Sodium Balance Regulation PDF

Regulate Sodium Balance Kidney is responsible for maintaining sodium balance, and can alter excretion to maintain homeostasis ANGIOTENSIN Na+levels lower than normal = renin angiotensin...

Regulate Sodium Balance Kidney is responsible for maintaining sodium balance, and can alter excretion to maintain homeostasis ANGIOTENSIN Na+levels lower than normal = renin angiotensin Na/H exchanger activity on luminal membrane increases as more Na and H move from aldosterone system (RAAS) activated, releases, angiotensin filtrate into tubule cells ll, and aldosterone Na/K ATPase increased activity on basolateral membrane resul5s in more Na being Na+ levels are too high RAAS pathway, decreased, atrial excreted out of proximal tubule cells into interstitial fluid, which is reabsorbed by blood natriuretic peptide (ANP) released vessels nearby Increased Na increased the ECF volume, ECF compartment is plasma, causes increase in total blood volume Angiotensin II is also a potent vasoconstrictor, vasoconstriction of the afferent arteriole alone results in a decrease in the GFR, reducing filtration production, and therefore reducing how much fluid can be excreted, including a reduction in Na+ excretion. Vasoconstriction of the efferent RAAS PATHWAY arteriole at the same time, still results in a net reduction of GFR, since so little blood enters the Produces an enzyme (renin) and two hormones (angiotensin ll, corpuscles of nephrons when the afferent arteriole is already vasoconstricted. and aldosterone) renin made by juxtaglomerular cells in response to low ANP levels of Na a cardiac atrial cells produce and release ANP into blood protein made Renin cleaves angiotensinogen (452 amino acids long) when blood volume and pressure increases, it stretches atrial cells peptide attaches to angiotensin l (10 amino acids long), Atrial cells contain mechanoreceptors that detect stretching, which releases angiotensin l cleave again by angiotensin-converting ANP into blood enzyme (ACE) -> Froungs Which makes angiotensin ll (8 amino acids long) Actions Prevent actions of aldosterone- blocks aldosterone release from adrenal gland ↓ hormone Increase GFR - ANP causes afferent arteriol to vasodilate, increasing GFR CONTROL OF RENIN RELEASE when more filtrate produced, travels faster Chemoreceptors Less opportunity for Na to be reabsorbed and more is then excreted composition of filtrate detected by macula densa cells Baroreceptors located on aortic arch Connect to cardiovascular centre in medulla oblongata as elk as innervated the juxtaglomerular cells in kidney Lower than normal Na+ levels will cause the macula densa cells to secrete a chemical messenger (paracrine factor) that causes the nearby juxtaglomerular cells to secrete the enzyme renin in the blood. CONTROL OF ALDOSTERONE RELEASE Aldosterone is a steroid Released by adrenal gland (endocrine tissue on top of kidney) Angiotensin ll is a stimulus for aldosterone higher than normal [k+] can also be a stimulus ALDOSTERONE Na channels increase on luminal membrane of principle cells allows for more movement of Na from filtrate into tubule cells Na/k ATPase activity increases, transport Na out into intersititum into blood vessels K channels can increase on luminal membrane