Lecture 31 - Na-K-H2O homeostasis

diuresis

• increased production of urine

where is ADH (vasopressin) made?

• in the hypothalamus and secreted by the posterior pituitary gland

what kind of response is ADH

• mostly acute response

• can be released and cause changes within minutes

what is the stimuli for ADH

• decreased blood pressure

• high plasma osmolarity

  • angiotensin II

sensors for ADH

• baroreceptors in blood vessels

• osmoreceptors in hypothalamus

draw feedback loop for ADH

what is the response generated by ADH in the collecting duct?

when dehydrated, plasma osmolarity will

increase

dehydration will ___ the release of ADH, increasing water ____

• stimulate; reabsorption

what is the renin-angiotensin-aldosterone system?

• critical regulator of blood volume, electrolyte (Ma/L) balance, and blood pressure

• involved in acute and long term physiological responses to these variables

• extremely clinically relevant

  • many areas where things can go wrong

  • many points of pharmacological control

what is the assembly line for angiotensin II

• liver = angiotensinogen

• kidneys = renin

• prod: angiotensin I

• lungs = ACE

• prod: angiotensin II

what are the effectors of RAAS?

• kidneys

  • PCT in kidneys→ inc Na+ reabs.+ inc. BP/BV

  • adrenal glands → aldosterone → inc H20 reabs. and inc. BP/BV

• posterior pituitary → ADH secretion → inc. H2O reabs.

• arterioles → inc constriction → inc BP

• brain → inc SNS → inc. BP

aldosterone and the DCT

• aldosterone binds to internal receptors in the cell and it makes changes in the nucleus that lead to the ENaC

• inc. in number of ENaC (luminal)

  • bring in Na+

• inc. activity of the Na-K-ATPases

  • bring sodium out of cell

• inc. K+ secretion on luminal side

• IMP for LONG TERM BP reg.