Physiology- Renal III Flashcards by Amy Garinger

Extracellular fluid Na conc and osmolarity are regulated by

Amt of extracellular water

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Osmolarity determined by

Amt of solute/vol ECF

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Total body water controlled by

Fluid intake

Renal excretion of water

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As water levels in body increase, what happens to osmolarity

Decreases

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Antidiuretic hormone AKA

Vasopressin

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Role of antidiuretic hormone

Regulates plasma osmolarity and sodium conc by altering renal excretion of water independently of rate of solute excretion

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Antidiuretic hormone feedback loop

Increased osmolarity sensed by osmoreceptors in hypothalamus–> posterior pituitary secretes ADH–> increases permeability of distal tubule and collecting ducts to water

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What parts of the kidney does ADH act on?

Distal tubule

collecting duct

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Tonicity of glomerular filtrate compared to plasma

Isotonic (same osmolarity)

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Proportion of solutes and water absorbed in proximal tubule

Equal proportions—> little change in osmolarity

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How is water absorbed in descending loop of henle

Osmosis

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Obligatory urine volume

Amount of urine necessary to be excreted per day to to rid body of metabolic waste products
In normal person = .5 L/day

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What is obligatory urine volume dictated by?

Maximal concentrating ability of kidney

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Why you shouldn’t drink sea water

1 L sea water in = 1.5 L water excreted

Leads to dehydration

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Requirements to excrete a concentrated urine

High level of ADH
high osmolarity of renal medullary interstitial fluid
-countercurrent mechanism

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Major factors contributing to hyperosmotic renal medullary interstitium

Active transport of Na ions and co-transport of K Cl and other ions out of thick ascending loop of henle into medullary interstitium
Active transport of ions from collecting ducts into medullary interstitium
Facilitated diffusion of urea from inner medullary collecting ducts into medullary interstitium
Diffusion of less water than reabsorption of solutes from medullary interstitium

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Countercurrent multiplier

Repetitive reabsorption of NaCl by thick ascending limb of loop of henle and continued inflow of new NaCl from proximal tubules into loop of henle

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How cortical collecting ducts play a role in concentrating urine

If ADH levels are high, cortical collecting ducts become permeable to water
-large amts of water get reabsorbed from tubule into cortex interstitium, where it is swept away by capillaries

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Why is water reabsorbed into cortex from collecting ducts instead of renal medulla?

To preserve high medullary interstitial osmolarity

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Role medullary collecting ducts play in concentration of urine

Wen ADH present, water gets further reabsorbed in interstitium and carried away from vasa recta
-urea is reabsorbed from medullary collecting duct into medullary interstitium and is “recycled”

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2 features of renal medullary blood flow that contribute to preservation of hyperosmolarity of renal medulla

Low medullary blood flow

Vasa recta serve as countercurrent exchangers

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Level plasma osmolarity is maintained at

280-295

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What level is plasma osmolarity at when thirst is sensed

294 mOsm/L

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What level does osmolarity have to raise by for ADH release to be stimulated

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Disturbances in osmolarity are reflected by

Alterations in serum Na concentrations; hyper/hyponatremia

ADH secretion is stimulated by

Hyperosmolarity | Volume depletion

What is hyperosmolarity sensed by

Hypothalamic osmoreceptors

What is volume depletion sensed by

Carotid sinus baroreceptors

Extracellular fluid volume determined mainly by

Balance between intake and output of water and NaCl

If ingestion of NaCl is greater than excretion of NaCl, what will happen to ECF volume?

Will increase

If excretion of NaCl is greater than ingestion of NaCl, what happens to ECF volume?

Decreases

Sensors that control ECF volume

Vascular low pressure volume sensors* Vascular high pressure volume sensors* CNS hepatic system

Where vascular low pressure volume sensors are located

Walls of cardiac atria Right ventricle Pulmonary vessels

How much of a change in blood volume is required to evoke a response from vascular low pressure volume sensors

5-10% change in blood volume and pressure

What happens in response to vascular low pressure volume sensors sending signals to brainstem

Modulation of sympathetic nerve outflow and ADH secretion - decrease in filling increases sympathetic nerve activity and stimulates ADH - dissension of structures decreases sympathetic nerve activity

Where are vascular high pressure volume sensors located

Arterial side of circularity system Wall of aortic arch Carotid sinus Afferent arterioles in kidney

How much of a change in blood pressure is required for vascular high pressure volume receptors in aortic arch and carotid sinus to send signals to brainstem

5-10%

Decrease in BP sensed by vascular high pressure volume sensors causes what?

