Hormonal Mechanisms Flashcards
Hypervolemia
Increased ECF volume
Can be with or without high perfusion pressure
Causes: nephrotic syndrome, advanced renal failure
Symptoms: nocturia, pruritis, edema, nausea, vomiting, appetite loss tiredness, protienuria, hypoalbuminemia
Hypovolemia
Decreased ECF volume
Loss of total body Na+
Causes:haemorrhage, d and v, poor fluid intake, polyuria
Symptoms: dry mucous membranes, fainting, tachy cardia, arthostatic hypertension
N
Effector mechanisms on renal Na+ transport: Sympathetic stimulation
Increase Na+ reabsorption
Noradrenaline influences proximal Na+ reabsorption
Activates RAA
Decreases GFR-> less Na+ filtered
Atrial naturetic peptides
Increase GFR by vasodilation
Decrease proximal Na+ reabsorption
Inhibit aldosterone and renin release
Natriuretic factors
Decrease tubule reabsorption
Inhibit renin release
Prostanoids-> decrease GFR
Factors effecting renin release
Macula densa-> decreased salt delivery to distal tubule-> decreased salt to macula densa co transporter-> increased renin release
Renal Baroreceptor-> decreased renal perfusion pressure detected-> increased renin release
Catecholamines-> decreased ECF/BP->increased sympathetic activity-> bets adrenoceptors-> increased renin release
RAA
Renin, inhibited by ANP and ADH
Angiotensinogen
Angiotensin 1
Angiotensin 2-> vasoconstriction, proximal Na+ uptake, increased CO
Aldosterone release by adrenal cortex-> distal Na+ uptake
Osmoregulation sensors and effectors
Sensed: plasma osmolality
Sensors: hypothalamic osmoreceptors
Effectors: ADH, thirst
What’s affected? Urine osmolality, water uptake
Volume regulation, sensors and effectors
Sensed: effective tissue perfusion
Sensors: macula densa, renal baroreceptors, atria and carotid sinuses
Effectors: RAA,SNS,ANP, naturetic factors, ADH
Effected: urinary sodium, thirst
Ingestion of hypertonic saline
Increased osmolality and increased volume
Osmolality-> increased ADH and thirst
Volume-> decreased RAA (high salt delivery to distal tubule and high ECF), increase ANP to inhibit ADH (reduce water reabsorption)
Produce concentrated urine
Eating salt without drinking water
Increased osmolality with out volume increase
ADH release by post pit. neurohypophysis
Thirst
Ingestion of isotonic salt
Increase volume but osmolality stays the same
Baroreceptors decrease RAA
SNS decreased stimulation
Increased ANP to inhibit ADH
Decreased water reabsorption-> increased urine volume, hypo osmotic
Drinking large amounts of water
Decreased osmolality and increased volume
Decreased ADH by osmoreceptors
Decreased RAA by baroreceptors
Increased ANP
Excrete dilute urine, excreting the water returns osmolality to normal
Factors effecting K+ secretion
Aldosterone: Increase Na reabsorption leads to increased electro negativity of lumen, increase Na/K activity, increased luminal permeability to K Increased plasma K conc: Increased luminal permeability, increased Na/K activity, aldostone secretion Distal flow rate: K washout means less in lumen Na reabsorption without Cl-: Decreased luminal charge Acid base balance: Decreased Na pump Decreased apical permeability to K Increase H/K