebound in aldosterone excretion was observed. The increase in aldosterone excretion was associated with corresponding changes in electrolyte excretion. The increase in aldosterone excretion and in plasma aldosterone concentration induced by the saluretic thiabutazide was markedly reduced by the administration of spironolactone (10 mg/kg). The sodium and water retention which was caused by the hyperaldosteronism, was almost completely abolished, and the increased potassium excretion returned to normal.

Effect of actinomycin D on aldosterone-mediated changes in electrolyte excretion.

ARTICLESEffect of actinomycin D on aldosterone-mediated changes in electrolyte excretionMD Lifschitz, RW Schrier, and IS EdelmanMD Lifschitz, RW Schrier, and IS EdelmanPublished Online:01 Feb 1973https://doi.org/10.1152/ajplegacy.1973.224.2.376MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited BySodium-Potassium-Adenosinetriphosphatase-Dependent Sodium Transport in the Kidney: Hormonal ControlEric Féraille, and Alain Doucet1 January 2001 | Physiological Reviews, Vol. 81, No. 1Corticosteroids and the Kidney1 January 2011Chapter 12 Development of Epithelial Na+ Channels and Regulation by Guanine Nucleotide Regulatory (G) Proteins and PhospholipidsNaCl Transport in the KidneyAldosterone increases the maximal turnover rate of the sodium pump1 November 1987 | Pflügers Archiv - European Journal of Physiology, Vol. 410, No. 4-5On the Mechanism of Action of AldosteroneTubular Processing of Glomerular Ultrafiltrate: Mechanisms of Electrolyte and Water TransportClinical disorders of aldosterone metabolismDisease-a-Month, Vol. 30, No. 8Excretion of SodiumSyndromes of Aldosterone Deficiency and ExcessMedical Clinics of North America, Vol. 67, No. 4Membrane TransportIntracellular Action of Mineralocorticoids: The Role of the Flavin Coenzymes and Riboflavin Analogs in HypertensionDifferential effects of acute mineralo- and glucocorticosteroid administration on renal acid eliminationKidney International, Vol. 21, No. 4Mechanism of drugs action on ion and water transport in renal tubular cellsEffect of aldosterone on the transepithelial potential difference of the rat distal tubuleKidney International, Vol. 19, No. 5Aldosterone Action in Target EpitheliaAntihypertensive effect of riboflavin analogs in rats with mineralocorticoid-induced hypertension.Hypertension, Vol. 3, No. 1Aldosterone and dopamine receptors in the kidney: Sites for pharmacologic manipulation of renal functionKidney International, Vol. 18, No. 5Primary hyperaldosteronismPharmacology & Therapeutics, Vol. 9, No. 3Steroid receptors in exocrine glands: The pancreas and prostateJournal of Steroid Biochemistry, Vol. 11, No. 1STEROID RECEPTORS IN EXOCRINE GLANDS: THE PANCREAS AND PROSTATERole of RNA in the action of aldosterone on Na+ transportThe Journal of Membrane Biology, Vol. 40, No. S1Cellular Defects in Urinary Acidification and Renal Tubular AcidosisThe Adrenal Cortex of AmphibiaThe Actions of AldosteroneRelationship of renal ammonia production and potassium homeostasisKidney International, Vol. 11, No. 616α,18-dihydroxydeoxycorticosterone and the binding of aldosterone to mineralocorticoid receptors in kidney of adrenalectomized ratsJournal of Steroid Biochemistry, Vol. 7, No. 5Effects of aldosterone, actinomycin D, puromycin and cycloheximide on RNA synthesis, carbonic anhydrase and atpase activities of the kidney and on urinary excretion of sodium in adrenalectomized miceJournal of Steroid Biochemistry, Vol. 7, No. 6-7MECHANISM OF ACTION OF STEROID HORMONESThe mechanism of aldosterone functionPharmacology & Therapeutics. Part B: General and Systematic Pharmacology, Vol. 2, No. 2Effect of aldosterone on flavin coenzyme biosynthesis in the kidneyJournal of Steroid Biochemistry, Vol. 6, No. 11-12Alteration in the labelling of renal ribosomal protein by aldosteroneJournal of Steroid Biochemistry, Vol. 6, No. 7Mechanism of action of steroid hormonesJournal of Steroid Biochemistry, Vol. 6, No. 3-4Cellular Receptors and Mechanisms of Action of Steroid HormonesAldosterone: Current conceptsMetabolism, Vol. 23, No. 5 More from this issue > Volume 224Issue 2February 1973Pages 376-380 Copyright & PermissionsCopyright © 1973 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1973.224.2.376PubMed4686492History Published online 1 February 1973 Published in print 1 February 1973 Metrics

The relationship between water intake and the production of "wet" droppings in the domestic fowl.

