Cadiovascular control

Question 1

Recall how the resting membrane potential is created, and how it is calculated.

Answer 1

The membrane is impermeable to ions. There is more K+ inside and Na outside
ion channels partially open, letting K ou and Na in, creating a charge imbalance-when the chemical gradient is balanced with the electrical balance-chemoelectreical equilibirum
Use the nenrst equation for 1 ion -K -9mv and Na+66mv
Use Galdman hodkin Katz for more ions-takens into account channel opennning-with 5% K and nome Na reach -70mV

Question 2

Describe the general characteristic of cardiac (ventricular) action potential

Answer 2

Its lng (300ms), and has a long absolute refractory period (Na channel closed and blocked by current) and relative refractory period (Na imbalance in cell makes it harder to activate)
Phase 0 is the upstoke- caused by rapid uptake of naa ions. Partially due to Ca2+ intake for Ca mediated Ca opening, as Pca open
Phase 1 is early repolarisation-opening of specialised K channels cause a little dip before plateau
phase 2 is plateau-Na are refractory. L type Ca channels open and balance K+ efflux
phase 3 is repolarisation-K+ channels open slowly, then specialise Ik1 open fast once reach a certain current-cause immediate RMB. Increase in k channels allows Ca to be taken back in
Phase 4 is rmb

Question 3

Are all the action potentials similar in heart cells?

Answer 3

No-nearly all are different
His, endo cardium, Myo caridum and epicardium are similar to ventricular
But Atrial AP are very different

Question 4

What are the intrinsic electrical properties of the heart due to?

Answer 4

Sinoatrial node are capable of spontaneous generation-followed by bundle of his coordtinated popagation
SA node is linked by internodal fibres to atriventricular node and left side atrium. Atrioventriclar node delays the AP to allow filling of ventreicules, then passes the AP down to the Apex (1st to beat, then ventricular fibres to propagate along myocardium)

Question 5

What is the shape of Sinoatrial AP due to?

Answer 5

Most ion channels are the same-but different expression leads to a different prolife
Starts with Slow and long Na intake bu “funny receptors”-slow depolarisation. T type Ca (slow and rare) open-little more depolarisation ->then Ca2+ intake (L type channel, faster) causes rapid depolarisation (and necessary for muscle)-K+ open (near peak)
Ca close-K+ repolarise cell (hyperpolarise), then na start again and repeat
No Ik1-never reaches RMB, always fluctuating

Question 6

What is the main regulator of Sinoatrial contraction?

Answer 6

Sympathetric (faster) and parasympathetic (slower)
Sympathetic just shortens the wave-reaches threshold faster (from spinal nerves). Increases heart rate (chrotropy) and contractility (inotropy)
Parasympathetic makes it slower-readch threshhold slower. Uses vagus nerve -caranial nerver)

Question 7

How is impulse propagation achieved in Heart cells?

Answer 7

The cells are connexcted by gap junctions (2 connexons made of 6 connexin)-allows passage of the AP along the cells and the ions-When first one opens, passive spead through gaps allows spread

Question 8

What is flow control and how is it achieved in humans?

Answer 8

Flow control is regulation of blood flow from the heart. Flow is calculated as difference in pressure/resistance, with Vessel radius being the maine changer-2x shrink is 16 reduce in flow
2 main ways of regulating: local instinsic to SNC, and nervous system regulation/hormones (systematic

Question 9

What is autoregulation of blood flow? What are 2 theories concerning its function?

Answer 9

Autoregulation is the intrinsic capacity of SMC to constrict vessels as flow increases (or pressure increases)
Its possibly due to mygenic theory: SMC respond diretctly as pressure rises and fibres contract-strech channels activate and constirct
Metabolic theory says that as flow decreases, metabolites accumulate, causing dilation
=>probably both at the same time

Question 10

Summarise local and circulating hormone action on flow regulation.

Answer 10

Local homnoes are made by epithelium-such as NO, prostacyclins, Thromboxanes (platelets) and endohelis
Circulating such as Vasopressin, Kinnins (dilate), Angiotensin II, Noradernalin (all other constrict)

Question 11

How are the 2 main branches of the Autonomic nervous system designed

Answer 11

Sympathetic-fight or flight-mostly controls circulation. ganglions proximal to spine (and use spine nerves), use ach at ganglion and noadrenaline at target
Parasympathetic-rest and digest (control heart rate)-ganglions distal to spine and use cranial nerves or spine. USe ach at ganglion AND target

Question 12

How are blood vessels nervated? What part of the brains control this?

Answer 12

Sympathetic innervates the heart and ALL vessels except capilarries, but not every organ-mostly kidney gut spleen and skin
Noradrenaline is transmitter of choice
Its connected to vasomotor centre the medulla and power part of pons in brain stem, and is made of vasoconstrictor, avsodilateor and cardioregulator area
Many higher parts of the brain apss by the VMC-and has effects on the VMS

Question 13

How exactly does the nervous system control vessel diameter?

Answer 13

Vessels are contantly lightly constircted (muscle tone)-increase in activity constricts and decreased dilates-done by barosensors

Question 14

How is the heart innervated, especially in relation to heart rate

Answer 14

SNS and PSNS both link to sinoatrial node-and SNS increases it while PSNS decreases it. if cut SNS, decrease, and if PSNS cut, increase (so controlled constantly
The main regulator is noradrenaline-B1 GCPR camp PKA increases intake of Ca, release of Ca by SR and need for Ca per sarcomere

Question 15

Recall all the different impacts of cardiac output

Answer 15

Cardiac output is stroke volume x heart rate
Stroke volume is contolled by SNS (increase) and end diastolic volume (by sterlings law)-itself controlled by arterial pressure (venous return). Also intrathortacic pressure reduces EDV
Adrenaline ahs increase of both SV and HR
SNS also increases HR
But PSNS decreases HR

Question 16

How does the feedback loop for BP work?

Answer 16

Baroreceptors measure the BP contantly, and if not correct, control center can activate PSNS, SNS, or homones to regulate it, as Barosensors sense again
Barosensors are mechanoreceptos in carotid sinus and aortic arche (PNS afferent) and lead to efferent to sinoatrial
Mostly senses pressure changes between 60 and 180, but most sensitive around 90-100

Question 17

What is reciprocal innveration, and how does it impact PSNS and SNS regulation of HR?

Answer 17

One afferent nerve connects to PSNS and SNS-if activated, PSNS increase and decrease of HR
On the other side, connected to inhibitory interneuron, then SNS nerves-therefore activation leads to inhibition of SNS and reduced HR (and vasodilation)
for PSNS As BP rise, baro receptor stretch activates them, going to CMV, then back down reciprocal innervation
For SNS-as BP rise, similar actions but nerve from spine and ganglion close-and also goes to arteries and veins (dilating-reduce venous retun, therefore stroke volume)

Question 18

Explain and factors in controlling Arterial pressure (MAP), then repeat with hemmorhage

Answer 18

Blood volume, respiration, skeletal ,muscle pump and SNS activation increase all lead to increase in venous pressure, therefore venous return, therefore arterial pressure
In haemorrhage, BV, VP, VR EDV, SV, CO and BP goes down-barorecptor feedback leads to increase of SNS, contriction and venous pressure
SNS up and PNS down increase contractility
SNS up increase venous tone, therefore pressure, therefore return, therefore EDV
SNS increase also increase contriction, and increase total peripheral resistancce
Contractility increase Cardiac output, and with TPR increase, it lead to increase of MAP