BP Regulation: Hormone Control Flashcards
Neuronal control of Bp?
1) regulate CO via SV & HR by changing preload and contractility
2) controls distribution of blood between body and heart
3) re-allocate the CO from ischemic tolerant organs to critical organs
4) regulate EDV (preload)
Hormonal control of BP?
1) catelchoamines
2) Neuronotic Peptides (ANP/BNP)
3) Renin-Angiotensin- Aldosterone system
4) Anti-Diuretic hormone (vasopressin)
What is the sympathy-adrenal system and what does it respond to?
- when SNS fires onto adrenal medulla (on top of both kidneys) and causes releases of catelchoamines
- in response to stress, exercise, hypovolemia, hypoglycemia
How does norepinephrine effect the body?
- preferentially acts on alpha 1 receptors, causes vasoconstriction in skin/gut arterioles
- can work on beta 1 receptors of SA & myocardium to promote increased HR, contractility, and diastolic reaction
how does epinephrine effect the body?
1) preferentially acts on beta 1 in SA & myocardium
2) can work on beta-2 and cause vasodilation in heart & sk muscles, main effect though is metabolic not vasculutre
3) pharm doses can act on alpha 1, causes systemic vasoconstriction to increase SVR & arterial pressure
Ionotropic agent
affects contractility
lusiotropic agent
affects diastolic relaxation (positive increases, negative decreases)
Adrenal gland structure/histology and secretions? (2 main structures)
- located at top of kidneys has outer cortex & central medulla
- medulla- secretes catelchoamines
- zona glomerulosa: secretes aldosterone in response to AT-II
- zona fasciculata: secretes cortisol in response to ACTH from pituitary
How do heart transplants experience increased HR and contractility during exercise w/o innervation from SNS or PNS?
-due to catelchoamine release during exercise from the adrenal medulla
hormone vasoconsctiors?
- NE binds alpha 1, promotes constriction in gut/skin
- AT-II initiates vasoconstriction when released
- ADH-vasopressin
hormonal vasodilators?
-Epi acting on Beta-2 receptor prominent in heart & sk. muscle for fight/flight response
What is the Natriuretic peptide family?
-fam of peptides that promote exertion of Na and urine
-consist of ANP and BNP both in cardiac myocytes
-are cardiopulmonary vol receptors, decrease SNS when activated
-
How are natriuretic peptides activated? What else is activated in this process?
- when cardiac myocytes are over stretched (hypervolumia) ANP/BNP released to tell body have too much blood/pressure
- hypervolumia also stimulates cardiopulmonary vol receptors to decrease SNS
What are renal & vascular effects of ANP/BNP release?
1) inhibit RAA to increase Na and urine excretion
2) causes vasodilation & decreased SVR
3) decrease salt & h20 appetite & ADH secretion
* ANP/BNP= Anti-RAA, do everything to decrease blood volume by decreasing the BP
Natriuresis? Diuresis?
- Naturesis= Na excretion
- Diuresis= urine output
CHF patients and natriuretic peptides?
- have significantly elevated ANP/BNP since have poor kidney profusion due to poor heart functioning
- kidneys take poor profusion as sign of low BP and BV so excrete less fluid to increase preload
- now heart OVERFILLED (hypervolumia), myocytes stretching & releases ANP/BNP
What does anti-diuretic hormone (vasopressin) do?
- regulates H20 permeability of kidney distal tubule & collecting ducts
- causes decreases urine output, vaso/venoconstriction both compensatory for hypovolemia, hypotension & plasma hyper-osmolarity
What controls ADH release?
1) hypotension (from medullary CV center)
2) hypovolemia (atrial vol receptors)
3) plasma hyperosmolarity (hypothalmic osmoreceptors)
* plasma= strongest signal for ADH release*
Renin-Angiotensin- Aldosterone (RAA) System? How activated?
- a hormone cascade that increases BP & blood volume
- activated in response to hypotension, hypovolemia, SNS activity
What RAA mechanisms?
a) decreases arterial pressure causes JG cells to release renin
b) proteolytic enzyme renin cleaves angiotensinogen–> AT-I
c) AT-I –> AT-II via ACE converting enzymes in lungs
d) AT-II acts on hypothalmus to stimulate thirst & aldosterone release from adrenal cortex
AT-II effects (6)?
a) vasoconstriction
b) increase brain thirst response
c) aldosterone release from adrenal cortex
d) ADH secretion from pituitary
e) increased SNS
f) increase Na/ H20 retention
aldosterone effects?
