Can someone explain passive vs. active transport for urine formation for me?

VickyRN, MSN, DNP, RN · Mar 5, 2006

My book is not doing a good job explaining it...can anyone help?

Hmmm... let me see...

The kidneys have a very rich blood supply. They need to have large quantities of blood passing through so that it can be filtered well, and all the waste products removed. A blood supply of about 600-1300 ml/ minute, which is 20-25% of the cardiac output, flows to the two kidneys. That’s about 72 liters per hour.

Inside the kidney, the blood is cleaned (or filtered) through very small networks of tubes called nephrons. Each kidney has about 1 million nephrons.

The nephron is the functional and structural unit of the kidney. Each one can function independently. They are contained in the renal cortex and medulla.

The function of the nephon is to cleanse the blood by filtration, reabsorption, and secretion. The nephrons also must concentrate the urine to allow for filtration with maximal efficiency, with less fluid loss.

As it filters the blood of impurities, the nephron forms urine from the blood. As the blood passes through the blood vessels of the nephron, all unwanted waste is taken away, as the nephrons converge into a collecting duct, which eventually merges into a pyramid and empties via the papilla into a minor calyx.

Any nutrients needed by the body (such as glucose, amino acids, sodium) are kept or returned to the bloodstream by the nephrons. In this way, the kidney helps to regulate the levels of chemicals in the blood such as sodium and potassium. So the right levels are maintained to keep the body healthy.

A nephron is composed of a renal corpuscle and a tubular system.

The renal corpuscle consists of a glomerulus, which is a tuft of capillaries. The glomerulus is completely surrounded by the thin membranous glomerular capsule (or Bowman’s capsule).

Inside the glomerulus, waste products in the blood move by filtration from the bloodstream into the Bowman’s capsule. The Bowman’s capsule collects the filtrate and channels it into urine-carrying tubes inside the nephron. These tubes are called tubules.

The tubular system consists of the proximal convoluted tubule, the loop of Henle, and the distal convoluted tubule. The distal convoluted tubule ends in one of many collecting ducts.

The nephrons collect and eliminate wastes from the body in a three-step process: glomerular filtration, tubular reabsorption, and tubular secretion.

Glomerular filtration—filtering the blood that flows through the kidney’s blood vessels, or glomeruli. This is a passive process, fueled by blood pressure.

Filtration is the movement of fluid through a cell or blood vessel membrane because of hydrostatic or water-pushing pressure differences on both sides of the membrane.

Glomerular filtration is non-selective (this means that the body has no control over what is filtered, the glomerulus is like a sieve & any molecules small enough will pass through) and it is passive (it needs no ATP energy expenditure to occur).

Tubular reabsorption—reabsorbing filtered fluid through the minute canals (tubules) that make up the kidney. Reabsorption occurs by active transport (substances such as glucose, amino acids, bicarb, electrolytes) or by osmosis (water). Active transport is "against" the concentration gradient and requires expenditure of APT energy. Osmosis is a passive process, the diffusion of water from an area of higher water concentration to an area of lower water concentration.

Tubular reabsorption is the returning of essential materials (such as bicarb) from the urine filtrate back into circulation.

It is the tubular reabsorption of most of the filtrate that keeps normal urine output at 1-3 liters/day and prevents dehydration. The tubules reabsorb more than 99% of all filtered water back into the body. The tubules have the ability to concentrate urine during times of low fluid intake. This allows for maximum excretion of waste products with less fluid loss.

Tubular secretion—release of filtered substances by the tubules into the urine. This is the reverse of re-absorption. Solutes move from the peritubular capillaries into the lumen of the nephron, by both active (active transport) and passive transfer (diffusion) .

Tubular secretion is excreting nonessential substances (such as hydrogen ions) out of the blood stream into the urine filtrate to be excreted from the body. Tubular secretion regulates electrolytes and pH.

Potassium (K+) and hydrogen ions (H+) are some of the substances secreted from the blood into the tubular filtrate to maintain homeostasis of electrolytes and pH.

Reabsorption and secretion occur along the entire length of the tubule, causing numerous changes in the composition of the glomerular filtrate, according to the needs of the body at the moment, as the filtrate moves through the tubules.

So, you see, you have both active and passive processes occurring... Hope this helps :)

jenn_rn_nj · Apr 1, 2006

in an effort to not recreate the wheel i thought i would resurrect this post since i'm studying for my test on the urinary system. any input would be appreciated.

i think i am getting the whole filtration/reabsorption/secretion thing; i just want to clarify the hormones, specifically aldosterone.

my questions are: would edema be a possible result of hypersecretion of aldosterone? i just want to make sure i'm understanding this by trying to figure out what might come next.

would hyposecretion result in higher production of urine but not necessarily more dilute urine due to both Na & H2O being secreted instead of reabsorbed?

thanks in advance :)

VickyRN, MSN, DNP, RN · Apr 1, 2006

my questions are: would edema be a possible result of hypersecretion of aldosterone? i just want to make sure i'm understanding this by trying to figure out what might come next.
would hyposecretion [of aldosterone] result in higher production of urine but not necessarily more dilute urine due to both Na & H2O being secreted instead of reabsorbed?
thanks in advance :)

Yes, you are correct :) Let's see if this explanation will help:

Aldosterone synthesis is primarily regulated by the renin-angiotensin system. It is secreted from the adrenal cortex (via a negative feedback loop mechanism) in response to low serum sodium or high serum potassium. When too much sodium is lost, extracellular fluid volume is reduced, and pressure receptors are triggered. In response, the kidney secretes an enzyme, renin, which, via angiotensin II, stimulates the adrenal cortex to secrete aldosterone, which in turn stimulates sodium reabsorption in the distal tubule and collecting ducts.

