Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
33 Cards in this Set
- Front
- Back
|
Which mechanism of blood pressure control is most important for long-term BP regulation?
|
The renal body fluid system.
|
|
|
List all of the mechanisms of BP control.
|
1. Nervous regulation- ANS:
a. Sympathetic Vasocontrictor System b. Reflex mechanisms: i. Baroreceptors ii. Chemoreceptors iii. Low Pressure Receptors iv. CNS Ischemic Response 3. Renal Body Fluid System |
|
|
What are the roles of each branch of the ANS in controlling BP?
|
1. Sympathetic NS:
-plays the most important role - primary modulator of BP (unconscious control) - Innervation of BVs: small arteries and arterioles. - Innervation of the heart. - Circulating catecholamines. 2. Parasympathetic NS: - Plays a much smaller role in BP control. - Innervation of the heart. |
|
|
Describe the vasomotor system.
|
Part of the ANS regulation.
- located in medulla - its the filter/mediator/modulator of the ANS and it affects the CV system - transmits sympathetic impulses (vasoconstrictor center) - transmits parasympathetic impulses (vasodilator center) |
|
|
What are the 3 parts of the vasomotor center of the medulla of the brain?
|
Vasoconstrictor center, cardioinhibitor center, and vasodilator center.
|
|
|
What is the major transmission chain of the sympathetic NS?
|
The sympathetic chain. It tells the ANS nerves where they need to go.
|
|
|
Describe the sympathetic vasoconstrictor system.
|
- network of sympathetic nerves throughout the body.
- maintains continuous partial constriction of the BVs= sympathetic vasoconstrictor tone. - Primary controller of the sympathetic vasoconstrictor system is the vasomotor center. - Effects mediated though: * direct innervation by sympathetic nerves * stimulation of the adrenal medulla to secrete catecholamines (NE and Epi). |
|
|
What happens in spinal anesthetic is injected high in the spinal cord? Why does this matter?
|
Within second of the injection, there's a precipitous decrease in MAP in the body. This clearly demonstrates the presence of a constant vasoconstrictor tone via the Sympathetic NS.
|
|
|
What are baroreceptors? What do they do in terms of controlling BP?
|
- most well defined nervous mech of BP control.
- stretch receptors located in large systemic arteries. - increases in BP stretches them. - Negative feedback reflex mech controls BP. - They're abundant in the carotid sinus and aortic arch. - They don't just respond to increases in pressure but also to any changes in pressure. - signals are transmitted to the medulla. |
|
|
Describe how baroreceptors respond to pressure.
|
They are not stimulated between 0 and 50-60 mmHg. At pressures above 50-60 mmHg, they are stimulated and respond to both increases and decreases in pressure. A graph of the number of impulses from the baroreceptors per second vs. BP has a sigmoidal shape.
- The steep portion of the curve indicates that there is maximal sensitivity in the physiological range: small changes in pressure provide very large changes in outputs. |
|
|
Describe the circulatory reflex involved in baroreceptor-mediated BP control.
|
High arterial pressure causes:
- increased impulses to medulla - inhibition of vasoconstrictor center Low AP has the opposite effect. It causes the AP to increase. - excitement of vagal parasympathetic center - decrease in BP: due to decrease in peripheral resistance and decrease in CO. Bottom line: pressure goes up and baroreceptors bring it down. Pressure Buffer Function: 1. Primary purpose is to reduce the minute by minute variation in BP. 2. Baroreceptors either increase or decrease BP. |
|
|
What happens when baroreceptors are denervated?
|
The organism loses its ability to buffer changes in BP, leading to widely fluctuating BP. This experiment demonstrates the exquisite second-second conrol that baroreceptors offer for organisms.
|
|
|
What are chemoreceptors? How do they affect BP?
|
- closely associated with baroreceptors.
- located in carotid arteries (carotid bodies) and aorta (aortic bodies). - sensitive to low oxygen, elevated CO2 and H+ ions. - excitation of chemoreceptors stimulates the vasomotor system. At low BP (<80 mmHg): - decreased blood flow in chemoreceptors - decreased O2, increased CO2 and H+ - increase impulses to medulla (same pathway as baroreceptors) - excites the vasomotor center to increase BP, i.e., a relative decrease in parasympathetics and increase in sympathetics. - causes an increase in BP - not a fine tune mechanism for controlling BP on a second-to-second time span (like baroreceptors), but more of a fight or flight mechanism |
|
|
List the reflex mechanisms that control BP in order of importance.
|
1. baroreceptors
2. chemoreceptors 3. low pressure receptors 4. CNS ischemic response |
|
|
What are low pressure receptors?
|
- similar to baroreceptors
- stretch receptors located in the atria and PA - reduce BP variations in response to changes in blood volume - reflexes parallel baroreceptors response |
|
|
How does the CNS Ischemic response help to regulate BP?
|
- Vasomotor mediated
- low BP (<60 mmHg) sensed (=ischemia) - potent excitation of vasomotor center - on of the most powerful activators of the sympathetic vasoconstrictor system - emergency control system - not usually involved in normal BP control, but is the ultimate fight or flight response and often occurs physiologically in the OR to compensate for decreased BP. |
|
|
What is dominant mechanism for long-term BP control?
|
The renal body fluid system.
|
|
|
Describe the Renal Body Fluid System.
|
- Dominant mech for long-term BP control
- ECF volume is maintained by this system - Balance btwn intake and excretion of NaCl and water by the kidney - Infinite gain feedback control system (this system never quits as long as the kidney remains healthy--it will keep doing its thing until it reaches some desirable set point). - Simple system: * Too much fluid causes AP to rise--> kidneys excrete excess fluid and salt. * Too little fluid causes AP to fall --> kidneys excrete less fluid and salt. - Extracellular fluid volume is a balance btwn intake and output - interrelation between cardiac, renal, and vascular function - kidney function is central - Infinite gain feedback system |
|
|
Describe the feedback mechanisms of the renal body fluid system.
|
* Renal excretion or pressure natriuresis:
- increase urinary output in response to BP elevation * Renin-Angiotensin System: - modulator of renal excretion of salt and water |
|
|
Describe the renal urinary output curve.
|
Pressure Natriuresis:
- shows the approximate average effect of different BP levels on urinary volume by an isolated kidney - increases in BP increases both urine and sodium output= Pressure Natriuresis - At a BP of 50 mmHg, the urine output is essentially zero. - At a BP=100 mmHg, urine output is normal. - At a BP=200 mmHg, urine output is about 6-8x normal. - Infinite gain feedback: * Increase TPR causes increase in BP * Urinary output increases until BP is normalized. |
|
|
Describe the graphical analysis of renal body fluid mechanism.
|
* The major determinants of long-term arterial pressure control:
- based on renal function curve - salt and water intake line * equilbrium is where intake and output curves intersect. |
|
|
Describe the Renal Urinary Output Curve.
|
* Infinite Gain Feedback:
- increased TPR causes increase BP - Urinary output increases until pressure is normalized. |
|
|
How does TPR fail to elevate Arterial Pressure in the long run?
|
- Changes in TPR do not affect long-term AP level.
- One must alter the renal function curve in order to have long-term changes in AP. - Changing renal vascular resistance does lead to long-term changes in AP. |
|
|
Describe the Renin-Angiotensin System.
|
- A powerful neurohormonal mechanism for controlling AP.
- When AP falls, detected in the kidney (JG cells), which then secrete Renin (an enzyme). - Renin acts on angiotensinogen in the plasma, causing the release of angiotensin I. - Angiotensin I is then acted on by an enzyme called converting enzyme (in the lung) to release Angiotensin II, which has remarkable effects on the body. |
|
|
What are the effects of Angiotensin II?
|
1. Primary Effect: Vasoconstriction:
- throughout the body rapidly - primarily in the arterioles, but also in veins - increases TPR and therefore AP 2. Secondary Effect: decreased excretion of salt and water by kidney, thereby increased fluid volume in the extra- and intra-vascular spaces. |
|
|
How is Angiotensin II formed?
|
- Renin is synthesized and stored in modified smooth muscle cells in afferent arterioles of the kidney.
- Renin is released in response to a fall in pressure. - Renin acts on a substance called angiotensinogen to form a peptide called Angiotensin I. - Angiotensin I (AI) is converted to Angiotensin II (AII) by a converting enzyme located in the endothelial cells in the pulmonary circulation. - AII then causes vasoconstriction and renal retention of salt and water in order to increase AP. |
|
|
How is AII inactivated?
|
By Angiotensinase.
|
|
|
Describe the actions of the Renin-Angiotensin System/
|
- Causes vasoconstriction
- Causes Na and fluid retention by direct and indirect acts on the kidney - Causes rightward shift of the renal function curve, which increases AP |
|
|
What happens to BP if a hemorrhage occurs, causing BP to initially drop, in the presence and absence of the Renin-Angiotensin System?
|
In an intact system, BP is allowed to return back to its steady-state level, and the time course for the system are quite rapid (w/in 30 min or so). Without the R-A System, BP does not return to normal.
|
|
|
What is the effect of Na+ intake on the RAS?
|
- RAS is important in maintaining a normal AP during changes in Na+ intake.
- As Na+ intake is increased, renin levels fall to near zero. - As Na+ intake is decreased, renin levels significantly increase. - RAS causes the Na+ loading renal function curve to be steep. Increased Na+ intake--> increased extracellular volume--> increased arterial pressure --> decreased renin and angiotensin--> decreased renal retention of salt and H2O--> return of extracellular volume almost to normal --> return of arterial pressure almost to normal |
|
|
Which factors decrease renal excretory function and increase BP?
|
- Angiotensin II
- Aldosterone - Sympathetic NS activity - Endothelin |
|
|
Which factors increase excretory function and reduce BP?
|
- Atrial natriuretic peptide (ANP)
- Nitric Oxide (NO) - Dopamine |
|
|
Describe the integration of BP control.
|
* Several different mechanisms.
* Feedback Control Systems are time-dependent: - baroreceptors: powerful buffers that respond very quickly and adapt quickly, too. - Renal-Body Fluid System: unimportant in acute control, but extremely powerful over days. |
