Vascular Physiology 2 Flashcards
effects of the parasympathetic nervous system on the CV system
*parasympathetic nervous system responds chiefly when there is an INCREASE in BLOOD PRSSURE
*the increased blood pressure causes more nerve impulses
*the CNS inhibits the sympathetic system and increases signals down the vagus nerve
*parasympathetic system decreases heart rate by slowing automaticity and slowing the conduction velocity through the AV node (decreased dromotropy)
M2 acetylcholine receptor → decreased CO by lowering heart rate
*the binding of ACh to muscarinic receptors decreases automaticity (→ chronotropy) and decreases dromotropy
*by decreasing CO through lowering the heart rate, the parasympathetic system through the muscarinic receptor activated by the vagus nerve hopes to decrease blood pressure
*note that the arterioles cannot be directly stimulated by the parasympathetic nervous system
atrial stretch receptors
*a decrease in atrial stretch (i.e. volume depletion) results in increased RAS activity and increased vasopressin
*an INCREASE in atrial stretch results in release of atrial natriuretic peptide (ANP)
ventricular tension receptors
*an increase in ventricular stretch/tension results in release of B-type (Brain) natriuretic peptide (BNP)
*has similar action as ANP except BNP lasts longer
BNP and ANP - overview
*BNP: B-type (brain) natriuretic peptide
*ANP: atrial natriuretic peptide
*act at several sites:
1) renal:
-get rid of sodium and fluid through urine
-inhibits renin release
2) adrenal:
-inhibits aldosterone release
3) heart:
-prevents maladaptive hypertrophy
4) blood vessels:
-relaxes both arterial and venous tone
*net results: DECREASED PRELOAD & DECREASED AFTERLOAD
natriuretic peptide receptor
*leads to vasodilation through activation of guanylyl cyclase → INCREASED cGMP
*natriuretic peptides are broken down by the enzyme Neprilysin
*several different types of ANP/BNP receptors
cyclic GMP - overview
*inhibits Ca2+ influx into cell
*hyperpolarizes the cell
*stimulates myosin light-chain phosphatase to break myosin-actin bonds (decrease vasoconstriction)
systemic vs. local vascular control
*by vasoconstricting, the sympathetic system preferentially shifts flow to those areas where the metabolism causes vasodilation
*by raising blood pressure, you further increase the flow to those areas which are vasodilated due to metabolic need
*with sympathetic activation, beta-2 increases blood flow to liver (increase glucose and triglyceride availability) and skeletal muscle to support “fight or flight” response
vascular tone
*a general term used to denote the general contractile state of a vessel or a vascular region
*an increase in arteriolar tone is automatically taken to mean a decrease in arteriolar vessel diameter, which increases arteriolar resistance and decreases flow
*basal tone in the arterioles is a critical factor for determining SVR
myogenic response
*as transmural pressure increases, arterioles respond both passively and actively:
-an increase in internal pressure results in mechanical dilation
-followed by a mechanical constriction, which may completely reverse the initial distention
*the opposite occurs when there is a decrease in internal pressure
autoregulation of blood flow
*an abrupt increase in blood pressure is normally accompanied by an initial increase in organ blood flow, which then gradually returns toward normal, in spite of elevated blood pressure
*the subsequent return of FLOW to normal levels is caused by a gradual INCREASE in active ARTERIOLAR TONE (constriction), which INCREASES RESISTANCE to blood flow
*ultimately, a new steady-state is reached with only slightly increased blood flow
*PURPOSE: to maintain a CONSTANT FLOW OF BLOOD, regardless of what the blood pressure is
local metabolic influences on arteriolar tone: OXYGEN
*as oxygen saturation decreases, the blood flow INCREASES
*in systemic vascular beds, a vascular region starved for oxygen causes VASODILATION of the arteriole
*this vasodilation of the “feeding” arteriole lowers the resistance, which increases blood flow to this area in need of more oxygen
local metabolic influences on arteriolar tone: METABOLITES
*as the rate of metabolism in a particular organ increases, the blood flow to that organ increases to meet the needs
*as metabolism increases, the tissue levels of certain ions and products of metabolism change:
-increased CO2, H+ (more acidic), K+, ADP, adenosine)
*as these levels change, the arterioles dilate to provide more oxygen to this area and remove products of metabolism
adenosine & adenosine receptor
*adenosine is a very powerful VASODILATOR
*as metabolism increases, adenosine gets released and → vasodilation
*A2A is the adenosine receptor:
-increases cAMP by Gs protein signaling, which then inhibits the myosin light chain kinase, which ultimately prevents myosin-actin cross-bridge formation
*DECREASES VASCULAR RESISTANCE (vasodilation)
hyperemia
*hyperemia (HIGH FLOW) is the phenomenon of increased organ blood flow to increased products of metabolism
*active hyperemia is in response to local metabolic vasodilator feedback on an arteriolar smooth muscle as a result of increased metabolic rate
*REACTIVE hyperemia is in response to a transient period of arrested flow