Cardiovascular-Renal Pharmacology 2 Flashcards
Hydraulic equation of Hypertension
BP=CO x PVR
Volume of blood pumped out by the VENTRICLE PER MINUTE
Cardiac output
Volume of blood pumped out by the VENTRICLE PER CONTRACTION/BEAT
(ml/beat)
Stroke volume
It is the heart conductivity
Heart rate
Determinants of stroke volume
Heart rate
+ Chronotrope increase HR, SV, CO, BP
Strength or force of contraction
Inotropy
Determinants of stroke volume
Inotropy
+ Inotrope increase SV, CO, BP
Volume of blood in the ventricles PRIOR TO CONTRACTION
Preload/ End diastolic volume
Carries blood towards the heart
Veins
Venoconstriction
Venous capacitance is
Blood is
Preload
Reduced
Mobilized
Increase
Venodilation
Venous capacitance is
Blood is
Preload
Increased
De-mobilized
Decrease
Fluid content of blood
Blood volume
Increase fluid content=
Increase preload (Blood is more bulky)
Increase Blood Volume=
Increase preload - stroke volume
Decrease venous capacitance=
Decrease ability of vein to contain blood
Peripheral vascular resistance is also known as
Total vascular resistance
Systemic vascular resistance
Afterload
Pressure required for the blood to be ejected
Peripheral vascular resistance
Resistance ventricles must overcome to circulate blood
Peripheral vascular resistance
Increase afterload
Increase BP
More harder for ventricles to pump blood
Arterioconstriction
Decrease afterload
Decrease BP
Arteriodilation
A drug that is both vaso and arteriodilator
Sodium nitroprusside
A drug that is arteriodilator
Amlodipine
Uses of BP regulation
To not reach dangerous levels
Short term mechanism of BP regulation
Baroreceptor reflex
It detects the increase of BP
Carotid sinus baroreceptor
It detects the decrease of BP
Aortic arch baroreceptor
Carotid sinus to brain through?
Afferent nerve 9
Vasomotor center (brain) to execute parasympathetic action
Efferent nerve 10
Aortic arch to vasomotor or brain
Afferent nerve 10
Brain to Sympathetic action
Pre-ganglionic Sympathetic fibers
Increase in BP
SANS/PANS
SANS
The long term regulation for BP
Renin-angiotensin aldosterone system
Final effect of RAAS activation is always?
Increase BP
Inhibition of RAAS steps will lead to?
Decrease in BP
Where is angiotensinogen synthesized?
Liver
Where is renin synthesized
Kidneys
Where is angiotensin converting enzyme synthesized
Lungs
Triggers of renin release
Beta-1 Stimulation
Renal Hypoperfusion (Kulang sa dugo)
Renal Hypotension
ACE degrades what substance in the lungs
Bradykinin
Substance P
AG II binds to
AG IA receptors
Effects of angiotensin II binding
Stimulation of autonomic ganglia
Release and synthesis of Aldosterone
Release of vasopressin
Stimulation of autonomic ganglia is what activity
SANS activity
Aldosterone is hormone in the blood synthesized by
Adrenal glands
A main mineralocorticoid
Aldosterone
What does aldosterone increases
Increase sodium and water reabsorption
Vasopressin is what kind of hormone
Antidiuretic hormone
Effects of vasopressin
Vasoconstriction
Prevents urination=water retention (increasing BP & BV)
Example of Renin Inhibitor
Aliskiren (decreases BP)
Example of ACE inhibitor
“-prils”
- decrease BP
- Accumulation of Bradykinin and substance P
Accumulation of Bradykinin and substance P in the lungs leads to the common side effect
Dry cough
Example of ARB
“-sartan”
MOA of ARB
Competitive blockers to angiotensin 1A
It is a pharmacologic antagonist
ARB
Agonist of angiotensin 1a
Angiotensin II
Have affinity and intrinsic activity
Agonist
Have affinity but no intrinsic activity
Antagonist
