Renal 6 Regulation of ECFV Flashcards
how is extracellular fluid volume controlled
altering the excretion of Na. ISOTONIC PROCESS= does NOT change the concentration of Na
What is the regulated variable in regulated variable in regulation of ECFV
vascular pressure which is sneced by the systemic and intrarenal baroreceptors
Vascular Low Volume sensors
Low pressure: Right atrium (release ANP) and Right ventricle (release BNP)
Vascular High Volume sensors
High Pressure: Carotic sinus, aortic arch, intrarenal baroreceptor (afferent arteriole)
Volume sensor in the brain
Hypothalamus
Volume sensor in the liver
Portal pressure
What occurs during Hypervolemia
Increased Effective circulating blood volume (ECBV) leading to 1.) decrease in RAAS 2.) increase in ANP, BNP, and Urodilatin 3.) Na and water excretion increase (but NO CHANGE IN OSMOLALITY)
What occurs during hypovolemia
decreased ECBV leading to 1.) Increased RAAS 2.) Increased Sympathetic activity (vasoconstriction of the afferent and efferent arterioles) 3.) Na and water excretion decrease (but NO CHANGE IN OSMOLALITY)
does osmolality change in the regulation of extracellular fluid volume
NO - isostonic - control Na secretion and water moves with it (therefore doesn’t change the concentration of Na)
What happens in Hypernatremia
OSMOLALITY ISSUE: Increased plasma Na leads to increased ADH release resulting in excretion of free water (PLASMA OSMOLARITY DECREASES)
What happens in Hyponatremia
OSMOLALITY ISSUE: Decreased plasma Na leads to decrease in ADH release resulting in excretion of free water (PLASMA OSMOLALITY INCREASE)
Volume regulation vs osmoregulation
Volume regulation: involves the control of Na excretion to regulate ECBV (ISOTONIC- does not change the concentration of Na) Osmoregulation: involed the controle of water excretion and water consumption through ADH/thrist mechanisms to regulate Na concentration
what is the primary stimuli for aldosterone release
1.) Angiotensin II (increased in hypovolemic states) 2.) Hypokalemia
secondary stimuli for aldosterone release
1.) Hyponatremai (weak stimulus) 2.) ACTH (weak stimulus)
What supresses the release of aldosterone
ANP, BNP, and dopamine - Note : Aldosterone also works to supress these factors. Without this mechanism ist would impair our ability to defend volume
Role of aldosterone in Na excretion
Increases Na reabsorption in principle cells of the collecting ducts causing 1) K secretion and excretion 2.) Cl reaborption 3.) H secretion
Aldosterone vs Na intake
decrease in Na intake causes renin and aldosterone to go up
Factors that affect Na exretion
1.) Aldosterone 2.) GFR 3.) Natriuretic factors 4.) Redistribution of Flow 5.) Norepinephrine and angiotensin II 6.) Pressure Natriuresis/Diuresis 7.) Physocal factors
What happens with increases in Na intake
1.) Increase urine Na 2.) Decrease plasma renin 3.) Decrease plasma aldosterone 4.) Increase ECBV
What happens with decreases in Na intake
1.) Decreased urine Na 2.) increased plasma renin 3.) increased plasma aldosterone 4.) Decreased ECBV
effect of changes in GFR on Na excretion
Changes in GFR change the filtered load of Na (and other solutes that are coupled to Na reabsorption) - Na reabsorption is load dependent thereofre increases in GFR increase Na excretion and decreases in GFR decrease Na excretion (glomerulotubular balance)
Atrial Naturetic Peptide (ANP)
Released from the myocytes in the right atria in response to stretch (hypervolemia) to cause afferent arteriolar vasodilation (increases GFR and decreases FF) Decreases peritubular capillary reabsorption (can lead to back leak) Ingibits Na reabsorption in the colletcing tubules causing diuresis and inhibits alsoderone secretion
Brain (B-type) Natriuretic Peptide (BNP)
Released from myocytes in the right ventricle in response to stretch (hypervolemia) - similar effects to ANP
Urodilatin
ANP like hormone produced in the distal nephron. INTRINSIC (no significant levels in the plasma) renal hormal that inhibits NA and water reabsorption in MCD
Endogenous digitalis like hormone (natriuretic hormone)
released from the hypothalamus in response to volume expansion. Inhibits NaK-ATPase to reduce sodium reabsorbtion (promotes excretion of Na and water)
Cortical nephron Na capacity
lower capacity for Na and water reabsorption than juxtamedullary nephrons (due to shorter loop of henle)
Redistribution of flow in hypervolemic states
flow is shunted towards cortical nephrons (less capacity for Na and water reabsorption and increased excretion)
Redistribution of flow in hypovolemic states
flow is shunted towards juxtamedullary nephrons with greter reabsorptive capacity which decreases Na and water excretion (keeps more in the system to defend volume)
Angiotenensin II causes gretaer vasoconstriction in _____ afferent arterioles
cortical
Norepinephrina and Angiotensin role
In low volume states NE and Angiotensin II stimulate NA reabsorption in the proximal tubule. Angiotensin II stimulates the Na-H exchanger by increasing NaK-ATPase activity. Net effect is increased solute and water reabsorption
Importance of autoregulation
minimizes the impact of changes in MAP (renal perfusion pressure) on RBF and GFR
