Physio 11 Flashcards
what is the kidney’s response to increase in ECF volume?
increases Na+ excretion. kidney responds to increase in ECF volume, NOT sodium concentration
effective circulating volume
functional blood volume reflecting the extent of tissue/organ perfusion where blood pressure is sensed. normally parallels the ECF volume, bbut can be less than total ECF in congestive heart failures or other things causing edema
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)
other sensors of blood pressure
sensors are in the CNS and the liver. they are not as important as the other ‘central’ sensors
what are the four parallel effector systems?
RAA (renin angiotensin aldosterone), sympathetic nerve activity, ADH/AVP, and atrial natriuretic peptide
renin-angiotensin-aldosterone hormonal system
angiotensin II promotes sodium retention by stimulating Na/H exchange in the proximal tubule. decreases renal plasma flow, again promoting Na reabsorption. Aldosterone increases sodium reabsorption by the late distal tubule and early collecting duct.
angiotensinogen and renin
angiotensinogen substrate of the enzyme renin and is made by the liver and released into the systemic circulation
renin is synthed and stored in granular cells of the juxtaglomerular apparatus of the kidney. decreased effective circulating volume increases renin release. converts angiotensinogen into angiotensin I
angiotensin I
converted to angiotensin II by angiotensin converting enzyme. mainly found in the lungs, but is found in the entire body. located on the luminal surface of vascular endothelium. II is degraded by aminopeptidases to III, which is less active
three renal mechanisms regulating renin release
- local renal baroreceptors in afferent arterioles respond to low pressure and increase secretion of renin
- decreased systemic arterial blood pressure stimulates baroreceptor reflex which causes increased sympathetic drive to juxtaglomerular apparatus increasing secretion of renin
- cells of macula densa sense tubular fluid sodium concentration, and if low, cause increased release of renin
actions of angiotensin II
induces aldosterone release from adrenal cortex. acts on hypothal to increase thirst and induce release of ADH/AVP. vasoconstricts renal and other systemic vessels to increase GFR and increase starling forces to favor reabsorption. enhances Na/H exchange in the proximal tubule which increases sodium reabsorption. induces hypertrophy of the renal tubule cells
aldosterone actions
acts on kidney tubules to increase reabsorption of Na and water. acts on the distal nephron to increase the secretion and excretion of K+. induces increased Na reabsorption by prinicpal cells in the late distal tubule and early collecting duct. increases Na transporter expression (basolateral Na/K pumps, apical Na channels, and mitochondrial enzyme expression)
aldosterone mechanism of action
diffuses into cell and binds to an intracellular aldosterone receptor to form a receptor-aldosterone complex. complex enters nucleus and induces the transcription of mRNAs coding for membrane transport proteins mediating transcellular sodium reabsorption as well as mitochondrial enzymes mediating oxidative phosphorylation
secretogogues for aldosterone (things that cause increased aldosterone excretion)
angiotensin II, increased plasma K concentration, adrenocorticotropic hormone (ACTH) (induced by angiotensin II)
hey ab
hypernatremia
increase in plasma sodium concentration to a level above the normal range of 135-145 mEq/L. symptoms include lethargy, weakness, and irritability. severe symptoms like seizure and coma occur over 158 mEq/L. caused by a loss of water from the plasma due to inadequate consumption of water or an inappropriate renal excretion of water.
hypovolemic and hypervolemic hypernatremia causes
hypo: inadequate water consumption, extreme sweating, severe diarrhea, excessive renal excretion of water
hyper: excessive hypertonic fluid consumption (sea water) and hyperaldosteronism