Theme 3 - drug treatment for CVD Flashcards
what blood pressure is classified as hypertension?
150/95 mmHg
what the blood pressure equation?
BP = CO x TPR
what does TPR measure?
degree of constriction or dilation of arterioles
where are the main baroreceptors that detect blood pressure found?
aortic arch, kidney and carotid sinus
what hormone is released when low blood pressure is low and what does this cause?
when baroreceptors detect low BP - noradrenaline is released which causes construction of arterioles which increases BP
what receptors does NA simulate when released in response to low BP?
- alpha1 adrenergic receptors
as well as beta 1 adrenergic receptors on the SA node and ventricular myocytes in the heart
what is the main aim of the sympathetic NS when decreased aortic blood flow is detected?
to increase preload (blood back to the heart) therefore increasing CO
by what mechanism does activation of B1 receptors on the heart increase blood pressure?
- via cAMP
- increases calcium entry to the SA node cells
- increases frequency and force of contraction
what NT is released by the parasympathetic NS to decrease blood pressure and what receptors does it act on?
Ace release which acts on M2 receptors
what branch of the ANS solely regulates peripheral resistance and what does this result in?
- sympathetic NS
- NA release works on alpha 1 receptors which increases calcium via IP3 = vasoconstriction
which receptors can the sympathetic NS act via to cause vasoconstriction?
- alpha 1 adrenergic (IP3)
- beta 2 receptors (cAMP)
what does decreased renal perfusion cause?
the juxtaglomerular apparatus to release renin
what does renin do?
converts angiotensinogen to AG I
where is ACE found?
in the endothelium
what NS response does AGII stimulate and what does this lead to?
- sympathetic NS
- causes aldosterone release from the adrenals (increased Na retention)
- ADH release from posterior pituitary (increased waer reabsorption)
what does activation of ADH and aldosterone by the sympathetic NS ultimately lead to?
increased blood volume, increased stroke volume, increased cardiac output and therefore increased blood pressure
what receptor does AGII work on and what does stimulation of these receptors cause?
AT1 receptors that increases arteriole and venous constriction increased blood pressure
what cells does aldosterone work on and what receptor does it bind?
works on principal cells in the DT and CD and binds a mineralocorticoid receptor
what is the result of aldosterone binding to its receptor in principal cells?
- upregulates Na/K ATPase on the BL membrane
- upregulates ENac in apical of CD cells
- results in increased reabsorption of Na+ and water in the blood
what would be the first choice of hypertensive drug for someone under 55
ACE inhibitor or angiotensin receptor blocker
what would be first choice hypertension treatment for those over 55 or from black origin?
calcium channel blockers/thiazide diuretics
what is the mechanism of action of ACE inhibitors and give an example
- reduced AGI –> AGII (doesn’t block it)
- RAMIPRIL
what is first dose hypotension, what drugsf class is it associated with and how can it be avoided?
- associated with ACE inhibitors
- patient can get very big drop in BP the first time they take an ACE inhibitor
- can be avoided by telling the patient to take it at night - prevents fainting
what is the main side effects of ACEIs and why does this occur?
- dry tickly cough (25-40%)
- occurs as ACEIs also reduces kininase II levels which breakdown bradykinin - results in increased bradykinin which is an irritant = cough
