Comparative Role of Hormonal and Non-Hormonal Factors in Sodium Tubular Reabsorption

2015 ◽  
pp. 75-83
Author(s):  
A. Nizet
Keyword(s):  
Tubular Reabsorption ◽  
Hormonal Factors

Lack of effect of chronic renal denervation on altered sodium reabsorption during increased ureteral pressure

1980 ◽  
Vol 58 (5) ◽  
pp. 477-483 ◽  
Author(s):  
D. R. Wilson ◽  
M. Cusimano ◽  
U. Honrath
Keyword(s):  
Isotonic Saline ◽  
Urine Osmolality ◽  
Tubular Reabsorption ◽  
Renal Nerves ◽  
Sodium Reabsorption ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Water Excretion ◽  
Renal Nerve Activity

The role of the renal nerves in the altered sodium reabsorption which occurs during increased ureteral pressure was studied using clearance techniques in anaesthetized rats undergoing diuresis induced by isotonic saline infusion. In rats with a sham denervated kidney, an ipsilateral increase in ureteral pressure to 20 cm H2O resulted in a marked and significant decrease in sodium and water excretion, increased fractional sodium reabsorption, and increased urine osmolality with no significant change in glomerular filtration rate. A similar significant ipsilateral increase in tubular reabsorption of sodium occurred in rats with chronically denervated kidneys during increased ureteral pressure. The changes in tubular reabsorption were rapidly reversible after return of ureteral pressure to normal. These experiments indicate that enhanced tubular reabsorption of sodium during an ipsilateral increase in ureteral pressure is not mediated by increased renal nerve activity. During the antinatriuresis of increased ureteral pressure there was a decrease in the fractional reabsorption of sodium from the opposite normal kidney. The role of the renal nerves in this compensatory change in function in the opposite kidney was studied in two further groups of animals. The renal response to a contralateral increase in ureteral pressure was similar in denervated and sham-denervated kidneys. The results indicate that altered renal nerve activity, through ipsilateral or contralateral renorenal reflexes, is not responsible for the changes in tubular reabsorption of sodium which occur during increased ureteral pressure induced by partial ureteral obstruction.

Ultrafiltration of renin in the mouse kidney studied by inhibition of tubular protein reabsorption with lysine

1988 ◽  
Vol 75 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Ingrid Mazanti ◽  
Kirstine Lintrup Hermann ◽  
Arne Høj Nielsen ◽  
Knud Poulsen
Keyword(s):  
Intraperitoneal Injection ◽  
Excretion Rate ◽  
Plasma Renin ◽  
Basic Amino Acid ◽  
Tubular Reabsorption ◽  
Renal Tubules ◽  
Plasma Renin Concentration ◽  
Protein Reabsorption ◽  
Glomerular Ultrafiltration

1. In order to study the role of the kidney in the elimination of endogenous plasma renin, renin was measured in the plasma and urine of female mice. 2. The renin concentration was two orders of magnitude lower in urine than in plasma, but it increased after intraperitoneal injection of submandibular mouse renin. No correlation between the plasma renin concentration and the urinary renin concentration and renin excretion rate could be demonstrated. 3. Blockade of the tubular reabsorption of proteins by intraperitoneal injection of the basic amino acid lysine increased the urinary renin concentration, renin excretion rate and renin clearance two to three orders of magnitude, without affecting the plasma renin concentration. 4. This finding demonstrates that ultrafiltered renin is reabsorbed almost completely in the renal tubules and that the mechanism most likely is the same as for other filtered proteins. 5. The large renal renin clearance obtained after intraperitoneal lysine is in accordance with a major role of the kidneys in the elimination of renin from the circulation, by a glomerular ultrafiltration and tubular reabsorption and metabolization of renin.

scholarly journals The role of sex steroids in white adipose tissue adipocyte function

Reproduction ◽  
2017 ◽  
Vol 153 (4) ◽  
pp. R133-R149 ◽  
Author(s):  
A E Newell-Fugate
Keyword(s):  
Adipose Tissue ◽  
Sexual Dimorphism ◽  
White Adipose Tissue ◽  
Hormonal Factors ◽  
Obesity Epidemic ◽  
Health And Disease ◽  
Males And Females ◽  
Hormonal Milieu ◽  
Gender Influences

