lecture 13 - renal system 3 Flashcards
what is diuresis?
the removal of excess water in urine
what are diuretics?
drugs that promote urine excretion
what does ADH do?
vasopressin
controls permeability of cells in the collecting duct to water
• makes collecting duct more permeable
• results in conc urine and water conservation
can also have cardiovascular effects - causes vasoconstriction
what are water pores also called?
aquaporins
action of ADH
1) ADH binds to receptor on basolateral cell surface
2) stimulates adenyl cyclase to generate cAMP and activates protein kinases
3) increases insertion of aquaporin 2 into apical membrane
4) increases water permeability
5) increases water absorption
6) produces concentrated urine
7) water conservation
what are the 2 main mechanisms of ADH release?
osmoreceptors are the main controllers of ADH
cardiovascular effects - decreased blood volume or pressure can stimulate ADH release
where is ADH produced?
by cells in the supraoptic and paraventricular nuclei of the hypothalamus
where is ADH stored?
in vesicles in the posterior pituitary gland
what do osmoreceptors detect?
changes in plasma osmolarity
increased plasma osmolarity = increased ADH
decreased plasma osmolarity = decreased ADH
how is ADH removed?
by the liver and kidney
quickly metabolised
half life of 15 minutes
osmolar control of ADH secretion
when osmolarity is low there is little plasma ADH
set point = 280mOsm
steep relationship
when you get to 300mOsm there is no further increase
full range over 20mOsm increase is osmolarity
non-osmolar control of ADH secretion
need atleast a 10% reduction in blood volume before any ADH is released
causes a larger amount of ADH to be released
ADH is a potent vasoconstrictor
physiological stimuli for ADH release
- heightened emotions
- stress
- high temperature
- exercise
- pain
alcohol inhibits ADH release
inappropriate secretion of ADH
- post operative pain
- intracranial disease/injury
- ectopic ADH production - tumours
- opiates
- chloropropamide, MDMA - ecstasy
- pneumonia
- TB
- pulmonary disease
- nicotine
why do you get nocturnal enuresis (bed-wetting)?
delay in the development of normal circadian rhythm of ADH
how does MDMA dramatically alter fluid balance?
can result in increased circulating volume and hyponatremia (low Na concentration in the blood)
it triggers thirst reflex so increases fluid in but also increases ADH secretion so decreases fluid out
can result in people drowning internally
ADH deficiency
diabetes insipidus
polyuria due to deficiency of ADH or its action
what is polyuria?
excessive urine production
what are the 2 types of diabetes insipidus?
central
nephrongenic
central diabetes insipidus?
deficiency of ADH secretion
nephrogenic diabetes insipidus?
nephrons do not respond to ADH
how do you increase Na+ reabsorption in the nephron?
activate the renin-angiotensin-aldosterone axis activated to increase Na+ reabsorption
what stimulates renin release?
decreased NaCl at macula dense
stretch receptors in afferent arteriole sense decrease in BP
increases sympathetic nerve simulation due to central decrease in BP
what is ACE?
angiotensin converting enzyme
what does renin do?
converts angiotensinogen to angiotensin I
what does ACE do?
converts angiotensin I to angiotensin II - the more active agent
what does angiotensin II do?
causes release of aldosterone from the adrenal cortex
what does aldosterone do?
causes an increase in Na+ reabsorption in the DCT and CD
this increases extracellular fluid
this restores volume
renin no longer produced
how does the renin-angiotensin-aldosterone axis work?
1) renin converts angiotensinogen to angiotensin I
2) ACE converts angiotensin I to angiotensin II – the more active agent
3) this travels to the adrenal cortex & causes the release of aldosterone
4) aldosterone causes increased Na+ reabsorption in the DCT & CD
5) this increases extracellular fluid
6) restoration of volume
7) renin no longer produced
cellular action of aldosterone
1) aldosterone binds to receptor in cytoplasm of principal cell
2) initiates transcription
3) increases number of ENaC channels in apical surface
4) increases Na+/K+ pump
5) Na+ reabsorption, Cl- follows
6) K+ secretion by ROMK
what are principal cells?
aldosterone can diffuse into these and find a steroid hormone receptor in the cell (nucleus)
what are ENaC?
epithelial sodium channels
what are ROMK?
renal outer medulla potassium channels
what is aldosterone?
a steroid hormone synthesised in the adrenal cortex following stimulation by angiotensin II
promotes reabsorption of Na+ by principal cells in DCT and CD
overall effect:
• decreased NaCl and H2O secretion
• increased blood volume
angiotensin II
- stimulates release of aldosterone from the adrenal cortex
- acts on the brain to create the sensation of thirst
- powerful vasoconstrictor
- inhibits the baroreceptor reflex and increases the release of norepinephrine from the sympathetic postganglionic fibres
overal effect:
• decreased NaCl and H2O secretion
• increased blood volume and BP
what is ANP?
atrial natriuretic peptide
where is ANP produced?
by the atria in response to stretch - increases blood volume / BP
what does ANP do?
regulation of plasma volume and [Na+]
increases renal water and Na+ excretion
opposite actions to ADH and aldosterone
inhibits thirst, ADH, aldosterone, and renin release
overall effect:
• increased NaCl and H2O excretion
• decreased blood volume and BP
what is micturition?
the action of urinating
what is urine?
fluid that leaves the collecting duct
flows through the ureter to the bladder
what is the bladder?
hollow organ that can expand to hold 500ml
smooth muscle wall
neck of bladder continuous with urethra
has 2 rings of sphincter muscles
what are the 2 rings of sphincter muscles in the bladder?
internal
• smooth muscle
• has normal tone that keeps in contracted
external
• skeletal muscle controlled by somatic motor neurones
• tonic stimulation from CNS maintains contraction
mechanism of micturition
1) stretch receptors fire
2) parasympathetic neurones fire
3) motor neurones stop firing
4) smooth muscle contracts
5) internal sphincter passively pulled open
6) external sphincter releases
