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Flashcards in Anti-hypertensives Deck (116):
1

Clonidine

centrally acting alpha 2 agonist

MOA: activate alpha 2 receptor-->decrease central sympathetic outflow-->decrease NE release

Effect:-->decrease TPR

Uses:
1. HTN
2. Clonidine used in withdrawal from abused drugs

Advantages of using:
1. No change in lipids
2. used in nicotine dependence

2

Clonidine Toxicities

1. dry mouth
2. sedation
3. rebound HTN

3

Methyldopa Toxicities

1. positive Coombs test (hemolytic anemia)

4

DOC to treat anti hypertension in pregnancy

Clonidine; also doesn't cause a change in lipids

5

Methyldopa

centrally acting alpha 2 agonist

MOA: activate alpha 2 receptor-->decrease central sympathetic outflow-->decrease NE release

Effect:-->decrease TPR

Uses:
1. HTN in pregnancy--DOC

6

Reserpine
MOA; Effects & Uses

Sympathetic nerve terminal blocker

MOA: blocks vesicular uptake & depletes transmiter stores

Hemodynamic effects: Decrease TPR & CO

Uses: rarely used to treat HTN

7

Reserpine Toxicities

Toxicities: sedation & depression
Disadvantages/Contraindicated: depression

8

Guanethidine toxicities & disadvantages/contraindications

Toxicities:
1. Orthostatic Hypotention
2. Fluid retention
Disadvantages/Contraindicated: CHF

9

Guanethidine MOA, Effects & Uses

Sympathetic nerve terminal blocker

MOA: interferes with amine release & replaces NE in vesicles

Hemodynamic effects: Decrease TPR & CO

Uses: rarely used to treat HTN

10

Use of Alpha 1 blockers to treat Hypertension

MOA:
1. selectively block alpha1A receptors
2. reduce prostatic SM tone

Hemodynamic effects: Decrease TPR

Uses: 1. HTN 2. BPH

Toxicities: orthostatic hypertension

Disadvantages/contraindications: none

Advantages: Decreases VLDL & LDL

11

Alpha 1 blockers used to treat HTN

1. prazosin
2. terazosin
3. doxazosin

12

Use of Beta blockers to treat Hypertension

MOA:
1. Block B1 receptors
2. decrease renin secretion

Hemodynamic effects--> Decrease CO

Clinical Uses: 1. HTN 2. HF

Toxicities/interactions: Bronchoconstriction

Contraindication:
1. Bronchial asthma
2. Heart Block

Advantages: Prolong survival
***labetalol is DOC in pregnancy

13

Beta Blockers used to treat Hypertension

1. metoprolol
2. atenolol
3. carvedilol (blocks B1 & alpha receptors)

14

Drugs used to treat HTN that work by decreasing CO

1. beta blockers
2. calcium-channel blockers (work by decreasing HR & FOC)

15

Vasodilators used to treat HTN that work by decreasing systemic vascular resistance

1. alpha blockers
2. direct-acting vasodilators
3. Angtiotensin-converting enzyme inhibitors (ACE inhibitors)
4. angiotensin receptor blockers (ARBs)

16

Antihypertensives that work at the vasomotor center

1. methyldopa
2. clonidine
3. guanabenz
4. guanfacine

17

Antihypertensives that work at sympathetic ganglia

Trimethaphan

18

Antihypertensives that work at sympathetic nerve terminals

1. guanethidine
2. guanadrel
3. reserpine (not used bc it depletes MO-->depression)

19

Antihypertensives that work at beta receptors of heart

beta blockers ie propranolol

20

Antihypertensives that work at angiotensin receptors of vessels

1. losartan
2. other angiotensin receptor blockers

21

Antihypertensives that work at alpha receptors of vessels

1. prazosin
2. and other alpha 1 blockers

22

Antihypertensives that work at vascular smooth muscle

1. hydralazine
2. minoxidil
3. nitroprusside
4. diazoxide
5. verapamil & other CCB
6. Fenoldopam

23

Antihypertensives that work at kidney tubules

1. thiazides, etc

24

Antihypertensives that work at beta receptors of juxtaglomerular cells that release RENIN

Propranolol & other beta blockers

25

Angiotensinogen is converted to angiotensin 1 by _____ which is inhibited by _______

1. renin
2. alskiren

26

angiotensin 1 is converted to angiotensin II by _________ which is inhibited by ___________

1. Angiotensin-converting enzyme (ACE)
2. Captopril & other ACE inhibitors

27

How do diuretics treat HTN?