Synopsis Production of “wet” droppings by laying hens was associated with polydipsia. Restriction of “wet droppers” to a “normal” water intake did not lead to dehydration, loss of body weight, decline in water balance or changes in electrolyte excretion and retention. It is concluded that “wet” droppings were the direct result of a primary polydipsia rather than an obligatory loss of body water followed by an increased water intake.

Mechanisms of renal lithium handling and their relationship to mineralocoticoids: A dissociation between sodium and lithium ions

Lithium-induced alterations in electrolyte excretion were studied in 16 patients with manic-depressive disease and in one normal subject under conditions of controlled sodium, potassium and fluid intake. An increase in urinary sodium and potassium excretion and in urine volume were noted on the first day of lithium administration. By lithium day 3, transient sodium retention occured. These changes in electrolyte excretion were not correlated with measurable changes in endogenous creatinine clearance. Sodium loading diminished and sodium depletion increased lithium retention. While sodium depletion always raised serum lithium levels, in one patient signs of lithium toxicity appeared despite relatively low serum lithium concentrations. These observations suggest that serum lithium may not be an accurate indicator of lithium overdose, especially during states of acute sodium depletion. Chlorothiazide and the aldosterone antagonist spironolactone produced a striking sodium diuresis, but lithium excretion did not increase consistently and at times decreased. Differences in renal sodium and lithium handling were also observed in response to desoxycorticosterone acetate (DOCA) administration. In rats, DOCA failed to cause lithium retention despite prompt retention of sodium. During the DOCA ‘escape’ period, lithium excretion increased and serum lithium concentration fell. Thus, renal lithium handling, unlike sodium handling, appears independent of mineralocorticoids. These characteristics of lithium excretion during DOCA administration in rats and aldosterone blockade in man suggest that the proximal tubule is the major site of lithium reabsorption in these species. These in vivo studies in man and animals indicate a decreased capacity of active transport systems in the kidney to handle the lithium ion as effectively as the sodium ion. These differences in sodium and lithium handling by the kidney may be related, in part, to lithium's mechanism of action, particularly if active transport systems in the central nervous system are qualitatively similar to those of the kidney with respect to lithium handling.

CONTRIBUTION OF BARORECEPTORS TO THE CONTROL OF RENAL FUNCTION.

Electrical stimulation of the left stellate ganglion of the dog is associated with an increase in urine flow, in electrolyte and total solute excretion, and in the renal clearance of inulin. These changes appear rapidly, are well maintained during prolonged stimulation, and stop soon after stimulation has ceased. The hemodynamic responses associated with these changes are an increase in arterial pulse pressure, an increase or no change in mean arterial blood pressure, and a decline in mean left atrial pressure. The diuretic response to stellate ganglion stimulation is diminished, but not abolished, by bilateral cervical vagotomy as are the changes in electrolyte excretion, total solute excretion, and the renal clearance of inulin. However, the hemodynamic responses are not greatly modified by cervical vagotomy. Vagotomy just above the diaphragm does not appear to modify these responses. The effect of vagotomy on the renal responses to stellate stimulation appears to be a result of sectioning baroreceptor afferent nerves which traverse the vagus nerves. The rapidity of the renal response to stellate stimulation, its temporal relation to the hemodynamic changes, and the effect of cervical vagotomy indicate that the diuresis is, to a large degree, secondary to withdrawal of renal sympathetic vasoconstrictor nerve discharge. The similarities between the renal responses to stellate stimulation and to intravenous infusions indicate that infusion diuresis may be mediated, at least in part, by the same mechanism. When renal blood flow is measured directly in the perfused kidney, carotid occlusion is associated with little change or with a decrease in renal blood flow at a time when renal arterial pressure increases. When renal blood flow is maintained constant in the perfused kidney, carotid artery occlusion is associated with an increase in renal arterial pressure. The intrarenal administration of the adrenergic blocking agent, phenoxybenzamine, can prevent the increase in renal vascular resistance during carotid occlusion indicating that it is due to an adrenergic mechanism. The renal pressure-flow curve is displaced down and to the right during carotid occlusion; autoregulation of renal blood flow is still observed, although at a lower level of blood flow. All these changes indicate that the primary renal response to carotid occlusion is vasoconstriction mediated by the renal sympathetic nerves. It is well-known that urine flow increases when renal arterial pressure is increased independent of a change in the activity of the renal vasoconstrictor nerves and independent of a change in renal blood flow. Consequently, the rise in arterial pressure associated with carotid occlusion can contribute directly to the response of the kidney to carotid occlusion. The variability of the changes in water and electrolyte excretion by the kidney during carotid occlusion may represent a varying contribution of direct and reflex mechanisms to the total response.