2. Renal Physiology 5

Physiology 210 with E.sanders at University of Alberta

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By: Rachel Fung
Created: 2012-02-09
Size: 41 flashcards
Views: 13

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How is plasma osmolarity evaluated?

Measuring plasma sodium concentration

Hyponatremia

Below normal sodium concentration

Hypernatremia

Higher than normal sodium concentration

What is the main determining factor of the amount of water excreted?

Water reabsorption

Anti-diuretic hormone or vasopressin

Peptide hormone secreted from posterior pituitary gland - helps in osmoregulation by altering permeability of luminar membrane in cells from collecting ducts via aquaporins

Where is ADH made?

Supraoptic nucleus of hypothalamus

Where is ADH secreted?

Posterior pituitary

What occurs in the absence of ADH?

Late distal tubules and collecting ducts are almost impermeable to water - water diuresis

Diabetes insipidus

Caused by tumors - ADH not synthesized

Nephrogenic diabetes insipidus

Nephron tubules don't bind/respond to ADH

What increases ADH?

Shock, pain, warm/hot weather, water deprivation

What decreases ADH?

Cold, humid environment, alcohol

Aquaporins

Water channels in renal tubules

How many types of aquaporins are there?

More than 10

AQP1

In proximal tubules

AQP2, 3, 4

In collecting ducts

AQP2

Insertion on luminal side is regulated by ADH via gene transcription

AQPs on basolateral membrane

Not regulated by ADH - 3 and 4

ADH and thirst - antidiuresis

Water deprivation

High plasma osmolarity

Hypothalamic osmoreceptor stimulation

Increase ADH release

Increased plasma ADH

Thirst and water intake, renal water retention and antidiuresis

ADH and thirst - diuresis

Water intake

Low plasma osmolarity

Hypothalamic osmoreceptor block

ADH block

Decreased plasma ADH

Renal water excretion

Large water diuresis

Osmotic diuresis

Excess solute in excreted urine is always associated with high levels of water excretion (uncontrolled diabetes mellitus) - lots of glucose increases volume of urine

Water diuresis

Only excess water is excreted without excess solute in urine

Regulation of sodium

Total body sodium varies by a small percent, though intake and loss vary within a large range

Physiologically regulated by changing the volume of urine excreted

Sodium excreted - sodium filtered - sodium reabsorbed (never secreted!)

Blood pressure and sodium regulation link

Sodium is most abundant solute in ECF - changes in sodium affect plasma volume

Any changes in sodium cause changes in blood pressure

Low sodium in plasma

Barorecpetors and ANS respond to changes in blood pressure (monitor filtered load of sodium - short term)

Aldosterone affects reabsorption in long term - regulated by renin and angiotensin II

High sodium in plasma

ANP inhibits aldosterone function

Baroreceptors

Nerve endings sensitive to stretch - in carotid sinus, aortic arch, major veins

Increasing blood pressure increases stretch, increasing nerve impulse frequency

Information processed in medulla oblongata

Decreasing arterial blood pressure in response to water/sodium loss

Increases renal sympathetic activity by venous, atrial, and arterial baroreceptors, stimulating afferent arteriole constriction, lowering GFR and decreasing excretion of sodium and water

Long term regulation of sodium

Aldosterone is secreted from adrenal cortex to affect sodium reabsorption

Acts on very distal part of distal tubule and cortical collecting duct to induce synthesis of sodium transport protein and insert water channels to stimulate reabsorption

Range of sodium excretion without aldosterone and with high aldosterone

Fine tuning

No aldosterone - 2% filtered load excreted

High aldosterone - 0% filtered load excreted

Aldosterone actions

Acts on sodium channels in luminar membrane and sodium/potassium pump in basolateral membrane

Regulation of aldosterone secretion

Sodium content in diet - high sodium intake, low secretion

Low total body sodium stimulates aldosterone secretion

Angiotensin II acts on adrenal cortex to control secretion of aldosterone (helps make it)

Aldosterone production

Angiotensinogen (liver) -> renin stimulation -> angiotensin I (kidney) -> ACE stimulation -> angiotensin II (sensitive to osmolarity) -> adrenal cortex stimulation -> aldosterone secretion

Renin

Secreted from juxtaglomerular cells of JGA - rate limiting enzyme

How does sodium depletion control renin secretion

Juxtaglomerular cells secrete renin

JGA receives input from external baroreceptors (sympathetic), intrarenal baroreceptors, and macula densa

Atrial natriuretic peptide

Synthesized in cardiac atria - inhibits sodium reabsorption in tubular cells, inhibits aldosterone

What stimulates ANP secretion?

Increased blood volume and increased sodium concentration

Atrial distension

Pressure natriuresis

Increase in arterial pressure can regulate sodium

Potassium regulation

Most of filtered K+ is reabsorbed in proximal tubule and loop of Henle

Collecting duct secretes small amount of K+

K+ in urine is regulated in cortical collecting duct

Hyperkalemia

Excess of potassium

Hypokalemia

Low potassium

About this deck

By: Rachel Fung
Created: 2012-02-09
Size: 41 flashcards
Views: 13

About StudyBlue

“I have been getting MUCH better grades on all my tests for school. Flash cards, notes, and quizzes are great on here. Thanks!”
Kathy