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Aldosterone & ANP
Terms in this set (10)
Na+ affect blood pressure
1. in the proximal tubule and loop of Henle, there is a constant % of sodium reabsorption regardless of the sodium load in the body
2. the extent of controlled reabsorption is inversely proportional to the magnitude of sodium load in the body:
if too much Na+, decrease reabsorption, and more Na+ loss in urine
Na+ depleted in the body, increase reabsorption, decrease Na+ loss in urine
goal of RAS: change ECF changes BP
expansion of plasma volume increase BP, contraction of plasma volume decrease BP.
-increase Na+ load, increase ECF's osmolarity, extra Na+ holding extra water, expansion ECF volume, increase BP
-decrease Na+ load, decrease ECF's osmolarity, less water than normal held by ECF, ECF volume reduction, decrease BP
how does kidney detect when blood pressure is low
each nephron has 2 arterioles and 2 sets of capillaries associated with. when the blood pressure is low, the granular cells in juxtaglomerular apparatus produce renin.
renin, ACE, ADH, aldosterone, angiotensin
renin covert angiotensinogen to angiotensin I, ACE conver angiotensin I to angiotensin II. ANG 2 stimulate the adrenal cortex produces aldosterone.
aldosterone made, where it act, what does it do
-synthesized in adrenal cortex, secreted in to the blood and transported on a protein carrier to its target.
-target of aldosterone is last 1/3 distal tubule and collecting duct.
-target cells are principle cell. P cells look like other polarized transporting cell with Na+/K+-ATpase pumps on the basolateral membrane
-various channels and transporter on the apical membrane
what causes aldosterone to be released, inhibits its release
-direct, at the adrenal cortex, increased extra cellular K+. an increase in K stimulates aldosterone production and results in secretion by the nephron. this reflex protects the blood from hyperkalemia (elevated blood K+)
-indirect through the RAAS pathway: decrease blood pressure and decrease flow past the macula densa
(-):direct, at the adrenal cortex, increase osmolarity. An increase in ECF osmolarity inhibits aldosterone secretion. less aldosterone means increased Na+ excretion, which helps decrease osmolarity
-aldosterone enters cells by simple diffusion.
-In the target cells, aldosterone combines with a cytoplasmic receptor. The hormone-receptor complex moves in to the nucleus and binds to DNA, initiating the synthesis of new protein channels and Na+/K+-ATPase pumps
-the new protein must be inserted into the cell membrane before their effect can be noticed
-the entire process takes 1-2 hours, a slow response for a hormone that is to increase ECF volume.
-in the distal nephron, Na+ and water reabsorption are separately regulated. Water does not automatically follow Na+ reabsorption: ADH must be present.
-In contrast, in the proximal tubule, Na+ reabsorption is automatically followed by water reabsorption because the proximal tubule epithelium is always freely permeable to water
ANP (atrial naturetic peptide), goal, what triggers release
secreted when atrial cells stretch more than normal, as would occur with increase in blood volume
ANP enhances sodium excretion and urinary water loss
functions of ANP
1. increase GFR, by relaxing the the contractile surrounding the filtration slits
2. decrease Na+ and water reabsorption in the collecting ducts
3. inhibits release of renin, aldosterone and ADH
4. secreted by neurons in the brain which lower blood pressure
5. short half-life
factors occurring during the rest and voiding phases of micturition
-higher CNS input
-the motor neuron fires
-external sphincter(skeletal muscle) stays contracted
-internal sphincter (smooth muscle) passively contracted
-stretch receptor sends signals to sensory neuron to CNS
-high CNS input facilitate or inhibit reflex
-parasympathetic neuron facilitate
-motor neuron inhibit
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