Unit 7 - Long term control of blood pressure Flashcards
what are the set points for hypotension and hypertension? what if it’s transient VS chronic?
hypo: low BP where systolic is less than 90 mmHg
HTN: sustained above 140/90
-transient are normal, from fever, exercise, emotions
-chronic is major cause of heart failure, vascular disease, renal failure, and stroke
what is the most important regulator of MAP set point?
RAAS
-major regulation of total Na+ content and long-term MAP, ANS, ADH, and ANP
what are fast VS intermediate VS slow factors that change arterial blood pressure/
fast: baroreceptor reflex (cardiac and vascular)
- adapts to long-term changes and effects are blunted (low gain)
intermediate: renal actions (PVR)
slow: renal salt and water excretion
there are many things in the acute response, but less so in the chronic response
how does the kidney directly and indirectly act on blood pressure?
maintains long term BP
- direct: alters blood volume
- indirect: RAAS mechanism with juxtaglomerular apparatus
what do macula densa, juxtaglomerular cells, and mesangial cells do? (entire juxtaglomerular apparatus)
MD: collective name for specialized group of epithelial cells in initial part of distal tubules; sense osmolarity changes
JX: granular cells that make renin
MC: provide anchor, may be involved in response to hypotension since they have actin and myosin, and act under sympathetic stimulation
what are local VS global effects of RAAS?
local are more important, but global are more known
- many tissues have local RAAS that is less understood, but provides local control of hemodynamics
- global has almost unlimited capacity, and is not a neural reflex
what are 3 determinants of renin secretion?
- neural baroreceptors signal via renal sympathetics to granular cells in JGA
- intrarenal baroreceptors in afferent arterioles (granular cells)
- can function w/o innervation - NaCl delivery to MD of JGA
- osmotic swelling releases transmitter that inhibits renin secretion
this system is very redundant, meaning it’s very important
autoregulation of JGA if decreased arterial pressure?
decreased MAP causes decreased glomerular hydrostatic pressure, which decreases GFR, and decreases flow rate in the LoH which increases NaCl resorption
- decreased MD NaCl causes increases renin and decreased arteriole resistance/tone
- -increased renin causes more AII and efferent arteriole resistance/tone, causing increased GFR
- -decreased AA resistance/tone causes increased GFR
mechanism of RAAS?
- renin from juxtaglomerular cells is proteolytic enzyme that acts on angiotensin (liver plasma alpha2-globulin) to convert to angiotensin I (decapeptide)
- ACE from lungs converts to angiotensin II (octapeptide)
what are three critical functions of AII?
- powerful vasoconstricter to increase peripheral vascular resistance
- constricts mesangial cells to reduce GFR
- stimulates aldosterone secretion (stimulate proximal Na/H exchange, increase blood volume via pressure naturesis and diuresis)
does AII have negative or positive feedback on granular/juxtaglomerular cells?
negative feedback to inhibit renin production by granular cells
-bind to AT receptor to decrease intracellular Ca to inhibit renin
what is ultimately responsible for maintaining BP setpoint in longterm? shortterm?
kidneys longterm, baroreceptor reflex short term
-sympathectomy has little impact, exccept in resistant HTN
-
what is renal nerve ablation’s effect?
“purported” cure for resistant HTN (ablate from ilaic –> femoral –> renal arteries will drop BP)
-but no significant change from ablation and sham procedures
what are the main factors influencing blood pressure? the equation?
BP varies directly with cardiac output, peripheral resistance, blood volume
-BP = CO x PVR
what is ECF determined by? what is the osmotic content of Na?
total osmotic content; 90% Na
how do the kidneys know about Na+ content?
indirectly sensed
what are some effectors of Na content?
- change in GFR - sympathetic nerve activity (minor), and AII (major)
- ADH and ANP sometimes
what are factors that control aldosterone?
circulating level of AII
- minor factors are plasma K concentration and ANP
- stimulates Na+ reabsorption in cortical connecting tubules and collecting ducts
- -influences about 2% of total filtered Na+
why are chronic diseases of PCT not usually seen?
b/c such a huge part of monitoring Na level, that if there is a disease they will die very quickly due to hypovolemia
what is tubuloglomerular feedback?
acts in opposite direction to other reflexes in order to blunt effectiveness and prevent “over-correction”
-effects do NOT predominant, but blunts the increase in renal blood flow and GC
what are naturetic peptides?
ANP and BNP
- inhibit release of renin
- relax afferent arteriole
- used diagnostically
out of these, which increase and decrease Na+ reaborption?
- cortisol
- progesterone
- estrogen
- GH
- TH
- insulin
- glucagon
- PTH
increase Na reabsorption: cortisol, estrogen, GH, TH, insulin
decrease Na reabsorption: progesterone, PTH
how do baroreceptors and osmoreceptors control water excretion?
B: assess vascular fullness
O: assess plasma osmolarity
how do proximal and distal nephron compare in water control?
proximal: regulates ECF based on BP
- affects Na and water together
distal: determined by ADH (major regulator of total body water)
- aldosterone and ADH affect Na and water excretion independently
what is the Guyton hypothesis?
abnormal renal Na handling in the pathogenesis of HTN
what are causes of secondary HTN?
- renal disorders
- endocrine disorders
- endogenous medications and drugs
- pregnancy
- coarctation of the aorta
- neurologic disorders
- psychosocial factors
- intravascular volume overload
- systolic HTN
how can obesity and insulin resistance cause increased blood pressure?
unknown mechanism, but causes hyperinsulinemia that can affect kidney, smooth muscle proliferation, and SNS
- kidney will increase Na+ reabsorption
- smooth muscle cell proliferation causes vasoconstriction
- increased SNS activity causes increased CO and vasoconstriction
what are the drugs that block renin?
- beta-blockers
- alpha-agonists
- aliskirin
what are drugs that block aldosterone?
spironolactone
