Long Term Control of Blood Pressure Flashcards
what inherent flaws exist in the way we analyze blood pressure?
everyone has a different set point for normal and it changes over the course of the day
how are hypertension and hypotension defined?
hypertension is sustained pressure of 140/90 or higher
hypotension is systolic below 90
what types of hypertension are normal? abnormal?
transient elevation caused by fever, physical exertion and emotional upset are normal
chronic elevation is abnormal
what does chronic hypertension cause?
heart failure, vascular disease, renal failure and stroke
what are the fast, intermediate and slow ways to change blood pressure?
fast- baroreceptor reflex
intermediate- renal vascular resistance
slow- changes in renal and water excretion
describe the renin- angiotensin activation pathway
angiotensinogen is synthesized by the liver. it is activated to angiotensin I by renin (made by kidney) and is further activated to ACE in lung capillaries to angiotensin II
what are the two major effects of angiotensin II?
causes vasoconstriction to increase blood pressure and causes the adrenal cortex to secrete aldosterone
what is the effect of aldosterone?
increases water and sodium reabsorption and decreases urine volume. It also stimulates ADH release
what are the direct and indirect actions of the kidney to maintain blood pressure long term?
direct- altering blood volume
indirect- renin angiotensin mechanism
what is responsible for initiating the renin- angiotensin pathway?
macula densa cells detect decrease in sodium concentration and signal to the juxtaglomerular cells to release renin
what are the two levels of effect of the renin-angiotensin- aldosterone system on the body?
local effects and global effects
local effects are less understood but work within organs and can result in damage
what are the three determinants of renin secretion?
renal SNS are triggered by neural baroreceptors
intrarenal baroreceptors in afferent arterioles
sodium chloride delivery to macula densa
how do transplanted kidneys still function in maintenence of blood pressure?
they can function without innervation from the CNS in the release of renin
how does the NaCl sensing of the macula densa reflect blood pressure?
with low GFR caused by low blood pressure, there is increased NaCl reabsorption due to low flow rate. this decreases the delivery of sodium to the macula densa
what two effects occur with decreased macula densa NaCl reception?
increased renin release and decreased afferent arteriole resistance to increase GFR
how does angiotensin II impact GFR?
by constricting mesangial cells in the kidney to decrease surface area and reduce GFR
how does angiotensin II impact granular cells?
provides negative feedback to inhibit renin production by binding AT receptors and decreasing intracellular Ca
when does sympathetic tone have more of an influence on the kidney? does a renal nerve ablation fix this?
in resistant hypertension
there was no statistically significant difference between the sham procedure and the actual one
what three factors influencing blood pressure?
cardiac output, peripheral resistance and blood volume
what does blood pressure equal?
cardiac output x peripheral vascular resistance
what three factors influence to cardiac output?
blood volume, arterial/venous compliance and resistance to venous return
what four effectors exist for the control of sodium content of the blood?
changes in GFR driven by sympathetic nerves and angiotensin II as well as antidiuretic hormone and atrial naturetic peptide
what is pressure diuresis?
increased fluid loss from the kidney with increased blood pressure
what does the equilibrium point for pressure naturesis reflect?
an equilibrium between intake and renal output at a normal water and salt intake.
what is the effect of increased blood pressure on GFR, angiotensin levels, fluid resorption in the proximal tubule and excretion of salt and water?
increased GFR, decreased A II, decreased fluid resorption and increased excretion of salt and water to decrease blood pressure
what is a major problem with ACE inhibitors? what are they used for?
that they prevent conversion to angiotensin II in a hypotensive situation
used to prevent water retention in people with high blood pressure
other than angiotensin II, what controls aldosterone secretion?
plasma K concentration and atrial naturetic peptide
what is the effect of aldosterone? how much effect does it have?
stimulates Na reabsorption in cortical collecting tubules and collecting ducts. only increases sodium reabsorption by 1-2% (a lot of volume because of high passage of Na through those tubules)
what are the 5 major effects of angiotensin II synthesis?
increased SNS activity, increased Na, Cl and decreased K reabsorption (H2O retention), increased aldosterone secretion, arteriolar vasoconstriction and ADH secretion by the posterior pituitary
how does aldosterone change solute composition of the urine?
activates and increases synthesis of Na/K pump and other channels that transport these ions. leads to increased Na resorption and increased K secretion
what prevents over correction of other reflexes in the kidney?
tubuloglomerular feedback acts in the opposite direction to other reflexes by inhibiting the increase in renal blood flow and pressure at the glomerular capillary during high renal arterial pressure
what are two of the naturetic peptides and what are their two actions? what are they used for?
ANP and BNP
inhibit the release of renein and relaxation of afferent arterioles
used diagnostically to assess congestive heart failure
what is the function of antidiuretic hormone?
increases water reabsorption
what other hormones increase and decrease Na reabsorption?
increase- cortisol, estrogen, growth hormone, thyroid hormone and insulin
decrease- glucagon, progesterone and PTH
where are osmoreceptors located?
in the hypothalamus along the ventricles
what are the different controls of ECF homeostasis in the proximal and distal nephron components
proximal- regulates ECF based on BP (both sodium and water)
distal- two mechanisms to maintain water and sodium separately (ADH and aldosterone)
under what conditions is ADH secreted? inhibited? which prevails when they conflict?
secreted with decreased blood pressure sensed by baroreceptors (more important than osmolality)
inhibited with decreased fluid osmolality sensed by chemoreceptors
why do people get hypertension?
there is a shift of the renal function curve that impairs naturesis and increases sodium and water retention
how does obesity lead to hypertension?
hyperinsulinemia increases sodium reabsorption and smooth muscle cell proliferation (increasing vasoconstriction) also increases overall inflammation
