L5 Flashcards
Physiological Control of Blood Pressure (3)
- Cardiac output
- contractile state of resistance arterioles
- volume
Cardiac Output
- heart rate
- sympathetic & vagus
- stroke volume
- Filling pressure & contractility (sympathetic)
Contractile state of resistance arterioles
– Neural
* sympathetic & parasympathetic NS
– Hormonal
* Renin-angiotensin-aldosterone system (RAS)
– Local transmitters
* Nitric Oxide (NO)
Volume
– Hormonal (RAS, ADH, ANP)
Antihypertensive Drug Strategies
- Reduce cardiac output
- Dilate resistance vessels
- Reduce vascular volume
Antihypertensive Drug Strategies
Reduce cardiac output
– (b-adrenergic blockers: not 1st line)
– Ca2+ channel blockers
Antihypertensive Drug Strategies
Dilate resistance vessels
– Ca2+ channel blockers
– Renin-angiotensin system blockers
– a1 adrenoceptor blockers
– Nitrates**
Antihypertensive Drug Strategies
Reduce vascular volume
– Diuretics. RAS blockers
Renin-angiotensin system
- triggered by low blood pressure, low blood volume, or low sodium levels in the bloodstream.
- A decrease in blood flow to the kidneys and/or increased sympathetic stimulation of the kidneys triggers the release of renin.
- Renin converts angiotensin precursor (angiotensinogen) released from the liver to inactive angiotensin I in the circulation.
- In the lungs, angiotensin I is further cleaved to the active angiotensin II by angiotensin converting enzyme (ACE).
- Angiotensin II activates angiotensin II type 1 (AT1) receptors on blood vessels
- resulting in vasoconstriction and thus increased blood pressure.
- Angiotensin II also activates AT1 receptors in the adrenal cortex,
- causing release of aldosterone.
- In turn, aldosterone stimulates mineralocorticoid receptors to increase reabsorption of sodium and water from the kidneys.
- This increases blood volume which also leads to elevated blood pressure.
RAAS system to whole
- triggered by low blood pressure, low blood volume, or low sodium levels in the bloodstream
- A decrease in blood flow to kidneys and/or increased sympathetic stimulation of the kidneys triggers the release of renin.
- Renin converts angiotensin precursor (angiotensinogen) from the liver to inactive angiotensin I in the circulation.
- (lungs), angiotensin I cleaved to active angiotensin II by angiotensin converting enzyme (ACE).
- Angiotensin II activates angiotensin II type 1 (AT1) receptors on blood vessels = vasoconstriction
- increased blood pressure.
- Angiotensin II activates AT1 receptors in the adrenal cortex
- Release of aldosterone.
- Aldosterone stimulates mineralocorticoid receptors to increase reabsorption of sodium and water from the kidneys.
- This increases blood volume which also leads to elevated blood pressure.
RAAS for increase blood volume and pressure and reabsroption
Angiotensin II also activates AT1 receptors in the adrenal cortex, causing the release of aldosterone. In turn, aldosterone stimulates mineralocorticoid receptors to increase reabsorption of sodium and water from the kidneys. This increases blood volume which also leads to elevated blood pressure.
RAAS to increase blood pressure
- triggered by low blood pressure, low blood volume, or low sodium levels in the bloodstream
- A decrease in blood flow to kidneys and/or increased sympathetic stimulation of the kidneys triggers the release of renin.
- Renin converts angiotensin precursor (angiotensinogen) from the liver to inactive angiotensin I in the circulation.
- (lungs), angiotensin I cleaved to active angiotensin II by angiotensin converting enzyme (ACE).
- Angiotensin II activates angiotensin II type 1 (AT1) receptors on blood vessels = vasoconstriction
- increased blood pressure.
ACE Inhibitors
- Perindopril
- Ramipril
- anything else ending in -pril
Angiotensin receptor blocker
(ARB)
- Candesartan
- Irbesartan
- anything else ending in -sartan
Autonomic Nervous System regulates blood pressure by effects on both pump output and what
Autonomic Nervous System regulates blood pressure by effects on both pump output and resistance in the circulation