When you think of aldosterone, think SALT and WATER. Aldosterone enhances sodium reabsorption. Since water always follows sodium, aldosterone therefore promotes the reabsorption of both sodium and water (isotonic fluid gain). Since the fluid gain is isotonic, serum sodium will remain within normal limits.

Aldosterone also promotes potassium and hydrogen ion secretion (loss from the body, into the urine).

Usual Effects of too much aldosterone (hyperaldosteronism)

Hypertension (secondary to hypervolemia - too much isotonic fluid in the intravascular space)
Hypokalemia
Peripheral Edema (but no third-spacing - the fluid gain is isotonic and therefore will remain in the extracellular space [intravascular, interstitial])
Metabolic alkalosis (secondary to renal tubule urinary hydrogen ion secretion)

The effects of too little aldosterone (hypoaldosteronism) are just the opposite. In fact, atrial naturetic peptide (ANP) is an aldosterone antagonist and has the opposite effect (opposes the renin-angiotensin-aldosterone system). ANP promotes excretion of both sodium and water in isotonic proportions (increased urinary output of salty [hyperosmolar] urine). So, with both hypoaldosteronism and increased ANP, you will have increased amounts of salty (hyperosmolar) urine. And, there will be less salt and water (in isotonic proportions) in the bloodstream. Serum sodium will not be affected, since this is isotonic fluid loss into the urine. Serum sodium will remain within normal limits.

ADH (antidiuretic hormone) promotes PURE water conservation (without salt). (When you think of ADH, think WATER.) ADH is secreted (as a negative feedback loop mechanism) from the hypothalamus via the pituitary when osmoreceptors in the hypothalamus sense too high serum sodium (too high osmolarity of blood). ADH makes the walls of distal tubules and collecting ducts more permeable to water, and thus the urine becomes more concentrated. Pure water enters the blood stream, making the fluid in the intravascular space more dilute (hypotonic). Serum sodium will decrease (perhaps to the point of hyponatremia).

lisabeth · Apr 2, 2006

Yes, you are correct :) Let's see if this explanation will help:
Aldosterone synthesis is primarily regulated by the renin-angiotensin system. It is secreted from the adrenal cortex (via a negative feedback loop mechanism) in response to low serum sodium or high serum potassium. When too much sodium is lost, extracellular fluid volume is reduced, and pressure receptors are triggered. In response, the kidney secretes an enzyme, renin, which, via angiotensin II, stimulates the adrenal cortex to secrete aldosterone, which in turn stimulates sodium reabsorption in the distal tubule and collecting ducts.
When you think of aldosterone, think SALT and WATER. Aldosterone enhances sodium reabsorption. Since water always follows sodium, aldosterone therefore promotes the reabsorption of both sodium and water (isotonic fluid gain). Since the fluid gain is isotonic, serum sodium will remain within normal limits.
Aldosterone also promotes potassium and hydrogen ion secretion (loss from the body, into the urine).
Usual Effects of too much aldosterone (hyperaldosteronism)
Hypertension (secondary to hypervolemia - too much isotonic fluid in the intravascular space)
Hypokalemia
Peripheral Edema (but no third-spacing - the fluid gain is isotonic and therefore will remain in the extracellular space [intravascular, interstitial])
Metabolic alkalosis (secondary to renal tubule urinary hydrogen ion secretion)
The effects of too little aldosterone (hypoaldosteronism) are just the opposite. In fact, atrial naturetic peptide (ANP) is an aldosterone antagonist and has the opposite effect (opposes the renin-angiotensin-aldosterone system). ANP promotes excretion of both sodium and water in isotonic proportions (increased urinary output of salty [hyperosmolar] urine). So, with both hypoaldosteronism and increased ANP, you will have increased amounts of salty (hyperosmolar) urine. And, there will be less salt and water (in isotonic proportions) in the bloodstream. Serum sodium will not be affected, since this is isotonic fluid loss into the urine. Serum sodium will remain within normal limits.
ADH (antidiuretic hormone) promotes PURE water conservation (without salt). (When you think of ADH, think WATER.) ADH is secreted (as a negative feedback loop mechanism) from the hypothalamus via the pituitary when osmoreceptors in the hypothalamus sense too high serum sodium (too high osmolarity of blood). ADH makes the walls of distal tubules and collecting ducts more permeable to water, and thus the urine becomes more concentrated. Pure water enters the blood stream, making the fluid in the intravascular space more dilute (hypotonic). Serum sodium will decrease (perhaps to the point of hyponatremia).

Those pictures look scarey. LOL. I guess I will understand it when I get there.

jenn_rn_nj · Apr 2, 2006

wow!!

thank you so much. :) i thought i was on the right track to "understanding" it but i wasn't sure. that info was 100 million times better than what is in my current book and much better than my google hits for "aldosterone and edema".

sometimes my prof likes to simplify things to "make it easier on us" but i find if i just memorize what she wants i'm not really "getting it" and then i can't answer those "critical thinking" type questions that she loves to throw at us.

thanks again!!

VickyRN, MSN, DNP, RN · Apr 2, 2006

Glad to be of assistance :)

jenn_rn_nj · Apr 7, 2006

made a very high A on my test today (1 wrong).

thanks again :)

VickyRN, MSN, DNP, RN · Apr 7, 2006

made a very high A on my test today (1 wrong).
thanks again :)

Congratulations!!! :balloons: