Regulation of Arterial Pressure Flashcards
Regulation of Arterial Pressure
- Regulation of arterial pressure is accomplished by a complex system of positive and negative feedback involving multiple nervous and hormonal systems, to achieve a mean arterial pressure that allows for adequate nutrient delivery to all tissues at all times
- At critical flows / pressure levels, blood will be shunted to the organs systems most critical for life, the CNS, heart and kidneys
- Maladapations of the systems which control arterial pressure are a very common in clinical practice
- Regulation of arterial pressure, at the most basic level, is determined by two intertwined variables, Cardiac Output (C.O.) and Total Peripheral Resistance (TPR)
Nervous Control of Arterial Pressure
– An Autonomic Function
– Responsible for very rapid changes in arterial pressure, crucial to survival
Baroreceptors
o Located in walls of carotid sinus and aortic arch
o Baroreceptors act as mechanoreceptors, transducing pressure and pressure changes, to nervous action potentials which are transmitted to the CNS
o Baroreceptors are sensitive to:
- Changes in pressure
- Rate of change of pressure
Baroreceptor Reflex Sequence
- Baroreceptor stimulation ->
2 Nervous impulse carried via cranial IX & X to medulla and pons ->
- Medulla / Pons direct regulation of blood pressure via autonomic nervous system modulating parasympathetic / sympathetic outflow to heart, and blood vessels. (Heart rate / contractility increased or decreased; the level of sympathetic “tone” to arterioles and venules causes contraction / relaxation of vascular smooth muscle.
Chemoreceptors
CNS Chemoreceptors react to levels of O2, CO2, and pH in blood and CSF. Stimulation of these receptors results in modification of sympathetic or parasympathetic outflow modifying blood pressure.
Nervous Control of Arterial Pressure : Pathophysiology
- Acute hemorrhage
- Autonomic disreflexia, aka. autonomic hyperreflexia (higher spinal cord injuries, multiply sclerosis)
- Acute hypertension resulting from intracerebral bleed
- Brain stem damage resulting in wild BP fluctuation
- Orthostatic hypotension may result from lesions of brain stem
- afferent neuron disease, peripheral neuropathies (diabetes mellitus, alcoholic neuropathy, tabes dorsalis)
- Autonomic insufficiency - efferent connections spinal cord disease
Hormonal Control of Blood Pressure
Renin – Angiotensin – Aldosterone System
- A hormonally mediated system
- Components:
o The slower component of blood pressure control regulates blood volume, thereby affecting arterial pressure (hours to days)
o A faster component (not nearly as fast as autonomic control) is mediated through hormone induced vasoconstriction
oUnderstanding this system is of major importance in evaluation and treatment of hypertension and congestive heart failure
Hormonal Control of Blood Pressure : Sequence
- Decrease in arterial pressure causes decrease in renal profusion
- Mechanoreceptors in afferent arterioles of kidney sense the decrease in arterial pressure and juxtaglomerular cells convert prorenin to rennin which is released into the circulation
- Renin converts angiotensinogen to angiotensin I
- Angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) primarily in the lungs and kidney
- Angiotensin II acts on the adrenal cortex (zona glomerulosa cells), stimulating release of aldosterone
- Aldosterone acts on distal renal tubule cells promoting increased reabsorption of Na+, increasing blood volume
***Angiotensin II - additional actions:
o Acts as a direct acting vasoconstrictor, increase total peripheral resistance (TPR) and blood pressure
o Preferentially mediates constriction of renal efferent arterioles – attempting to preserve intra- renal profusion pressure and glomerular filtration
o Stimulates Na+ – H+ exchange in renal proximal tubule increasing Na+ / HCO3 reabsorption
Pathophysiology: Rennin –Angiotensin – Aldosterone System
Useful Adaptive Response: In the event of circulating volume depletion, (ex. acute blood loss; dehydration) this system attempts to preserve blood volume and flow
Pathophysiology: Rennin –Angiotensin – Aldosterone System
Maladaptive Responses: clinical situations where these “adaptive” responses to a “decreased” blood pressure, actually do harm.
Pathophysiology: Rennin –Angiotensin – Aldosterone System Maladaptive Responses
Volume overload: In systolic heart failure with low cardiac output, the kidneys sense decreased blood flow which activates the renin-angiotensin- aldosterone system. Activation of the RAAS system results in increasing blood volume and increased peripheral resistance which aggravates the heart failure.
Pathophysiology: Rennin –Angiotensin – Aldosterone System Maladaptive Responses
In some individuals, their “set point” for blood pressure is higher than normal resulting in chronic hypertension. Their hypertension may be well controlled by giving them ACE inhibitors (ex. Lotensin) or ACE receptor antagonist (ex. Cozaar)
Pathophysiology: Rennin –Angiotensin – Aldosterone System Maladaptive Responses
In cirrhosis of the liver with low serum albumin (and some other edematous state) inappropriate aldosterone secretion contributes to the development of ascites. The ascites may be treated with spironolactone which antagonizes the actions of aldosterone
Pathophysiology: Rennin –Angiotensin – Aldosterone System Maladaptive Responses
In individuals with unilateral renal artery stenosis from atherosclerotic cardiovascular disease, increase serum renin levels may elevate blood pressure to levels which risk stroke, myocardial infarction and further damage to the kidneys