-released from adrenal cortex, causes decreases urine output by increases Na and H20 reabsorption
Juxtaglomerular Renal Barorecrptors and main goal?
- JG cells (juxtaglomerular cells) compose juxtaglomerular apparatus (JGA)
- they are in afferent renal arterioles & deceit changes in wall dissension or Renal Perfusion Pressure
- release renin is response to hypovolemia, hypotension or increased SNS signaling
-to increase BP back to normal
JG cells release?
1) renal hypoperfuson (decreased MAP) causes JG cells to release renin
2) Hypotension in body causes SNS activation & it stimulates JG cells to release renin
- when blood flow & pressure restored, JG cells loose stretch & SNS signals and release is halted
- this
1) lisinopril
2) losartan
1) ACE inhibitor (pri=ACE inhibitor); AT-I can’t convert to AT-II so RAA response blunted
2) angiotensin receptor blocker (ARB); (artan= ARB)
- similar effects as ACE inhibitor
what happens if have persistent RAA activation?
-results in hypertension
What is shock? 4 types of circulatory shock? common feature for all of them?
- shock= when BP is inadequate to support critical organs
1) cariogenic shock
2) hypovoluminc
3) obstructive
4) distributive - all have common feature of atrial hypotension
cariogenic shock
- issue w/ hearts ability to contract (decreased contractility)
- due to MI, ischemic heart disease, arrhythmia causing uncoordinated ventricle contraction
Hypovolumic shock?
- inadequate filling of heart due to low EDV (preload), not enough blood to fill vessels
- due to hemorrhage (also called hemorrhagic shock)
obstructive shock?
- when heart can’t contract (Cardiac tamppenade) or when have a pulmonary embolism (obstruction) so blood flow is blocked
- only 2% of shock cases
distributive shock
- lumps together septic and anaphylactic shock, is when CO is normal but loose SVR
- most common type of shock
septic shock
-gram negative bacteria release endotoxins, causes macrophages to release cytokines that cause systemic vasodilation & failure of SVR
anaphylactic shock
- allergic rxt causes cytokine release that increases mast cell granulation and causes vasodilation & a loss of SVR
what are the effects of arterial hypo perfusion?
a) brain:altered mental status/ thirst
b) skin: cool, clammy, since baroreflex diverting blood from skin
c) kidney: oliguria (few urine), baroreflex causes blood to divert from kidneys so retain fluids
d) heart: tachycardia due to baroreflex trying to increase CO
how long until brain/heart, kidney/lung/liver, and sk. muscle/gut/skin have irreversible ischemic damage?
a) brain/heart: 2-5 min
b) kidney/lung/liver: 120-150 min
c) sk muscle, gut, skin= 360-600 min
4 stages of shock (due to blood loss)?
a) compensated (initial)
b) compensated (non-progressive)
c) decompensated
d) irreversible
compensated (initial) shock?
- loose 0-15% of blood volume
- may have no symptoms
- compensatory systems activated and working
- MAP drops below 5mm HG
- -treat aggressively,s top bleeding, keep warm, give fluids & O2
compensated (non-progressive) shock?
- loose 15-25% of blood volume
- compensatory mechanisms are failing
- thirsty
- anxious, restless weak
- cool, clammy skin
- decreased PP
- tachycardia/tachypena
- treat aggressively,s top bleeding, keep warm, give fluids & O2
decompensated shock
-25-35% blood volume lost
-absent or weak pulse
-altered mental status (maybe unconscious)
-acidosis
-slow breathing
-toxin accumualtion
is reversible if act quickly if not start positive feedback spiral towards death
irreversible
- organ failure
- heart failure
- collapse of SVR
- widespread cell death
- is a positive feedback spiral that instigated by low MAP and propagated by low MAP to cause even lower MAP and lead to death since organs no longer professed*
how is blood volume restored after hemorrhage?
- renal fluid conservation
- drink water (thirst)
- transcapillary refil