Increases sympathetic nerve activity and ADH secretion

Increase in BP sensed by vascular high pressure volume sensors causes

Decrease in sympathetic nerve activity

When vascular high pressure volume sensors sense a change in volume at afferent arteriole of kidney, what structure responds to these changes

Juxtaglomerular apparatus

Juxtaglomerular apparatus response to reduced perfusion pressure in afferent arteriole

Release of renin

Juxtaglomerular apparatus response when an increased perfusion pressure is sensed

Suppression of renin release

Volume sensor signals

Sympathetic nerves Renin-angiotensin-aldosterone system Natriuretic peptides Antidiuretic hormone

With ECF depletion, stimulation of renal sympathetic nerve activity leads to

Constriction of afferent and efferent arterioles Renin secretion stimulated by granular cells NaCl reabsorption along nephron stimulated directly

What is the net effect of renal sympathetic activity

Decrease excretion of NaCl | Restore ECF volume to normal

Renin secretion stimulated by

Reduced perfusion pressure Sympathetic nerve activity Reduced delivery of NaCl to macula densa

Functions of angiotensin II

Stimulation of aldosterone secretion by adrenal cortex Arteriolar vasoconstriction, increasing BP stimulation of ADH secretion and thirst Increase NaCl reabsorption by proximal tubule, thick ascending loop of henle, distal tubule, and collecting duct Stimulates secretion of aldosterone

Natriuretic peptides

ANP and BNP are secreted when heart dilates to relax vascular smooth muscle and promote excretion of NaCl and water by kidneys

Hi and low pressure volume sensors send signals to kidneys to increase excretion of NaCl and water by:

``` Decreasing sympathetic nerve activity Releasing natriuretic peptides Inhibit ADH secretion Decrease renin secretion Decrease aldosterone secretion ```

General responses of nephrons to the need for volume sensors to want to get rid of sodium and water

GFR increases Reabsorption decreases in proximal tubule and loop of henle Sodium reabsorption decreases in distal tubule and collecting duct

Extracellular volume depletion cause kidneys to

Reduce excretion of NaCl and water

Reduced excretion of NaCl and water is done by

Increasing sympathetic nerve activity Increased secretion of renin Decreasing natriuretic peptides Increased secretion of ADH

The kidneys effort to reduce excretion of NaCl and water results in

Decreased GFR Increased Na reabsorption by proximal tubule and loop of henle Increased Na reabsorption by distal tubule and collecting duct

Acidemia

Fall in pH (more acidic)

Alkalemia

Rise in pH (more basic)

Most metabolic processes in the body result in the production of

Acid

Largest source of acid from within the body

Catabolism and oxidation of glucose and fatty acids...ultimately CO2+H2O= carbonic acid

What gets rid of volatile acid production

Pulmonary ventilation

Nonvolatile acids formed primarily from

Metabolism of sulfur-containing amino acids

What gets rid of nonvolatile acids

Excretion of H ions thru kidney

H ion conc determined by

Ratio of PCO2 and bicarbonate concentration

3 primary systems to prevent acidosis or alkalosis

1. Chemical acid-base buffer systems of body fluids 2. Respiratory center 3. Kidneys

Chemical acid-base buffer systems of body fluids

Bicarbonate and phosphate buffer systems | Proteins as infra cellular buffers

How respiratory center prevents acidosis/alkalosis

Removal of CO2 and therefore bicarbonate from ECF

How kidneys prevent acidosis/alkalosis

Excrete either acidic or alkaline urine

Body produces how much nonvolatile acid/day?

~80 mEq

Reabsorption of bicarbonate and secretion of H are accomplished through process of

H secretion by tubules | -bicarbonate must combine with H to form H2CO3 before it can be reabsorbed

3 mechanisms used by kidneys to regulate ECF H conc

Secretion of H Reabsorption of filtered bicarbonate Production of new bicarbonate

H ion secretion and bicarbonate reabsorption occur in all parts of tubules except

Descending ans ascending thin limbs of loop of henle

What must happen for each bicarbonate to be absorbed

One H must be secreted

How H is secreted in proximal tubules, thick segment of ascending loop of henle, and early distal tubule

Secondary active secretion of H is coupled with Na transport

How intercalated cells of late distal and collecting tubules secrete H

Active transport

Phosphate buffer system

Phosphates are ultimately responsible for holding H+'s in urine so that H+'s can be expelled from the body in urine. This also allows HCO3- to be reabsorbed from the kidney back into the body, without H+ following the HCO3- back into the body.

Ammonia buffer system