Hypertension Flashcards
Hypertension?
Persistently elevated blood pressure (>140/90mmHg)
What is the formula for BP?
BP = CO x PR
At rest are CO & PR stable?
CO is stable however PR fluctuates for varying reasons (such as vasoconstriction & vasodilation occurring in the body)
Systole?
Pumping phase; usually around 120 mmHg
Diastole?
Filling phase; usually around 80 mmHg
What are the 4 mechanisms to monitor BP?
- Baroreceptors
- Vascular Autoregulation
- Renin Angiotensin Aldosterone System
- Fluid volume regulation by the kidneys
Baroreceptors?
Detect changes in pressure (feed information to the nervous system, homeostatic mechanisms engage to return pressure to original state)
“baro-“?
Pressure
Where are baroreceptors located on the blood vessel?
In the tunica external/adventitia
Explain the pathophysiology of baroreceptors.
Type of mechanoreceptor sensory neutron that is excited by stretch of the blood vessel -> creates an action potential -> CNS -> stimulation of vascular smooth muscle -> constrict/dilate -> alters PR -> alters BP
In the body, where are baroreceptors located and why?
Located in the aorta (BP going to the body) and located in the carotid arteries (BP going to the brain)
Vascular Autoregulation?
Blood vessels constrict and dilate
What does vascular auto regulation occur in response to?
Changes in the body (such as change in pH)
How should vascular autoregulation be controlled?
In a localized way so only the area perfused by that specific vessel is affected
What does RAAS stand for?
Renin Angiotensin Aldosterone System
What is RAAS?
A homeostatic mechanism triggered by a decrease in BP, with the end result of an increased BP to normal range.
In RAAS what detects the decrease in BP?
Juxtaglomerular cells (granular cells) detects a decrease in BP [less stretch ]
Explain in detail what occurs in RAAS.
Juxtaglomerular cells (or granular cells) in the kidneys release renin into the blood. The release of renin causes the precursor protein angiotensinogen to transform into angiotensin 1. Angiotensin 1 circulates until ACE is made by pulmonary capillaries. ACE converts angiotensin 1 into angiotensin 2. Angiotensin 2 has multiple functions to increase BP such as:
- Stimulates thirst by increasing plasma volumes which increases the venous return, stroke volume, and cardiac output which increases blood pressure.
- Constricts efferent arteriole to increase pressure within the glomerulus and restores GFR.
- Stimulates the release of 2 hormones [aldosterone and anti-diuretic hormone]
- Aldosterone -> secreted from the adrenal cortex and promotes the insertion of Na+ channels-> reabsorption of Na+, following by H20, increases blood volume, increases blood pressure
- ADH secreted by the posterior pituitary gland and promotes the insertion of H20 channels into distal convoluted tubule and collecting duct -> reabsorption of H20 -> increased blood volume -> increased blood pressure. [It also stimulates thirst which increases BP)
4. Angiotensin 2 is a potent vasoconstrictor itself. It constricts arterioles throughout the body which increases PR -> increases BP
What is renin?
An enzyme
What releases renin?
Juxtaglomerular (or granular) cells from the kidneys
Where is angiotensinogen made?
In the liver
ACE?
Angiotensin converting enzyme
Where is ACE made?
Pulmonary capillaries
In a nutshell, what are the 4 main functions of angiotensin 2 that help it increase BP? (You don’t have to describe the 4)
- Stimulates thirst
- Constricts efferent arteriole to increase pressure within the glomerulus and restores GFR
- stimulates the release of aldosterone and antidiuretic hormone
- angiotensin 2 is a potent vasoconstrictor itself