CASE 7 Flashcards
reabsorption involves two types of transport
- epithelial transport
2. paracellular transport
epithelial transport
- substances cross the apical and basolateral membranes of the tubule epithelial cell to reach the interstitial fluid.
- solutes moving down their gradient use open leak channels or facilitated diffusion carriers to cross the cell membrane
- molecules that need to be pushed against their gradient are moved by either primary or indirect, secondary active transport
paracellular transport
- substances pass through the cell-cell junction between two adjacent cells.
active reabsorption of Na+
- primary driving force for most renal reabsorption
- filtrate entering the proximal tubule is similar in ion composition to plasma, with higher Na+ concentration than is found in cells
- Na+ can enter tubules by moving down the gradient
- NHE, Na+ H+ exchanger plays a major role in Na+ reabsorption
sodium linked secondary active transport
- responsible for reabsorption of many substances, like glucose, amino acids, ions
urea
- passively reabsorbed
- can move across the epithelium by diffusion if there is a urea concentration gradient
concentrations and secretion into the tubule
- Proximal convoluted tubule: secrete uric acids, organic acids
- Loop of Henle: no secretion takes place here
- End of ascending limb: secretion of H+
- distal convoluted tubule: secrete K+ and H+
- end of collecting duct: secretion of H+
RAAS, Renin-Angiotensin-Aldosterone System
- control of blood pressure
- juxtaglomerular cell is key cell, they are in the blood vessels of kidney, release renin
- renin helps raising blood pressure
- system shuts down when flow through convoluted distal tubule goes up; it inhibits renin release by granular cells
Triggers for release of renin by juxtaglomerular cells
- low blood pressure is sensed by juxtaglomerular cells and baroreceptors
- juxtaglomerular cells are triggered by sympathetic nerve cells during a period of stress as it triggers B1 adrenergic receptors, which stimulate renin production
- Macula densa cells, sense sodium. With low blood pressure not a lot of salt is being reabsorbed. Sense low NaCl concentration –> trigger the juxtaglomerular cells to release renin.
Angiotensinogen
- plays a role in RAAS
- produced by liver
- moves around the body in a nonactive state –> when it meets renin –> chops off a big chunk of angiotensinogen –> becomes angiotensin 1.
Angiotensin 1
- moves through blood vessels
- endothelial cells in lungs are able to convert angiotensin 1 into angiotensin 2
angiotensin 2
- very active hormone
- increases sympathetic activity, vasoconstriction and increased heart rate
- this all converts via ACE, angiotensin converting enzyme
Places angiotensin 2 goes to
- smooth muscle cells. Causes blood vessels to constrict, which causes increased resistance
- it causes kidney cells to hold on to more water, which increases blood volume
- pituitary gland –> secretes ADH (vasopressin) (oppose effects are caused by ANP) –> increases resistance of blood vessels and causes kidney to hold on to more water
- adrenal gland is triggered to produce aldosterone, which tends to promote Na+ and water reabsorption in distal convoluted tubule and lower plasma K+ concentration –> increasing blood pressure
dehydration effect on heart rate and respiration
- leads to high blood concentration and low blood pH –> increased respiration rate
- high blood concentration means high viscosity, which increases resistance and increases Mean Arterial Pressure
- dehydration triggers homeostatic responses
severe dehydration: compensatory mechanisms are aimed at restoring normal blood pressure, ECF volume and osmolarity by:
- conserving fluid to prevent additonal loss
- triggering cardiovascular reflexes to increase blood pressure
- stimulating thirst so that normal fluid volume and osmolarity can be restored
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Decreased volume is sensed by the atrial volume receptors
- the baroreceptors signal the cardiovascular control center to raise blood pressure
- decreased peripheral blood pressure directly decreases GFR
- paracrine feedback causes the granular cells to release renin
- granular cells respond to decreased blood pressure by releasing renin
- decreased blood pressure, decreased blood volume, increased osmolarity and increased ang 2 production stimulate ADH
The baroreceptors signal the cardiovascular control center to raise blood pressure
a. heart rate goes up as control of AV node shifts
b. the force of ventricular contraction increases under sympathetic stimulation.
c. sympathetic input activates the vasomotor center and causes arteriolar vasoconstriction, increasing peripheral resistance
d. sympathetic vasoconstriction of afferent arterioles in kidneys decreases GFR, helping conserve fluid
e. increased sympathetic activity at the granular cells of kidneys increases renin secretion, which leads to increased reabsorption of water
decreased peripheral blood pressure directly decreases GFR
- a lower GFR conserves ECF volume by filtering less fluid into the nephron
paracrine feedback causes the granular cells to release renin
- lower GFR decreases fluid flow past the macula densa, which triggers renin release
granular cells respond to decreased blood pressure by releasing renin
- the combination of decreased blood pressure, increased sympathetic input onto granular cells, and signals from the macula densa stimulates renin release and ensures increased production of antiotensin 2
decreased blood pressure, decreased blood volume, increased osmolarity and increased angiotensin 2 production all stimulate ADH and the thirst centers of hypothalamus
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Control pathways ensure that all four main compensatory mechanisms are activated
- cardiovascular responses
- angiotensin 2
- vasopressin
- intake of water
cardiovascular responses
- combine increased cardiac output and increased peripheral resistance to raise blood pressure
angiotensin 2
- stimulation of thirst
- vasopressin release
- direct vasoconstriction
- reinforcement of cardiovascular control center output
- stimulated aldosterone release –> but high osmolarity inhibits aldosterone release