Glomerular capillaries in hypvolemia (efferent vasoconstriction)
keep Pg from faling too much and increase the filtration fraction
Peritubular capillaries in hypovolemia (efferent vasoconstriction)
decreased hydrostatic pressure and increased oncotic pressure resulting in an increase in the reabsorptive capacity
Glomerular capillaries in hypervolemia (efferent vasodilation)
increase PG and decrease the FF
Peritubular capillaries in hypervoleia (efferent vasodilation
increasd hydrostatic pressure (Pc) and decreased oncotic pressure leading to decreased reabsoprtive capacity
RAAS in Na-Volume regulation
low blood pressure = hypovolemia - potent stimulus for renin release
what is involved in RAAS Na-Volume Regulation
1.) Intrarenal baroreceptors (afferent artreiole - JG cells release renin) 2.) Cardiopulmonary baroreceptors (High pressure- cartotid sinus and aortic arc Low pressure- Right atrium and ventricle) 3.) tunulogolomerular feedback (decreased delivery of tubular filtrate and/or Cl- to the macula densa signals that GFR is too low) = Intrinsic release of renin that leads to efferent arteriolar vasoconstriction and increased GFR
what do we release if we want to increase GFR
dilatory elements
what do we release if we want to decrease GFR
adensosine - to cause vasoconstriction
Renin (RAAS)
catalyzes the conversion of angiotensinogen to angiotenin I
Converting enzyme (RAAS)
catalyzes the conversion of angiotensin I to angiotensin II (AKA ACE- angiotensin converting enzyme)
Angiotensin II compensates for what
geared to compensate for a hypovolemic state - whether real or percieved
Roles of Angiotensin II (10 roles)
1.) Stimulates aldosterone secretion to increase Na and water reabsorption 2.) Stimulates sympathetic vasoconstriction to increase blood pressure 3.) Stimulates thirst to increase water intake (only with sigificant hypovolemia) 4.) Stimulates ADH release to increase distal nephron reabsorption to water WHEN THERE IS >10% REDUCTION IN ECBV. 5.) Causes vasoconstricyion of effernt arterioles - decreases RBF, helps maintain GFR, increases fitration rate to increase peritubular capillary reabsorption) 6.) Enhances Norepinephrine syntheiss 7.) greater vasoconstriction in the outer cortical afferent arteroles (shunts blood toward juxtamedullary nephrons) 8.) Stimulates prostaglanidinsg that modulate vasoconstriction to help prevnet excessive vasoconstriction. 9.) Stimulates Na reabsorption in the proximal tubule via NaK-ATPase 10.) inhibits renin secretion (negative feedback)
Pathological changes leading to increased Na exretion
1.) osmotic diuresis (presence of unabsorpbed solutes in the tubule that pull water) 2.) Impermeant anions in filtrate (diffusion trapped) 3.) aldosterone deficit
Aldosterone deficit leads to
1.) hypvolemia 2.) Hyperkalemia (remember: aldosterone normally causes potassium secretion) 3.) metabolic acidosis (remember: aldosterone causes H+ secretion)
Pathological changes leading to a decrease in Na exrcretion
1.) Aldosterone excess 2.) Aldosterone escape
Aldosterone excess leads to
1.) Hypervolemia (decreased Na excretion) 2) Hypokalemia (casues K secretion) 3.) Metabolic alkalosis
Aldosterone escape
diuresis that opposes excess Na and water retention
Increased Na intake and changes in Na excretion
Water retention (increased ECBV) - fluid and weight gain
Decreased Na intake and changes in Na excretion
water elimination (decreased ECBV) - fluid/weight loss
Conditions that can cause altered ECBV
immersionin water (zero g, recombinant position) - redistricution of intravascular fluid resulting in PERCIEVED HYPERVOLEMIA
Response to percieved hypervolemia due to altered ECBV
increased Na and water excretion - long latency (60-90 minutes)
Heart Failure (changes in Na excretion)
Decreased cardiac output leads to decreased ECBV causing increased ranal Na and water retention to create increasd ECBV which cause venous pressure leading to peripheral edema (decreased ECBV= percieved hypovolemia)
Role of the kidney in long term regulation of blood pressure
Kidney sets areterial pressure at 100 mmHg by controlling the reabsorption and secretion of Na which controls water reabsorption and REGULATES THE EFFECTIVE CIRCULATING BLOOD VOLUME
Renal response to real or percieved hypvolemia
Renal hypoperfusion (decreaed arteriolar stertcha nd decreased NaCl delivery to the macula densa) leads to the release of renin which causes increased Angiotensin II which can stimulate aldosterone secretion resulting in increased renal Na to increace the extracellular volume- the increased volume in addition to the increase in sympathetic blood pressure will cause a decrease in renin (feedback)
Cirrhosis and change in Na excretion
Changes peritubular capillary oncotic pressure due to decreased production of plasma protiens leading to edema causing percieved hypvolemia resulting in renal Na and H20 retention which causes further edema
Nephrotic syndrome and change in Na excretion
Changes in peritubular capillary oncotic pressure due to loss of protiens throough the urine resulting in edema and decreased ECB (percieved hypovolemia) resulting in renal Na and water retention leading to more edema
