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1

How is MAP calculated using syst/diast BP?

Diastolic + 1/3 (syst-diast.)

2

How is MAP calculated or what are its components?

MAP=COxSVR

3

How is Cardiac output calculated?

CO=HRxStroke volume

4

What determines Systemic vascular resistance?

SVR is determined by vessel diameter (resistance is inversely proportional to 4th power of vessel radius).

5

What affects vessel diameter?

Vessl diameter is affected by vessel anatomy (atherosclerosis, etc), as well as neurohumoral factors.

6

What affects stroke volume?

Stroke volume is determined by force of contractility (inotropy) as well as preload (how much blood enters the heart) which is affected by blood volume and venous compliance.

7

What are the 3 types of short term control of arterial pressure?

high pressure Baroreceptors, low pressure baroreceptors, and chemoreceptors

8

Explain how high pressrue baroreceptors work including the different nuclei in the brain and all the affects of it.

There are baroreceptors in the carotid sinus and in the aortic arch. With an increase in AP, they increase their firing velocity to stimulate the NTS. The carotid sinus fires through glossopharyngeal and the aorta through the vagus. From there, the NTS neurons stimulate neurons in the caudal venterolateral nucleus and these neurons inhibits neurons in the rostral venterolateral nucleus which decreases their sympathoexcitatory output. This results in less sympathetic activity. The NTS neurons also project to the RF and the dorsal motor nucleus of the vagus which results in less symp. activity and greater parasymp. output.

Therefore, overall, you'll get decreased heart contractility, decreased heart rate, and decreased constriction of blood vessels resulting in decreased MAP.

9

How do low pressure baroreceptors work? What is the net effect?

They are located int he atrium and large veins and are sensitive to changes in volume. When they sense stretch (greater volume), they send signals to hypothalamus which leads to less ADH. Less ADH leads to less water readsorption and thus less blood volume and lower MAP.

10

Where are the chemoreceptors located? What do they respond to? What is their affect?

Located in the carotid body next to the carotid sinus. These receptors respond to changes in levels of tissue CO2, pH levels (i.e. H+ ion concentrations) or reduced pO2 levels causing increased respiration and arterial pressure.

11

Explain the effects of the parasympathetic nervous system on arterial pressure.

The major neurotransmitter of the parasympathetic nervous system is acetylcholine. There are two

receptor subtypes in the PNS – muscarinic and nicotinic receptors. Most of the effects of the PNS

are non cardiovascular (glands, GI tract etc) but it is very important in controlling heart rate and

contractility. The heart is always under “vagal” tone. The vagus nerve is the major

parasympathetic input to the heart and if this nerve is cut, heart rate increases immediately

showing that the PNS is instrumental in causing cardiodeceleration and decreasing cardiac output.

Cardiac effects are mediated by the dorsal motor nucleus of the vagus (DMNX) and the nucleus

ambigious (NAmb). Parasympathetic activity will reduce heart rate (negative chronotropic effect)

and decrease conduction velocity in the sinoatrial (SA) and atrioventricular (AV) nodes of the

heart. Parasympathetic activity will also reduce atrial and ventricular contractility (negative

inotropic effect).

12

Explain the pathway of the SNS's effect on AP. What are the main effects?

Descending axons from the RVLM project to the intermediolateral cell column in the thoracic and

upper lumber spinal cord. They activate sympathetic preganglionic neurons that project to the

paravertebral or perivertebral ganglia to activate post-synaptic sympathetic neurons by releasing

acetylcholine. These neurons in turn project to the vasculature and the heart and release

norepinephrine.

i)vasoconstriction both arterioles and veins​
ii) cardioacceleration – chronotropy (rate), inotropy (force), dromotropy (conduction velocity) – tachycardia​
iii) reciprocal inhibition of parasympathetic vagal signals to heart

13

Explain how the effects on AP of the SNS occur?


Constriction of veins (α1,) – increased venous return incr. CO and incr.   AP​

Heart Rate and contractility (β1) – incr. CO  incresed AP (β2 – Epi)​

 Contraction of peripheral arterioles (α1) – incr. SVR  incr. AP​

Powerful response to acute insults – e.g. blood loss

14

Explain how NE and E affect AP and how they are released?