With the increasing knowledge that gender influences normal physiology, much biomedical research has begun to focus on the differential effects of sex on tissue function. Sexual dimorphism in mammals is due to the combined effects of both genetic and hormonal factors. Hormonal factors are mutable particularly in females in whom the estrous cycle dominates the hormonal milieu. Given the severity of the obesity epidemic and the fact that there are differences in the obesity rates in men and women, the role of sex in white adipose tissue function is being recognized as increasingly important. Although sex differences in white adipose tissue distribution are well established, the mechanisms affecting differential function of adipocytes within white adipose tissue in males and females remain largely understudied and poorly understood. One of the largest differences in the endocrine environment in males and females is the concentration of circulating androgens and estrogens. This review examines the effects of androgens and estrogens on lipolysis/lipogenesis, adipocyte differentiation, insulin sensitivity and adipokine production in adipocytes from white adipose tissue with a specific emphasis on the sexual dimorphism of adipocyte function in white adipose tissue during both health and disease.

scholarly journals The role of hormonal factors and endocrine therapy in ovarian cancer

2013 ◽  
Vol 1 ◽  
pp. 14-19 ◽  
Author(s):  
Krystyna Serkies ◽  
Marcin Sinacki ◽  
Jacek Jassem
Keyword(s):  
Ovarian Cancer ◽  
Endocrine Therapy ◽  
Hormonal Factors

Female Thyroid Cancer: The Role of Reproductive and Hormonal Factors in Switzerland

Oncology ◽  
1993 ◽  
Vol 50 (4) ◽  
pp. 309-315 ◽  
Author(s):  
Fabio Levi ◽  
Silvia Franceschi ◽  
Cristina Gulie ◽  
Eva Negri ◽  
Carlo La Vecchia
Keyword(s):  
Thyroid Cancer ◽  
Hormonal Factors

Role of hormonal factors in plasma K alterations in acute respiratory and metabolic alkalosis in dogs

1990 ◽  
Vol 258 (2) ◽  
pp. F305-F310
Author(s):  
H. Suzuki ◽  
A. Hishida ◽  
K. Ohishi ◽  
M. Kimura ◽  
N. Honda
Keyword(s):  
Metabolic Alkalosis ◽  
Control Level ◽  
Plasma Potassium ◽  
Respiratory Alkalosis ◽  
Plasma Norepinephrine ◽  
Hormonal Factors ◽  
Control Value ◽  
Norepinephrine Concentration ◽  
Induced Alkalosis

Studies were performed on previously nephrectomized dogs to examine roles of hormonal factors in plasma potassium alterations in acute alkalosis. Respiratory and metabolic alkalosis were induced by hyperventilation and intravenous NaHCO3 or tris(hydroxymethyl)aminomethane (Tris) infusion, respectively. Respiratory and NaHCO3-induced alkalosis provoked decreases in plasma potassium from the control value of 5.12 +/- 0.68 (SE) to 4.21 +/- 0.55 meq/l (P less than 0.01) and from 4.65 +/- 0.26 to 3.91 +/- 0.16 meq/l (P less than 0.01) within 180 min, respectively. In contrast, Tris-induced alkalosis elicited an increase in plasma potassium from the control value of 4.56 +/- 0.30 to 5.31 +/- 0.30 meq/l (P less than 0.01). Hypokalemia in respiratory alkalosis was associated with a decrease in the plasma norepinephrine concentration from the control level of 377 +/- 104 to 155 +/- 41 pg/ml (P less than 0.05) but not with changes in plasma levels of epinephrine, insulin, glucagon, cortisol, and aldosterone. However, this hypokalemia was not affected by phentolamine. Also, somatostatin did not modify the hypokalemic response. NaHCO3-induced hypokalemia was associated with a decline in the plasma aldosterone and norepinephrine concentrations. The decline in plasma norepinephrine in NaHCO3-induced alkalosis followed the decrease in plasma potassium. In Tris-induced alkalosis, plasma insulin increased but norepinephrine decreased. The findings do not suggest fundamental roles of the hormonal factors in the plasma potassium alterations in bilaterally nephrectomized dogs with acute alkalosis.

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