alpha 2 agonist = decreases sympathetic outflow

also interacts with imidazoline receptors = may contribute to BP lowering effect

initial pressor response after IV admin

oral and transdermal preps as well

adverse effects:

1) CNS = sedation, depression

2) dry mouth

3) orthostatic hypotension

4) possible hypertensive crisis on sudden withdrawl

prodrug

MOA: stimulation of alpha-2 receptors= decrease sympathetic outflow

Oral admin and IV prep

ADVERSE EFFECTS:

1) CNS = sedation; decrease concentration; depression; hyperprolactinemia

2) dry mouth

3) orthostatic hypotension

4) HEPATOTOXICITY

5) POSITIVE COOMB'S TEST; HEMOLYTIC ANEMIA

interaction with tricyclic antidepressants and cocaine

selective alpha-1 blocker

oral admin; extensive metabolism

ADVERSE EFFECTS: first dose phenomenon (start at bedtime to avoid orthostatic hypotension)

dizziness and headache

ex: tamulosin - used for BPH

decrease HR and contractility = decrease CO = decrease renin release

cardioselective; intrinsic sympathomimetic activity (partial agonist activity; membrane stabilizing activity

Adverse effects:

1) may worsen heart failure

2) bradycardia

3) bronchospasm

4) prolong hypoglycemia in patients taking insulin

5) increased VLDL, decreased HDL

6) CNS effects

7) BETA BLOCKER WITHDRAWL = upregulation of receptors - must taper them off of the drug

actions: combined alpha and beta blocker (alpha 1 selective; beta nonselective)

adverse:

1) same for alpha

2) same for beta

3) heptatotoxicity

use for heart failure

blocks beta receptors and produces vasodilation

MOA: nitric oxide release - not due to alpha blockade

arterial dilator

causes nitric oxide release

compensatory responses to the vasodilation =

use with beta blocker and diuretic

oral and parentral admin

metabolized by acetylation (phase II rxn) = drug induced lupus; not for slow acetylators

other adverse effects:

1) palpitations and angina

2) headache

(these are due to fact that you decrease BP so much, body compensates via increased HR)

stabilize membrane; open K channels

compensatory sympathetic stimulation; used with beta-blocker and loop diuretic

oral administration

adverse effets:

1) headache, palpitations, angina

2) hypertrichosis

3) pericardial effusion

4) EKG changes (T wave changes)

parentral drug for Hypertensive emergencies

acts on dopamine-1 receptors; vasodilation

rapidly metabolized - continuous IV infusion

adverse effects:

1) headaches, flushing

2) increase heart rate

3) increased intraocular pressure (don't give to a pt with glaucoma)

parentral; for hypertensive emergencies

MOA: open K channels

reflex sympathetic stimulation

adverse effects:

1) excessive lowering of bp

2) reflexive sympath. stim. = angina, ECG ischemia, cardiac failure in patients with ischemic heart disease

3) fluid retention

4) hyperglycemia

venous and arterial dilator

give IV for hypertensive emergencies

MOA: increase cGMP = release nitric oxide or direct stimulation of enzyme

adverse:

1) continous infusion because short half life

2) solution is light sensitive

3) close monitoring

4) CN and SCN poisoning

ACEi (many are prodrugs)

inhibit conversion of angiotensin I to angiotensin II = decreased A II = decreased vasoconstriction and aldosterone

BRADYKININ - similar enzyme as ACE

:( decreases GFR in bilateral renal artery stenosis, but :) decreases proteinuria and stabilizes renal function in pt's with chronic renal dz

Adverse effects:

Cough (due to bradykinin and PGs)

Angioedema

Proteinuria

Toxicity (in fetus)

hypOtension

Pancretitis

Rash

Increased K

Low Angiotensin II

ARBs

inhibit type 1 receptors (AT₁)

oral

adverse effects:

1) hypotension

2) increased K⁺

3) angioedema

4) cough

5) increased BUN and Creatinine in patients with bilateral renal artery stenosis

6) fetal toxicity

blocks renin activity; decreased angiotensin I and II

increased angiotensinogen

oral admin

adverse:

1) diarrhea

2) angioedema

3) cough

4) hyperkalemia

5) fetal tox.