The adrenal medulla is innervated by sympathetic nerves that, when activated, cause the release of

epinephrine and norepinephrine into the circulation. Epinephrine accounts for approximately 80%

of the catecholamine content of the adrenal medulla. Epinephrine is active at all adrenergic

receptors (α1, α2, β1, β2) whereas norepinephrine is only active at α1, α2, and β1 receptors. The

major cardiovascular effects of epinephrine and norepinephrine are much the same in that both

arteries and veins constrict (α1) and heart rate and contractility increase (β1, β2). One exception is

that vascular beds in skeletal muscle express β2 receptors that when activated by epinephrine lead

to vasodilation in those beds. This is important during exercise to ensure adequate blood flow to

skeletal muscle.

15

Where is ADH formed? What isanother named? Where is it secreted into the blood? What are its receptors? What occurs at each receptor and how does that affect AP? Which is more important for AP? How is its release stimulated?

Vasopressin – Anti Diuretic Hormone (ADH)​
Octapeptide formed in hypothalamus – transported to posterior pituitary (neurohypophysis) from where it is secreted into the blood.​

Receptors – V1, V2 ​

Actions: ​

1) Potent vasoconstrictor (V1) but not thought to play a major role in normal (physiological) AP control as only minute quantities released – important pathophysiologically e.g. hemorrhage circulating levels incr – AP​

2) Anti-diuretic effect (V2) more important physiologically – enhances the permeability of collecting ducts in kidney – incr H2O reabsorption into vascular system; incr. blood volume incr.  CO and incr.  MAP ​

ADH – stimulated by an increase plasma osmolality or decrease in AP​

16

What is ANP? Where is it released from? When is it released? What pathologic condition is it associated with? What are its effects?

atrial Natriuretic Peptide – ANP​

28 amino acid peptide ​
Released from specialized atrial myocytes in response to atrial stretch (caused by incr. extracellular fluid volume)​
Actions:​
Vasodilation – particularly in the kidney​
Inhibition of renin secretion in renal arterioles​
Inhibition of aldosterone secretion (adrenal medulla)​
Inhibition of vasopressin secretion (pituitary)​
Inhibition of sodium reabsorption by kidney​
Net effect – incr. sodium excretion,  incr.GFR,  incr. urinary volume   incr. H2O loss and ultimately decr.  Blood Volume​

Elevated levels of ANP are associated with Heart Failure​

17

What is the RAAS? How does it work? What receptors are involved? Explain the pathway including all the enzymes involved and where they're released from and each of their effects?

Renin – produced by kidney and released into circulation in response to  perfusion pressure, renal sympathetic nerve activity or plasma osmolarity ( Na+ flux across macula densa) ​

Angiotensinogen – plasma glycoprotein, (α2-globulin) produced and released into circulation by liver – cleaved by Renin – Angiotensin-1 (decapeptide) ​

Angiotensin-1 – inactive at vasculature – cleaved by Angiotensin Converting Enzyme (ACE; located on endothelial cell surface) – Angiotensin II (octapeptide)​

Angiotensin II – potent vasoconstrictor​

receptors – AT1, AT2 – GPCR – stimulates PLC and Ca2+​

Actions: AT1​

incr. vasoconstriction arterioles>veins​
 incr. norepinephrine overflow from sympathetic nerves​
 enhance norepinephrine’s (and other vasoconstrictors) effect​
 decreased Renin secretion​
 increased thirst via central activity ​
increased aldosterone and vasopressin (ADH) secretion -  increased Na+ reabsorption by proximal tubule of kidney ​
​Net effect is to increase fluid volume and AP​

Actions: AT2​

vasodilation –  NO and PG release from endothelial cells ​

18

What is angiotensin (1-7)? What are its actions? Where does it come from?

Angiotensin (1-7) – metabolite of ACE 2 activity on Angiotensin I​

Actions:​
1) vasodilation via AT2 and Mas receptor - stimulation of NO and PG​
2) may act as an antagonist to Angiotensin II at AT1​
3) inhibits sympathetic nerve outflow​

19

What are 2 effects of angiotensin II on arterial pressure? What are the different mechanisms?

Angiotensin II – acts directly on kidneys – decr. excretion of Na+ and H2O -->incr. extracellular volume –  incr. Arterial Pressure (hours-days)​

Angiotensin II – incr. aldosterone release from adrenal gland – acts on kidney to incr.Na+ reabsorption – can continue over days​

Interactions between RAS and aldosterone and  renal fluid mechanisms are extremely important in long term regulation of AP.