Hormonal Control of Blood Pressure Flashcards
Integrated systems regulate MAP
- when hemorrhage causes a sudden decrease in arterial pressure, the pressure control system faces 2 challenges: 1st- respond rapidly enough to ensure survival; 2nd- gradually reestablish blood volume to normal levels
- they are accomplished by integrated actions of systems that respond rapidly (sec - min); intermediate (min-hrs); and long term (days or longer)
Rapid acting control mechanisms
- typically nervous reflexes
- the baroreceptors, chemoreceptors, and CNS ischemic response
Intermediate control mechanisms to regulate MAP
- include the renin-angiotensin vasoconstrictor mechanism, the stress relaxation mechanism (e.g. increased pressure for min-hrs leads to continuous stretch of the vessel to relieve the pressure
- capillary fluid shift mechanism (e.g. if capillary pressure falls too low, fluid is fluid is absorbed from the tissues through the capillary membranes thus building up blood volume and pressure
- during this time, nervous mechanisms become gradually less effective
Long term control mechanisms to regulate MAP
-involves control by the kidneys, in particular the renin-angiotensin-aldosterone system
CNS ischemic response
- when blood flow to the vasomotor center in the lower brain stem becomes decreased enough to cayse ischemia- the vasoconstrictor and cardioaccelerator neurons in the vasomotor center respond directly to ischemia and become strongly excited
- this arterial pressure elevation in response to cerebral ischemia is known as the CNS ischemic response
- one of the most powerful of all the activators of the sympathetic vasoconstictor system
- it does not become significant until the arterial pressure falls far below normal, down to 60 mm Hg, and to greatest degree 15-20 mm Hg
High pressure baroreceptors
-decrease their firing rate leading to increased HR, cardiac contractility, and vasoconstriction
Low pressure baroreceptors
- decerase their firing rate in response to decreased circulating volume
- this leads to increased SNS mediated vasocontriction, especially the renal bed (they also stimulate ADH release)
Peripheral chemoreceptors
-respond to local hypoxia by increasing the firing rate of chemoreceptor afferents, leading to increased firing of SNS vasoconstrictor fibers and changes in ventilation
Central chemoreceptors
-respond to brain ischemia (a fall in pH/acidosis) leading to a powerful SNS output (the kidney can actually stop producing urine)
Angiotension II
-decreased arterial pressure -> renin (kidney) -> renin substrate (angiotensinogen) -> angiotensin I -> (by converting enzyme in lung ACE ) angiotensin II -> angiotensinase inactive, vasoconstriction, renal retention of salt and water -> increased arterial pressure
Recovery from hemorrhage with angiotensin
- hemorrhage causes arterial pressure to drop from 100 mm Hg to 50 mm Hg, the renin-angiotensin vasoconstrictor response is powerful enough to return pressure back to ~83 mm Hg
- this response can be life-saving, especially in circulatory shock
- in the presence of renin-blocking antibody recovery was much weaker returning to 60 mm Hg
Integrated responses to hemorrhage
- response to hemorrhage involves contributions of the baroreceptors, the renin-angiotensin-aldosterone system, as well as increased fluid reabsorption by the capillaries in response to a decrease in capillary hydrostatic pressure
- the unstressed volume refers to the volume of blood that the veins can hold, no pressure
- the stressed volume refers to the volume in the arteries. This volume of blood produces pressure by stretching the elastic fibers in the walls of the vessels
Increased salt intake
-increased salt intake -> increased extracellular volume -> increased arterial pressure -> decreased renin and angiotensin -> decreased renal retention of salt and water -> return of extracellular volume almost to normal -> return of arterial pressure almost to normal
Antidiuretic hormone (ADH; vasopressin)
- from the posterior pituitary function, synthesized in the supraoptic nuclei of the hypothalamus and stored and released in posterior pituitary
- main function is water balance; it is released in response to increase osmolarity of extracellular fluid and decreased blood pressure and has the major effect of promoting water reabsorption by the kidney.
- high ADH in plasma, a low volume of concentrated urine is produced
- vasopressin/ADH is also a vasoconstrictor
- released in response to increased body fluid osmolarity, decreased blood volume, and decreased blood pressure
- ANP (atrial naturetic peptide), ethanol, aldosterone decreases release
Control of arteriolar tone
- greatest resistance to flow occurs in the small arteries and arterioles
- the state of construction of relaxation of these vessels is regulated in part by the sympathetic nervous system and release of norepinephrine
- circulating hormones, including ADH, angiotensin, may contribute to constriction through their actions on vascular smooth muscle; atrial natriuretic peptide (ANP) is a smooth muscle dilator
- endothelium plays an important role in regulating vascular tone by its release of NO and prostacycline in response to shear stress, ACh, and bradykinin
- endothelin is a potent, endothelium-derived vasoconstrictor important in some pathophysiologic states
- the endothelial cell surface also has angiotensin-converting enzyme (ACE), which forms angiotensin II by cleavage of circulating angiotensin I