Blood pressure control Flashcards
Blood pressure rises slowly with increasing age. Since cardiac output stays relatively constant over time, what causes the increase in BP?
Increase in total peripheral resistance
What neuronal entities are responsible for short term regulation of blood pressure? Explain why these are only good for sensing short term changes and not long term changes.
What is feedback gain?
Baroreceptors and chemoreceptors
Baroreceptors are only good for the short term b/c of adaptation: they get used to an env of raised BP and so it would take an even higher increase in blood pressure to get the receptors to sense any changes
Feedback gain: the degree to which the blood pressure is returned back to normal (change in pressure/difference after correction)
Where are the 2 locations for the baroreceptors and what is different about what they do?
The carotid sinus and the aortic arch.
Carotid sinus baroreceptors: involved in maintaining regular/normal BP
Aortic arch receptors: only involved when BP rises significantly (i.e. by 20-30 mmHg)
The vasomotor center is the point in the brainstem where the signals coming from the baroreceptors splits into the X and Y, where X controls sympathetic outflow and Y controls parasympathetic outflow to the heart and blood vessels.
Vasoconstrictor and cardioinhibitor
Vasoconstrictor: sympathetic
Cardioinhibitor: parasympathetic
Describe the relationship between the firing range of the baroreceptors and arterial BP
Basically, the receptors have a higher firing rate at higher blood pressures
The point of maximal inflection is the point at which the receptors are most sensitive to changes in BP (maximal buffering occurs within that range)
Describe the “pressor” response to a decrease in blood pressure (outline the sequence of events).
What happens when the pressure falls to activate the medulla? What are the effects of sympathetic activation on the heart, arterioles and veins? What is the ultimate goal of the pressor response?
T/F: Excitatory emotions have the effect of inducing sympathetic activity and raising blood pressure levels
low blood pressure >> decreased baroreceptor firing >> increased medulla NTS activity >> activation of sympathetic response
Veins: decrease compliance >> decreased capacitance
Arterioles: increased resistance
Heart: increased contractility >> increased HR (increased CO)
Ultimate goal = raise blood pressure back to normal levels
True. Excitatory emotions (as well as stress etc) have the ultimate effect of raising BP. The only difference is that the cerebral cortex is stimulated >> hypothalamus stimulated >> medulla NTS activated (the rest = what’s described above)
Describe the “depressor” response to an increase in blood pressure (outline the sequence of events).
What happens when the pressure falls to activate the medulla? What are the effects of sympathetic activation on the heart, arterioles and veins? What is the ultimate goal of the depressor response?
high blood pressure >> increased baroreceptor firing >> decreased medulla NTS activity >> dampening of sympathetic response
Veins: increase compliance >> increased capacitance
Arterioles: decreased resistance
Heart: decreased contractility >> decreased HR (decreased CO)
Ultimate goal = reduce blood pressure back to normal levels
Describe the CNS ischemic response. When is this response most active.
CNS ischemic response: when intracranial pressure in the CNS is high, blood flow is reduced and blood pressure increases. (the goal at the end of the day is to increase BP >> increase HR >> increase blood flow to the brain)
The response is most active when blood flow to the brain is compromised.
Outline the renin-angiotensin-aldosterone system
What is the significance of the RAAS system in hemorrhage?
Maintains blood pressure and prevents shock
Describe the Atrial Natriuretic Peptide System
T/F:Positive emotions help to decrease blood pressure.
True. Too bad we don’t believe in that nonsense.
What does this graph demonstrate? (what is the effect of renin and angiotensin 2 on blood pressure regulation)
REnin and angiotensin work to absorb Na+ normally and maintain BP by shifting the renal function curve left or right as necessary
T/F: The renal function curve for all hypertensive patients will be shifted rightwards only for patients who are salt sensitive.
Falsehood. The curve as a rightshift for all hypertensive patients, regardless of their salt sensitivity. Salt sensitve pts: bp changes if salt intake is reduced; non salt sensitive pts: even if salt intake is reduced, BP stays same
What is the effect of Angiotensin 2 on the brain and the vasculature in maintaining BP? Which one of these mechanisms is more important for LONG TERM BP regulation?
On brain >> promotes thirst >> increased water intake; upregulation of ADH/AVP/Vasopressin >> increased water reabsorption
On vasculature>> vasoconstriction
The effect on the brain is more important for long term BP control (seoarate hypothalamic pathway promotes vasoconstriction)
Outline the pathway connecting Ang 2, Aldosterone, and Ouabain that gets activated and raises BP
Immediate effect when BP is low:
Circulating Angiontensin 2 >> SFO >> promotes Ang 2 signaling >> stimulates parvocellular paraventricular nucleas >> stimulates brainstem to send sympathetic output to periphery >> raises Blood Pressure
Chronic effect: Ang 2 signaling promotes Aldosterone secretion >> (also circulating aldosterone) aldosterone binds to mineralocorticoid receptors >> opens ENaCs >> promotes EO secretion >> EO further stimulates parvocellular paraventricular nucleas >> stimulates brainstem to release sympathetic outflow to periphery >> raises blood pressure
