Unit 7 - Regulation of Plasma Sodium and ECF Volume Flashcards Preview

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Flashcards in Unit 7 - Regulation of Plasma Sodium and ECF Volume Deck (40)
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why is maintaining plasma volume so important?

blood pressure drives blood flow, and blood pressure is dependent on volume
-so volume --> BP --> flow


what are the sensors, efferent pathways, effectors, and regulated parameters of osmolarity?

S: hypothalamic osmoreceptors
EP: ADH and thirst
E: kidney, brain (thirst)
RP: renal free water excretion, water consumption


what are the sensors, efferent pathways, effectors, and regulated parameters of ECF volume?

S: carotid sinus, aortic arch, renal afferent arteriole, and atria (actually pressure stretch receptors)
EP: renin-angiotensin-aldosterone, SNS, ADH, ANP (virtually never constant)
E: short term heart and blood vessels, but long term kidney
RP: short term blood pressure (PVR x CO), but long term renal Na excretion


what is the renal response to abrupt increases in dietary Na (to 150 mmol)?

if initially in Na+ balance, and Na+ intake is increased, the kidney takes 6 days to catch up (positive balance) by retaining osmolarity by retaining 1 L water (gain 1 kg weight)


what is the renal response to abrupt decreases in dietary Na (by 150 mmol)?

if initially in positive Na+ balance, and Na+ intake is decreased, the kidney takes 6 days to recover (negative balance) by retaining osmolarity by losing 1 L water (lose 1 kg weight)


what is hemorrhage an example of and what will it cause?

severe ECF volume contraction
-induces decrease in GFR


is kidney's increase in Na+ excretion in response to an increase in ECF volume, or an increase in Na+ concentration?

it's due to increase in ECF volume
-will increase excretion to retain osmolarity at 300 mmol/L (both 150 mmol Na+ and 150 mmol Cl-)


what is effective circulating volume? what does it do?

functional, not anatomical, blood volume reflecting extent of tissue/organ perfusion where blood pressure is sensed
-induces regulation of Na+ excretion
-normally paralleles total ECF volume, both intra- and extra-vascular volumes


which induces regulation of Na+ excretion: changes in effective circulating volume, or total ECF volume?

changes in effective circulating volume


when is effective circulating volume less than total ECF volume?

in disease states that cause edema (like CHF)


what is CHF in regards to edema?

increases end diastolic pressure, so increased capillary hydrostatic pressure driving fluid from intravascular to extravascular space


what does pulmonary edema cause volume-wise?

if secondary to left ventricular heart failure and pulmonary HTN
-caused by increased capillary hydrostatic pressure in the lung, driving fluid from intravascular to extravascular space, that severely compromises gas exchange in lung


what does liver disease do volume-wise?

caused by decrease in synthesis of albumin, so decreased plasma oncotic pressure that upsets normal Starling forces


what does neprhotic syndrome do volume-wise?

disease of renal glomerulus allows inappropriate filtration of albumin = albuminuria
-decreases plasma oncotic pressure, disrupting Starling forces


what do diuretic drugs do?

decrease plasma volume by "forcing" kidney to increase excretion of Na+ and water in urine
-this decreases hydrostatic pressure, and increases oncotic pressure in capilliaries, which favors absorption of edema in interstitial space back into intravascular space


what are the 3 types of ECF volume baroreceptors?

1. "central" vascular sensors
-Low pressure (very important): atria and pulmonary vasculature
-High pressure (less important): carotid sinus, aortic arch, and juxtaglomerular apparatus (renal afferent arteriole)
2. sensors in CNS (less important)
3. sensors in liver (less important)


what are 4 parallel effector systems that increase renal Na+ absorption and decrease renal Na+ excretion?

1. renin-angiotensin-aldosterone hormonal system
2. increased renal sympathetic nerve activity
3. posterior pituitary (ADH)
4. ANP


what is the RAA hormonal system?

-AII promotes Na+ retention by stimulating Na/H exchange in proximal tubule cells, and decreases renal plasma flow, which promotes increased Na+ resabsorption
-aldosterone induces increase in Na+ reabsorption by late distal tubule and early collecting duct


how does increased renal SNS activity affect blood volume?

induces renal vasoconstriction and increased Na+ reabsorption, which reduces renal Na+ excretion


how do ADH and ANP affect blood volume?

ADH - promotes water reabsorption
ANP - reduces Na+ excretion in response to reduced ECF volume


what is angiotensinogen?

substrate of renin, and is alpha2-globulin made by liver and released into systemic circulation


what is renin? what activates it?

made and stored in granular cells of JGA of kidney
-decreased effective circulating volume increases its release, converting angiotensinogen to AI (decapeptide)


what is ACE?

angiogensin converting enzyme (decapeptide AI to octapeptide AII)
-found on luminal surface of vascular endothelium throughout body, and abundant in vasculature of lung and kidney


what is angiotensin II's half life?

2 minutes (rapid degradation by aminopeptidases)
-cleaves AII to heptapeptide AIII with less activity


what is the most important factor controlling AII levels in plasma?

renin release from granular cells of JGA


what are the three renal mechanisms regulating renin release?

1. local renal baroreceptors in afferent arterioles respond to low pressure and increase secretion of renin by granular cells
2. decreased systemic arterial blood pressure stimulates baroreceptor reflex, that causes increased sympathetic drive to JGA, increasing renin secretion
3. cells of macula densa sense tubular fluid Na+ concentration and, if low, cause increased release of renin from granular/JG cells into afferent arteriole blood supply


what are actions of AII?

-induces aldosterone release from adrenal cortex
-acts on hypothalamus to increase thirst and induce release of ADH from posterior pituitary
-vasoconstricts renal and other systemic vessels:
--in kidney: constricts efferent more than afferent arterioles to increase GFR
--increases Starling forces favoring reabsorption of tubular fluid by peritubular capillaries
-enhances Na/H exchange in proximal tubule, which increases Na+ reabsorption
-induces hypertrophy of renal tubule cells


what does aldosterone do?

mineralcorticoid secreted by adrenal cortex
-is primary long term regulator of salt balance and ECF volume, thus blood pressure
-acts on kidney tubules to increase reabsorption of Na+ and water due to increase in osmolarity from increased Na+ reabsorption
--acts on "principal" cells in late distal tubule and early collecting duct in renal cortex
-acts on distal nephron to increase secretion and excretion of K+


how does aldosterone increase Na+ reabsorption?

induced increase in Na+ transporter expression
-increased basolateral membrane Na+/K+ pumps
-increased apical membrane Na+ channels
-increased mitochondrial enzymes (ATP)

doesn't work immediately


why doesn't solute reabsorption in cortical nephron participate in counter current exchange?

due to separate venous circulations in cortex and vasa recta of medulla; the cortical circulation is rapidly returned to renal vein

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