Fluid losses not compensated for by food intake can stimulate thirst mechanisms or other compensatory means, such as the sympathetic nervous system, angiotensin II, and
renal sodium excretion.
Atrial Natriuretic Peptide Stimulates Dopamine Tubular Transport by Organic Cation Transporters: A Novel Mechanism to Enhance
Renal Sodium Excretion.
Not exact matches
The observed increase in mortality and CVD events among those with daily
sodium excretion less than 3 grams is consistent with the findings of many other studies.3, 4,6,7,22 During follow - up, one hundred twenty - six patients (4.5 percent) developed end - stage
renal disease (ESRD).
-RCB- elevated
sodium level within kidneys, either as a result of pathological bottleneck such as reduced number of nephrons, or simply due to heightened intake - or both - may activate pro-inflammatory cytokines and chemokines in proximal tubular cells, may cause oxidative stress by activating ROS - producing NADH oxidase enzymes, or blood vessel constriction by inhibiting kidney arginine transport and nitric oxide synthesis; elevated
renal inflammation, oxidative stress and restricted blood flow all can impair the efficacy of
sodium excretion, more so combined (if extensive, it can also result in post-natal reduction of nephron units)
One measured fluid, electrolyte, and
renal indices of hydration over eleven days of caffeine consumption in human subjects, finding that doses of up to 6 mg caffeine per kilogram of body weight had no effect on body mass, urine osmolality (urine concentration), urine specific gravity (concentration of excreted materials in urine), urine color, urine volume,
sodium excretion, potassium secretion, creatinine content, blood urea nitrogen (forms when protein breaks down), and serum levels of
sodium and potassium.