BP Regulation: Hormone Control Flashcards
(41 cards)
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