1. they reduce venous pressure & CO by reducing blood volume
2. HOW? They act on the kidney to enhance Na & water excretion
3. Reducing blood volume not only reduces central venous pressure, but also CO!

28

What group of diuretics are preferred for HTN? WHY? Ex?

Thiazides, bc maximum antihypertensive action is at LOWER doses than the diuretic dose!

Ex) hydrochlorothiazide

Added BONUS: they reduce SVR with long-term use

Loss of Na-->decreased vessel stiffness-->decreased TPR

29

Toxicity of Thiazides

1. hypokalemia
2. decrease glucose tolerance and may unmask latent DM
3. increase plasma LDL, cholesterol & triglycerides (TG)
4. increase plasma uric acid & may precipitate acute gout

30

MOA for beta blockers as anti-HTN drugs

1. decrease in CO by blocking cardiac Beta 1 receptors
2. inhibition of renin release by blocking beta 1 receptors on JG cells

31

Hemodynamic effects of beta blockers in HTN

a) Decreased:
1. HR
2. CO
3. PVR

b)Unchanged: venous tone

c)Negligable: postural hypotension

32

all beta blockers are equally effective in lowering BP in??

mild to moderate HTN

33

in severe HTN, beta blockers are useful???

in preventing the reflex tachycardia that often results from treatment with direct vasodilators

34

beta blockers have shown to reduce mortality after

MI & heart failure

35

Propranolol
a) type
b) toxicities
c) prolonged use warning

a) non-selective comound
b)
1. bradycardia or cardiac conduction disease
2. asthma
3. peripheral vascular insufficiency
4. diabetes
c) DO NOT discontinue abruptly after prolonged regular use bc can result in reflex tachycardia

36

Cardio-selective beta 1 drugs

b) benefits?

1. atenolol
2. metoprolol

b) cause less bronchoconstriction than propranolol

37

beat blockers with additional alpha blocking activity

b) when would you use them?

1. labetalol
2. carvedilol

b) tumor in adrenal medulla (pheochromocytoma)

38

Calcium channel blockers act on

L type calcium channels

39

CCB effective in lowering BP

1. verapamil
2. diltiazem (has intermediate actions)
3. DHP (amlodipine, felodipine, isradipine, nicardipine, nifedipine, nisoldipine)

40

DHP
a) examples
b) selectivity
c) can cause

1. amlodipine
2. felodipine
3. isradipine
4. nicardipine
5. nifedipine (not for HTN bc too short acting!!)
6. nisoldipine

b) more selective as vasodilators
c) can cause slight reflex tachycardia

41

Verapamil

1. has the greatest depressant effect on the heart
2. may decrease HR & CO
3. How? L-type Ca channels-->decrease FOC

42

DHP not used for HTN bc too short acting

nifedipine

43

How do calcium channels lead to muscle contraction?

1. calcium comes in
2. binds to myosin light chain kins

44

Inhibitors of Renin Angiotensin Aldosterone System (RAAS)

1. ACE inhibitors: end in "-pril" (captopril, Enalapril, Ramipril, Benazepril, fosinopril, lisinopril, quinapril)
2. Angiotensin Receptor Blockers (ARBs): end in "-sartan" (Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan)
3. Renin antagonist: aliskiren
4. Aldosterone Receptor inhibitors: end in "-one" (spironolactone, elprenone)

45

ACE Inhibitors

end in "-pril"
1. captopril
2. Enalapril
3. Ramipril
4. Benazepril
5. fosinopril
6. lisinopril
7. quinapril

46

end in "-pril"

ACE inhibitors

47

Angiotensin Receptor Blockers (ARBs) (Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan)

1. Losartan
2. Valsartan
3. Candesartan
4. sprosartan
5. irbesartan
6. telmisartan
7. olmesartan)

48

End in "-sartan

Angiotensin Receptor Blockers (ARBs)
1. Losartan, Valsartan, Candesartan, sprosartan, irbesartan, telmisartan, olmesartan

