Effects of Drinking Water on Renal Function – Endocrine System Example

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"Effects of Drinking Water on Renal Function" is an incredible example of a paper on the endocrine system. Since a lot of water passes through the kidneys, this is a logical place to regulate body water content. Or ADH is a hormone that is released by the pituitary gland. Antidiuresis means “ against high urine volume” ; so this hormone, when released, causes the kidneys to pull water from the collecting ducts back into the body; ADH helps retain water. When there is a lack of ADH, the water stays in the lumen of the collecting duct and produces a large volume of dilute urine (diuresis. ) A disease where ADH is absent or produced in low amounts is called diabetes insipidus.   (Friedman 24)         The goal of this practicum was to compare the effects of drinking 800 ml water per 70 kg body weight with control (no drinking) on: Urine flow rate, Urine Osmolality, Urine sodium concentration And parameters calculated from these measurements.   As well,     the goal included interpreting the effects in terms of the hormonal control of urine flow rate.       To a large extent, these excretory and regulatory processes depend on the blood supply to the kidney.

It is not surprising therefore that it receives the highest blood flow per gram of organ weight in the body at 1 liter/min. As blood flows through these vascular organs, its composition is appropriately altered according to homeostatic requirements.   (Verbalis 18)         One manner of understanding the magnitude of the renal blood flow is to consider the renal fraction.   This is the fraction of the total cardiac output that flows through the kidneys.   A 70 Kg man with a cardiac output of 6 L/min.

has a normal renal blood flow of about 1.2 L/min. Rearranging these numbers (1.2 / 6.0), we find that the kidney is constantly fed 20% of the cardiac output or a renal fraction of. 2. Thus, a very substantial portion of the total cardiac output flows through the kidneys.   (Mulloy 22)         Considering the fact that each kidney in a normal 70 Kg man weighs about 130 – 170 g, the large magnitude of the normal blood flow through the kidney becomes even more apparent.   With a total flow of 1200 ml/min.

and 300 g of the kidney, the average flow per gram of kidney weight is about 400 ml/min/100g (see Table 1).   This is several times greater per unit weight of organ than the blood flow through most other organs.   For example, liver tissue has a blood flow of about 20 ml/min/100g and resting muscle has a flow of about 27 ml/min/100g. During various stress conditions or diseases, this renal fraction can vary considerably and be markedly affected.   (Mulloy 155) Blood flow to the kidneys will be dependent on a number of important systemic factors.

Clearly, if there is a problem with volume (dehydration, hemorrhage) or cardiac output (congestive heart failure, myocardial infarct) then blood flow is diminished. In less obvious ways hypoalbuminemia (cirrhosis, nephrotic syndrome, and starvation) affects the intravascular volume so that the effective blood (volume) flow is diminished despite many of these patients appearing total body fluid overloaded. Finally, hypotension from severe vasodilatation (anaphylactic shock, sepsis) would also diminish blood flow to the kidneys. (Rose 7)         Na+ and Cl- are the predominant ions in the extracellular fluid (ECF).

Because they are non-penetrating solutes, Na+ and Cl- produce an osmotic pressure that holds water in the ECF. Because the osmolarity of the ECF is kept constant, the amount of sodium and chloride in the body determines the volume of the ECF. We focus on sodium since sodium reabsorption is regulated. (Robertson 19)       To maintain the volume of the ECF constant, the amount of Na+ excreted needs to match Na+ input by the diet. On a typical day, a large amount of Na+ is filtered, and nearly 99% of filtered Na+ is reabsorbed.

Use 19)     Although the apical transporters differ along the length of the renal tubule, one thing that is always true is that the energy for Na+ reabsorption depends upon the Na+ concentration gradient. Na+ moves readily across the apical membrane of cells of the renal tubule because the Na+ concentration is high in the ECF and low inside of cells. The Na+ gradient is established by the Na+/K+-ATPase, which pumps Na+ across the basolateral membrane.     The principal regulator of Na+ reabsorption is the steroid hormone aldosterone, which is produced in the zona glomerulosa of the adrenal cortex.

Aldosterone, like all steroid hormones, works as a transcription factor to alter gene expression in cells. Aldosterone works in the cells of the distal tubule and cortical collecting duct depicted at left. Na+ reabsorption in this part of the renal tubule accounts for only 2% of total Na+ reabsorption, but this is the site where regulation of Na+ balance occurs.   (Chung 33)       Aldosterone secretion is stimulated by angiotensin II. Recall that the limiting step for the formation of angiotensin II is the hormone renin, which is released by the juxtaglomerular cells located in the afferent arteriole of the kidney.

The juxtaglomerular cells are stimulated to secrete renin by three mechanisms, all of which are activated in response to decreased ECF volume.   (Ayus 997) The sympathetic nervous system innervates the juxtaglomerular cells. A decrease in ECF volume will cause a drop in mean arterial pressure (MAP). Decreased MAP is detected by the carotid baroreceptors, which activate these sympathetic nervous system inputs to cause renin secretion. The juxtaglomerular cells act as baroreceptors.

A drop in MAP means less pressure in the afferent arteriole, with less stretch of the juxtaglomerular cells. Less stretch of the juxtaglomerular cells activates renin secretion. Less Na+ delivered to the distal tubule activates the juxtaglomerular cells via the juxtaglomerular apparatus.   Discussion:         Sixty percent of body weight consists of water, two-thirds of which is intracellular. Alterations in the concentration of salt, whether due to primary changes in the amount of water or the amount of salt in the body can be of pathophysiologic importance. Note that sodium chloride is the predominant solute in the extracellular fluid (ECF).

In contrast, cells contain mostly potassium, phosphate, and proteins. This distribution of solutes between cells and ECF is fundamental to the maintenance of normal cell function. Each solute has its own specific set of physiologic functions, yet the total concentration of solute is also an important parameter.


Rose BD. Clinical physiology of acid-base and electrolyte disorders. 3d ed. New York: McGraw-Hill, 1989:589-676

Friedman E, Shadel M, Halkin H, et al. Thiazide-induced hyponatremia: reproducibility by single dose rechallenge and an analysis of pathogenesis. Ann Intern Med 1989;110(1):24-30

Robertson GL, Mahr EA, Athar S, et al. Development and clinical application of a new method for the radioimmunoassay of arginine vasopressin in human plasma. J Clin Invest 1973;52(Sep):2340-52

Verbalis JG. Adaptation to acute and chronic hyponatremia: implications for symptomatology, diagnosis and therapy. Semin Nephrol 1998;18(1):3-19

Mulloy AL, Caruana RJ. Hyponatremic emergencies. Med Clin North Am 1995;79(1):155-68

Arieff AI, Llach F, Massry SG. Neurological manifestations and morbidity of hyponatremia: correlation with brain water and electrolytes. Medicine (Baltimore) 1976;55(2):121-9

Berl T. Treating hyponatremia: damned if we do and damned if we don't. Kidney Int 1990;37(3):1006-18

Chung HM, Kluge R, Schrier RW, et al. Clinical assessment of extracellular fluid volume in hyponatremia. Am J Med 1987;83(5):905-8

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