regulation of homeostasis by the kidney Flashcards
Body pH
Between 7.35 and 7.45
Death occurs at <6.8 or >8.0
Types of buffer systems
Carbonic acid/bicarbonate
Protein
Phosphate
HCO3- (must be reabsorbed by kidneys)
Relationship between pH and plasma CO2
Inverse relationship
Changes in pH detected by
Peripheral chemoreceptors
These act on respiration centres in the brain to adjust respiration rates
Regulation of acid base balance
HCO3- in filtrate is reabsorbed, and H+ is secreted or Renal Tubular Acidosis occurs
& vice versa
Intercalated cells help H+ secretion and HCO3- reabsorption
Preventing acidosis
Excretion of CO2 from lungs
Secretion of H+ from kidneys
Acidosis
Inadequate ventilation
Loss of HCO3- in diarrhoea and urine
Treatment of metabolic acidosis
IV isotonic HCO3-
IV lactate solution
Treatment of respiratory acidosis
Restore ventilation
Treat underlying dysfunction
Give IV lactate solution
Alkalosis
Hyperventilation
Use of H+ in metabolism
Loss of H+ in vomit/urine
Treatment of metabolic alkalosis
Electrolytes
IV Cl- solution
Treat underlying disorder
Treatment of respiratory alkalosis
Treat underlying disorder
Breathe into a paper bag
IV Cl-solution
Osmoreceptors and baroreceptors
Increased plasma osmolality stimulates osmoreceptors = ADH release = increased ECV
Increased plasma osmolality also triggers different osmoreceptors which trigger thirst
Low pressure blood volume receptors - v important
Large systemic veins
Cardiac atria
Pulmonary vasculature
High pressure arterial stretch receptors - less important
Carotid sinus
Aortic arch
Renal afferent arteriole
Baroreceptors
Detect changes in ECV
Central vascular sensors
Sensors in CNS and liver
Parallel effector pathways which act on kidney
RAAS Sympathetic NS ADH release ANP release These change renal haemodynamics and Na+ transport by renal tubule cells
What stimulates renin release from JGA cells
Decreased renal perfusion pressure detected in afferent arteriole
Decreased Na+ in distal tubule - macula densa - the renal Na+ sensor
Decreased systemic BP -> symptoms NS supplying JGA
Actions of Ang II
Enhances tubular Na+ transport in kidney
Stimulation of aldosterone release from adrenal cortex
Acts on hypothalamus to stimulate thirst and ADH release
Vasoconstriction of renal/systemic vessels so BP increases
Renal cell hypertrophy so more protein synthesis of Na+ transporters and channels
Actions of Aldosterone
Stimulates Na+ reabsorption in DT and CD
Increases ECV and lowers plasma K+
Conserves Na+ and water - but variation in plasma K+ levels
ANP
Lowers ECV
Increased ECV causes stretch -> ANP release, promoting natriuresis and renal vasodilation (again more Na+ excreted)
More Na+ reaches macula dense -> reduces effects of Ang II
What synthesises and stores ANP
Atrial myocytes