49

Aldosterone Receptor inhibitors

end in "-one"
1. spironolactone
2. elprenone

50

end in "-one"

Aldosterone Receptor inhibitors:
1. spironolactone
2. elprenone

51

Effects of ATII on the myocardium & kidney

1. mitogenic for vascular & cardiac muscular cells
Remodeling:

52

Remodeling effects of ATII

1. increased wall-to lumen ratio in bv
2. concentric & eccentric hypertrophy
3. fibrosis & stenosis of intimal surface of bv
4. due to increased migration & hyperplasia of vascular sm cells, myocytes & fibroblasts
**slowed, prevented & even reversed by ACE inhibitors

53

Effects of angiotensin II

b) inhibited by

1. vasoconstriction-->increased peripheral vascular resistance-->increased BP
2. aldosterone secretion-->increased Na & water retention-->increased BP

b) Angiotensin receptor blockers (ARBs)

54

Effects of aldosterone secretion

b) inhibited by

aldosterone secretion-->increased Na & water retention--> increased BP

b) inhibited by spironolactone, eplerenone (aldosterone receptor inhibitor

55

Effects of bradykinin

Bradykinin is an important vasodilator: normally it stimulates release of NO & prostacyclin--> decreases PVR

1. increased prostaglandin synthesis-->vasodilation
2. release of NO--> vasodilation-->decreased PVR--> decreased BP

**causes dry cough in ACEI (MC ADR w ACEI)

56

Role of ACE inhibitors

1. act by inhibiting the ACE converting enzyme (peptide dipeptidase)
2. enzyme normally hydrolyzes angiotensin I-->II
3. also inactivates bradykinin (an important vasodilator: normally it stimulates release of NO & prostacyclin--> decreases PVR)
4. ACEI lower BP principally by DECREASING PVR

57

How do ACE inhibitors treat HTN?

They lower BP principally by DECREASING PVR

58

When are ACEI DOC?

1. Diabetic nephropathy, bc they diminish proteinuria & stabilize renal function
2. They improve internal hemodynamics with DECREASED glomerular EFFERENT arteriolar RESISTANCE & a resulting REDUCTION of intraglomerular capillary pressure

Don't use concurrently with K+ sparing diuretics bc can result in HYPERkalemia

59

ACEI ADR

1. Severe HYPOtension can occur after initial doses in pots who are HYPOVOLEMIC
2. DRY COUGH = MC!!
* due to increased levels of BRADYKININ
3. Acute renal failure in patients with bilateral renal artery stenosis
**in renovascular HTN, glomerular filtration pressures are maintained by vasoconstriction of the post-glomerular arterioles, an effect mediated by AGII-->ACEI can therefore ppt a significant reduction in GFR & cause acute renal failure
4. Angioedema is rare but may be potentially fatal; more common in blacks
5. PREGNANCY CATEGORY D: DO NOT USE IN PREGNANCY bc can cause SEVERE renal pathology in fetus
6. DRUG interactions: HYPERkalemia: if K+ sparing diuretics & ACEI are concurrently used

60

Angiotensin Receptor Blockers (ARBs) uses & MOA

1. Block the ATII type 1 (AT1) receptor
2. have NO effect on bradykinin metabolism & are therefore MORE SELECTIVE blockers of angiotensin effects than ACEI
3. ARBS provide benefits similar to those of ACEI in patients with heart failure & chronic kidney disease

61

ARB ADR

1. Noticeably lower incidence of cough (bc no effect on bradykinin metab)
2. hyperkalemia
3. renal effects
4. pregnancy category D: DO NOT use in pregnancy! (bc can cause renal pathology in fetus)

62

Alpha Blockers

1. alpha 1 selective drugs produce their antihypertensive effects by selectively blocking alpha 1 receptors in arterioles & venues
2. postural hypotension can be seen
3. used in men with concurrent HTN & BPH
4. nonselective alpha blockers work by blocking both the presynaptic and postsynaptic receptors--> tachycardia

