• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/16

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

16 Cards in this Set

  • Front
  • Back

These antagonists bind α- or β-adrenoceptors at target organs, inhibiting α- or β-adrenoceptor mediated effects, respectively.




They block endogenous and exogenous ____ agonists (e.g. E, NE, phenylephrine, isoproterenol and salbutamol)

Adrenoceptor antagonists

This α-adrenoceptor antagonist blocks both α1 and α2 -adrenoceptors

Phentolamine

This α-adrenoceptor antagonist selectively blocks α1- adrenoceptors.




-> Reduce blood pressure of hypertensive patients.


Toxicities include nasal stuffiness, orthostatic hypotension and reflex tachycardia

Prazosin




-nasal stuffiness - due to􏰣 blood flow to the mucus membrane


-orthostatic hypotension - dilatation of veins thereby reducing return of blood to the heart


-tachycardia due to reflex increase in sympathetic discharge in response to a decrease in blood pressure (and subsequent β-adrenoceptor activation).

This β-adrenoceptor antagonist blocks β1- and β2– adrenoceptors



Mechanism of action involves blocking β1-adrenoceptors:


-in the central NS -> reduce sympathetic outflow


-in the peripheral NS (at pre-junctional sympathetic nerve terminal -> reduce NE release


Propranolol


This β-adrenoceptor antagonist selectively blocks β1-adrenoceptors antagonist




Mechanism of action involves blockade of β1-adrenoceptors in the CNS to reduce sympathetic outflow and peripherally (at pre-junctional sympathetic nerve terminal) to reduce NE release.

Metoprolol

Both Propranolol and Metoprolol are so-called cardiac protective, blocking B1 adrenoceptors -> decrease SNA, CO, HR/cardiac work...




Drug use?



Prevent increased HR and CO during exercise. Treat hypertension and angina/myocardial infarction.

Propranolol


blocks β1-adrenoceptor -> dec SNA


blocks β2– adrenoceptors -> reduce tremor inskeletal muscles




Drug use?

management of acute panic symptoms and performance anxiety.

Toxicities of β-adrenoceptors antagonists



β1-adrenoceptors blockers reduces heart rate and cardiac contraction -> toxicity?



β2-adrenoceptors blockers -> bronchoconstriction -> toxicity?

Reduced cardiac function, congestive heart failure (may worsen heart failure in patients with high β1-adrenergic tone).



Asthma attack in patients with asthma

These drugs inhibit transmitter (NE and E) release from adrenergic nerves, blocking adrenergic neurons -> reduce the activity of the SNS, but not the actions of already circulating E, NE or sympathomimetic drugs.

Antiadrenergic drugs

Both of these antiadrenergics activate central and peripheral prejunctional α2-adrenoceptors -> reduce sympathetic outflow and release of E and NE.

Clonidine and α-methyl dopa

This antiadrenergic drug blocks VMAT -> reduces uptake of DA and NE into storage vesicles -> prevents NT release.

Reserpine

This antiadrenergic drug is taken up via Uptake-1 into the sympathetic nerve terminal. Large [drug] in the nerve terminal -> blocks Na+ influx -> inhibits AP propagation -> blocks release of NE from storage vesicles.



->-> depletes NE stores at the nerve terminal.

Guanethidine

These drugs bind to and inhibit the action of nicotinic receptors at both sympathetic and parasympathetic ganglia; their influences depend on predominance of parasympathetic or sympathetic tone at a particular site.

Ganglionic blockers (e.g., hexamethonium)

Ganglionic blocker -> Inhibit activity in organs with high parasympathetic tone:


heart


eye


gastrointestinal organs


genitourinary organs




-> effect of inhibition?


(Think, what does PNS stimulation do? What is opposite?)

Increase heart rate


Mydriasis


Paralysis of accommodation


Decreased gastrointestinal tone and motility


Urinary retention

Ganglionic blocker -> Inhibit activity in organs with predominate sympathetic tone: BV--


arterioles


veins




-> effect of inhibition?


(Think, what does SNS stimulation do? What is opposite?)

Vasodilation (arterioles)


Venodilation (vein)




-> reduced BP


-> pooling of blood in the lower limbs

To review, Ganglionic blockers (e.g. hexamethonium) -> ?

To review, Ganglionic blockers (e.g. hexamethonium) -> ?