Renal control Flashcards
Changes in osmolarity through the nephron
- descending limb of loop of henle is only permeable to h2O, only water reabsorbed
==> high mOsM, it is more concentrated - ascending limb of loop of henle is selectively permeable to ions, ions reabsorbed but no water
==> low mOsM, it is more dilute urine - collecting duct, variable reabsorption of water and solutes
- urine osmolarity (low or high mOsM) depends on reabsorption in the collecting duct
cortex usually isosmotic and then it get more and more concentrated as we go deeper into medulla, e.g. descending limb of loop of henle becomes more concentrated
How is osmotic gradient maintained?
aim : create hypoosmotic fluid (low solute conc) and hyperosmotic interstitial fluid (high solute conc) == Blood is not considered interstitial fluid.
fluid in loop of henle and blood flow in vasa recta (capillaries surrounding the juxtamedullary nephrons) move in opposite directions
- ascending limb of loop of henle is only permeable to solutes so ions are exiting and osmolarity decreases
- blood moves opposite direction, picks up the solutes, osmolarity increases as this happens (300-1200 mOsM)
- descending limb of loop of henle only permeable to H2O so it loses water
- blood picking up H2O, osmolarity decreases (1200-300 mOsM), diluted and returns to circulation
how is the Distal tubule and collecting ducts
- Controlled variation in urine concentration
==> Alterations in water and Na+ reabsorption
Primarily under hormonal regulations:
- Vasopressin (ADH): Increases water reabsorption, concentrates urine, reduces urine output.
- Aldosterone: Increases sodium reabsorption and potassium secretion, increases blood volume and pressure.
- Natriuretic Peptides: Promote sodium and water excretion, reduce blood volume and pressure.
Control of water reabsorption – Vasopressin (ADH)
aim == increases water reabsorption
triggers : 1. decrease blood pressure, 2. low blood volume (less atrial stretch), 3. osmolarity greater than 280 mOsM
- hypothalamus neurons synthesis vasopressin (ADH), released posterior pituitary
- ADH travels through blood to collecting duct epithelium
- insertion of water pores/ aqua porin in apical membrane
- increased water reabsorption to conserve water, urine becomes more concentrated
triggers for vasopressin 3)
trigger : osomlarity/ conc of body fluid higher than 280 mOsM
receptors : hypothalamic osmoreceptors
neuron : interneuron to hypothalamus
signal : hypothalamus neurons to synthesise vasopressin
results : retain H2O to decrease osmolarity, make body fluid conc more dilute
triggers for vasopressin 1)
trigger : decreased blood pressure in arteries
receptors : carotid & aortic baroreceptors
neuron : sensory neuron to hypothalamus
signal : hypothalamus neurons to synthesise vasopressin
results : retain H2O to increase blood pressure
triggers for vasopressin 2)
trigger : decreased low volume ==> decreased atrial stretch
receptors : atrial stretch receptor
neuron : sensory neuron to hypothalamus
signal : hypothalamus neurons to synthesise vasopressin
results : retain H2O to increase blood volume
how does Aldosterone
aim - increase Na+ reabsorption (and K+ secretion)
trigger : low BP/BV = same as ADh
- aldosterone is a steroid homrone produced by adrenal glands, can be directly absorbed by cells from blood cross interstitial fluid
- aldosterone binds to aldosterone receptor in the membrane
- this hormone-receptor complex initiates transcription in the nucleus
- translation and protein synthesis makes new proteins channels and pumps
- these proteins induced by aldosterone modulate the exisiting channels and pumps
==> increased sodium reabsorption (lumen to blood), and potassium secretion (blood to lumen)
Renin Angiotension system (RAS) : activation of ANG II
trigger : reduction in NaCl, ECF volume, arterial blood volume
- low BP = Low GFR = less NaCl transport; macular densa cells (distal tubule) detects and sends signals to granular cells (afferent arteriole)
- granular cells produce renin
- renin triggers conversion of angiotensinogen made from liver –> angiotensin 1
- ACE enzyme converts ANGI –> ANGII active homrone
Renin Angiotension system (RAS) : mechanism of ANGII
- ANGII stimulate adrenal cortex to secrete aldosterone
–> produce more Na+/K+ ATPase pump
–> increase Na+ reabsorption, H2O as well
–> increase BP, BV - ANGII acts on arterioles
–> vasoconstrcition => BP - ANGII act on hypothalamus to secrete more vasopressin (ADH)
–>more aquaporins inserted and increase H2O reabsorption
–> increase BV
Natriuretic peptides overview
role : causes salt excretion, acts as endogenous RAS inhibitors (works opposite to renin angiotensin system)
trigger : Released due to increased stretch/ increase in BV
two most well known NP:
1. Atrial Natriuretic peptide (ANP) : Produced in myocardial cells of the atria
- Brain Natriuretic peptide (BNP) :Produced by ventricular myocardial cells and neurons in brain
Natriuretic peptides mechanism
triggered by increase in blood volume
what produces ANP/BNP = atria myocardial cells and ventricular myocardial cells/ brain neurons respectively
ways it acts
1. adrenal cortex = stimulates adrenal cortex to decrease aldosterone secretion
2. Less renin, less ANGII, no stimulation to adrenal cortex to produce aldosterone
3. kidney = vasodilates afferent arteriole to increase GFR, less renin produced, less Na+ reabsorption, all to have more NaCl H2O lost to urine to decrease BV and BP
4. hypothalamus = less vasopressin, no aquaporins for water uptake = more lost to urine to decrease BV/BP
5. medulla oblongata = decrease sympathetic activity => relaxation of smooth muscles in blood vessels and decrease Bp
==> “MD regulates BP & RP” (MD for Medulla oblongata, BP for Blood Pressure, RP for Respiratory Patterns)
Micturition
aka urination
Once filtrate leaves the collecting duct, now called urine
* Rhythmic contractions of ureter smooth muscle eject urine into the bladder
- Bladder is composed of smooth muscle and stores urine until it is voided
Opening of bladder and urethra closed by sphincters : Internal and external
- full bladder, stretched, stretch detected by receptors so stretch receptors fire
- parasympathetic neurons fire for smooth muscle of bladder to contract
- motor neurons stop firing and tonic discharge is inhibited (the signals keeping the external urethral sphincter contracted are turned off)
- smooth muscle contracts so ballder squeezed to push out urine, internal spincter is passively open, external spincter relaxes, peessssssss
Q: Explain how aldosterone regulates potassium balance in the body and the potential effects of hyperkalemia and hypokalemia.
A:
Aldosterone Regulation: Aldosterone controls potassium balance by promoting the reabsorption of sodium and the secretion of potassium in the distal convoluted tubule and collecting ducts of the nephron.
Hyperkalemia: High potassium levels trigger aldosterone secretion. This enhances cell excitability initially but leads to less responsive cells over time, causing cardiac arrhythmias and potentially dangerous heart and respiratory system issues.
Hypokalemia: Low potassium levels lead to muscle weakness and can affect the heart and respiratory system.
Q: Describe the role of the hypothalamus in regulating thirst and salt craving.
A:
Thirst Regulation: Thirst is controlled by hypothalamic osmoreceptors, which are triggered by increases in blood osmolarity above 280 mOsM. Drinking water relieves thirst.
Salt Craving: A decrease in plasma sodium levels triggers salt craving, which is also integrated in the hypothalamus.
