Physiology Stuff Flashcards
Increased gap junction uncoupling would
Decrease conduction of a signal through muscle.
This is not promoted by sympathetic stimulation
Aortic pressure during ejection is greater when
In protodiastole
Nicotinic receptor are where?
Muscarinic?
- at junction of prenganglionic and postganglionic psns and sns.
- muscarinic is released at junction of postganglionic and effector cells
Overdrive suppression (TA slides)
increased extracellular potassium is thought to decrease membrane potential (make more negative) in the pacemakers cells that are being suppressed. These pace making cells will not fire as they are further away from threshold
About funny current (TA slides)
E. Although we don’t know exactly why or how, the funny current contributes to the firing of the SA nodal AP.
Funny current is not connected to any single ion species. It is the difference in inward and outward current leading up to the AP.
LAyers of arterioles, muscular arteries and elastic areteries
Arteriole 1-5 layers, muscular artery up 6-40 layers, elastic artery 40-60 layers
veins or arteries have thicker tinuca intima?
typically arteries have a thicker intima with a more prominent IEL
angiotensin II. tell me about it
Although angiotensin II mostly regulates blood pressure in the long term, the sharp decrease in renal blood flow due to decreased arterial blood pressure will cause a large rise in angiotensin II which will actually help increase blood pressure in an emergency situation like a hemorrhage.
Atropine
is an inhibitor of PSNS neurons
are there no cholinergic neurons outside of the sacral/cranial parasympathetic ganglia
yes!
There are specialized cholinergic neurons in skeletal muscle which respond to sympathetic stimulation causing an increase in flow (along with beta 2 receptors)
Things about the SA nodal AP
- The Na-Ca Exchanger (NCX) is responsible for depolarization.
- The frequency of depolarization is affected by autonomic and metabolic signals
- Depolarization is facilitated by a pre-AP spike in Ca2+
- Phase 4 is characterized as a period of instability due to a gradual voltage rise.
Increased local blood flow after a period of vascular occlusion is referred to as:
Reactive Hyperemia via shear stress induced vasodilation