Session 4- Control of body fluid volume and osmolality Flashcards
what is renin
an enzyme that is synthesized and stpred in JGA in the kidney
what stimulates renin release
LOW BP
increased sympathetic innervation
-granular cells of the JGA are innervated by sympathetic system, resulting in an increase in renin release
fall in wall tension of afferent arteiole
Decreased Na+ to the macula densa
-if less NaCl reaches the macula densa, the macula densa is stimulated to release prostaglandins which act on granular cells causing renin release
how does the RAAS system work
angiotensiogen-> angiotensin I via renin
angiotensin I -> angiotensin II VIA ACE
angiotensin II-> aldosterone
action of angiotensin II
directly vasoconstricts efferent arteioles within the glomerulus which increases GFR
stimulates the zona glomerulosa of the adrenal cortex to release aldosterone
action of aldosterone
directly increases Na+ reabsorption from the DCT
releases ADH
stimulate thrist
where does prostaglandin synthesis occur
cortex
medulla
collecting duct epithelial cells
what do prostaglandins do
vasodilators
renin release
what stimulates prostaglandin release
a decrease in effective circulating volume of Na+
action of ANP
inhibit Na+/K+/ATPase and close Na+ channels of the collecting ducts and DCT reducing Na+ reabsorption. Thus, Na+ and water excretion by the kidney is increased
vasodilate afferent arterioles, thereby increasing GFR
inhibit aldosterone release
inhibit ADH release
decrease renin release
how do starling forces affect the reabsorption of sodium if blood pressure increases
if BP increases, there is more blood voluem meaning the hydrostatic pressure of the peritubular capillaries increases and the oncotic pressure decreases which causes water reabsorption to decrease in the PCT
in the PCT how is the intial BP rise diminished
reduced number of Na-H antiporters and reduced Na- K ATPase activity in proximal tubule
this causes reduction in sodium resorption in proximal tubule
reduction in water resorption
ECF volume decreased
what is pressure natriuresis
increased sodium excretion
what is pressure diuresis
increased water excretion
how does congestive heart failure affetc the kidneys
CO falls and heart fsils to perfuse kidneys adequately
hypoperfusoon results in Na+ and water retention by the kidneys leading to oedema
renal hypoperfusion following a fall in CO is sense by the kidneys as hypovolaemia
this results in compensation by retaining NaCl and water to increase circulating fluid volume - RAAS
how does cardiac failure affect the lungs
this increase in pulmonary venous pressure results in transudation from the capillaries in the lungs and in pulmonary oedema
what is hypervolaemia
excess of fluid
how does hypertension affect teh kidneys
arteriosclerosis of the major renal arteries
hyalinization of the small vessels with intimal thickening
this can lead to chronic renal damage and a reduction in the size of the kidneys
renal causes of secondary hypertension
most diseases of the kidney cause-
impaired Na+ and water excretion, increases blood volume
stimulation of renin release
renal artery stenosis also causes reduced perfusion of the kidney and therefore excessive activation of the RAAS
what senses changes in osmolarity in the brain
hypothalmic osmoreceptors located in the organum vasculature of the lamina terminalis- OVLT located in brain
Where is ADH produced
the supraoptic nucleus of the hypothalamus then transported to the posterior pituitary
what triggers ADH release
increase in plasma osmolality
ADH effect
reduced water excretion
blood vessel vasoconstriction
it binds to V2 receptors on the basal membrane
- G protein coupled receptors when activated cause fusion of inactive aquaporin 2 vesicles with the luminal membrane
- creates ac channel through with water can pass
- passive flow of water
what is diabetes insipidus
too little ADH
inability to reabsorb water from the distal part of the nephron due to failure of secretion or action of ADH
symptoms of diabetes insipidus
polyuria
polydipsia
low urine osmolality
cental diabetes insipidus
impaired ADH synthesis or secretion by the hypothalamus- damage to hypothalamus or pituitary
- brain injury
- sarcoidosis
- tumour
- aneurysm
- some forms of encaphalitis or meningitis
how do we treat central diabetes insipidus
administrating ADH
nephrogenic diabetes insipidus
acquired insensitivity of the kidney to ADH
water is inadequately reabsorbed from the collecting ducts so a large quantity of urine is produced
what is SIADH
syndrome of inappropriate antidiuretic hormone secretion
excessive release of ADH from the PP gland or another source
chracterized by dilutional hyponatraemia