63

Men with concurrent HTN & BPH should use

alpha 1 selective blockers
1. prazosin
2. terazosin
3. doxazosin

64

alpha 1 selective blockers

1. prazosin
2. terazosin
3. doxazosin

used primarily in men with concurrent HTN & BPH

65

Used in diagnosis & treatment of pheochromocytoma

nonselective alpha blockers:
1. phentolamine
2. phenoxybenzamine

work by blocking both the presynaptic and postsynaptic receptors--> tachycardia

66

nonselective alpha blockers

1. phentolamine
2. phenoxybenzamine

work by blocking both the presynaptic and postsynaptic receptors--> tachycardia

67

4 MOA Vasodilators use

dilate vessels by acting directly on SM cells through NONAUTONOMIC mechanisms
1. Release of NO
2. Blockade of Ca Channels
3. Opening of K+ Channels
4. Activation of D1 receptors

68

Vasodilators that act by releasing NO

1. Nitroprusside
2. Hydralazine
Other drugs that act by this mechanism are
1. Nitrates
2. Histamine
3. ACh

69

Vasodilators that act by Blockade of Ca channels

1. Verapamil
2. diltiazem
3. DHP like nifedipine, amlodipine

70

Vasodilators that act by Activation of D1 receptors

Fenoldopam

71

Vasodilators that act by Opening K+ Channels

1. minoxidil
2. diazoxide

72

MOA by which Vasodilators that act by Opening K+ Channels WORK

1. intercellular K ion concentration (150mM) > extracellular K ion concentration (3-4 mM)
2. K channel opening--> outflow of K ions ---> hyper polarization --> a series of cellular responses like smooth muscle relaxation

73

vasodilators that act on the venous bed

1. nitrates (more V>A)
2. ACEI (both venous & arterial beds)
3. alpha 1 antagonists (both venous & arterial beds)
4. Nitroprusside Sodium (both venous & arterial beds)

74

vasodilators that act on the arterial bed

1. ACEI (both venous & arterial beds)
2. alpha 1 antagonists (both venous & arterial beds)
3. Nitroprusside Sodium (both venous & arterial beds)
4. Ca-antagonists (almost entirely act on arterial bed)
5. hydralazine
6. minoxidil
7. nitrates (more V>A)

75

Hydralazine

1. acts by release of NO
2. arteriolar vasodilator
3. used in low doses bc of toxicities
4. combo of hydralazine w nitrates is approved for patients with both BPH & heart failure--esp blacks!
5. major route of metabolism = acetylation
a) rapid acetylators = reduced bioavailability (30%)
b) slow acetylators = 50% bioavailability

6. Toxicities: Compensatory respones:
1. tachycardia
2. salt & water retention

7. Drug induced REVERSIBLE lupus erythematous like syndrome, characterized by:
1. arthralgia
2. myalgia
3. skin rashes
4. fever (in slow acetylators)

76

Combo approved for patients with BPH & heart failure, especially blacks

Combo of hydralazine + nitrates

77

Toxicities assoc with Hydralazine

Toxicities:
Compensatory respones:
1. tachycardia
2. salt & water retention

Drug induced REVERSIBLE lupus erythematous like syndrome, characterized by:
1. arthralgia
2. myalgia
3. skin rashes
4. fever (in slow acetylators)

*Used in low doses bc of toxicities

78

Minoxidil

1. reserved for severe HTN
2. arteriolar vasodilator
3. acts as a K+ channel opener--> hyper polarization --> relaxes vascular smooth muscle
*after activation of a KATP channel, K+ efflux occurs from the vascular cell membrane-->hyperpolarization--> smooth muscle relaxation --> decreased BP
4. Toxicities:
a) Severe compensatory responses:
1. tachycardia
2. palpitations
3. angina
4. edema
b) hypertrichosis/hirsutism (increased hair growth)
5. Other use: topical minoxidil (as rogaine) is used as a stimulant of hair growth for correction of baldness

79

Reserved for severe HTN

Minoxidil

80

Arteriolar vasodilators

1. Minoxidil
2. Hydralazine

81

Toxicities assoc with Minoxidil

a) Severe compensatory responses:
1. tachycardia
2. palpitations
3. angina
4. edema

b) hypertrichosis/hirsutism (increased hair growth)

82

Rogaine

topical minoxidil used as a stimulant for hair growth to correct baldness

83

parenteral vasodilators (act on both arteries & veins) used in hypertensive emergencies

Sodium Nitroprusside & Diazoxide

84

Sodium Nitroprusside

1. Parenteral vasodilator (acts on both arteries & veins)
2. used in hypertensive emergencies
3. Structure: grease iron center complex w 5 cyanide moieties & a nitrosyl group (44% cyanide by weight)
4. SHORT acting drug (few minutes)--> so given by IV infusion
5. MOA: release of NO from the drug molecule (NO donor) stimulates GC & increases cGMP in smooth muscle
6. Toxicities:
1. Excessive hypotension
2. tachycardia
3. causes accumulation of cyanide (cyanide toxicity)
4. manifests as lethargy, disorientation, muscle spasms & convulsions
5. cyanide toxicity treated by Na thiosulfate or hydroxocobalamine

85

lethargy, disorientation, muscle spasms & convulsions
a) diagnosis
b) treatment

a) Cyanide toxicity
b) cyanide toxicity treated by Na thiosulfate or hydroxocobalamine

86

Toxicities associated with Sodium Nitroprusside

1. Excessive hypotension
2. tachycardia
3. causes accumulation of cyanide (cyanide toxicity)
-->manifests as lethargy, disorientation, muscle spasms & convulsions
-------->cyanide toxicity treated by Na thiosulfate or hydroxocobalamine

87

Diazoxide

1. Given by IV infusion, DOA several hours
2. acts by opening K+ channels (hyper polarization)
3. prevents/reduces smooth muscle contraction
4. also reduces insulin release-->used to treat hypoglycemia produced by insulinomas
5. ADR:
1. hypotension
2. hyperglycemia
3. salt & water retention

88

Used to treat hypoglycemia produced by insulinomas

Diazoxide bc it reduces insulin release

89

ADR of Diazoxide

1. hypotension
2. hyperglycemia
3. salt & water retention

90

Fenoldopam

1. peripheral arteriolar dilator
2. used for hypertensive emergencies
3. and postoperative hypertension
4. agonist @ D1 receptors
5. causes vasodilation particularly in RENAL VESSELS
6. 1/2 life = 10 minutes
7. administered by continuous IV infusion

91

alpha 2 selective agents

1. clonidine
2. methyldopa

92

alpha 2 selective agents: MOA

1. activates alpha 2 receptors in the CNS (bc readily enter CNS)
2. cause decrease in sympathetic outflow
3. -->decrease in BP ( bc decreases CO &/or TPR)
4. -->major compensatory response is SALT RETENTION

93

Clonidine

1. reduces BP by reduction in CO due to DECREASED HR & Relaxation of capacitance vessels, with a REDUCTION in peripheral vascular resistance

Toxicities:
1. Dry mouth
2. Sedation
3. Sudden withdrawal-->rebound HTN (this is treated with alpha blockers i.e. phentolamine)

94

How do you treat the rebound hypertension associated with sudden withdrawal of clonidine

alpha blockers ie phentolamine

95

Methyldopa

1. prodrug (converted into active metabolite methylnorepinephrine in the brain)
2. ----->this stimulates central alpha 2 adrenoceptors
3. widely used in the past but is now used primarily for HTN DURING PREGNANCY

Toxicity:
1. Sedation
2. methyldopa causes HEMATOLOGIC IMMUNE TOXICITY (POSITIVE Coomb's test)
-->may progress to hemolytic anemia

96

primarily used for HTN during pregnancy

methyldopa

97

Ganglion blocking drugs used to treat hypertension

1. Hexamethonium
2. trimethaphan
a) these are nicotinic blockers acting in the ganglion
b) cause a severe reduction in BP
*No longer used clinically
**Major compensatory response = salt retention

98

Hexamethonium & trimethaphan

1. Ganglion blocking drugs used to treat hypertension
2. these are nicotinic blockers acting in the ganglion
3. cause a severe reduction in BP
4. No longer used clinically
5. Major compensatory response = salt retention

99

Toxicity associated with ganglion blockers

a) symptoms associated with parasympathetic blockade:
1. blurred vision, dizziness, syncope
2. constipation*
3. urinary hesitancy--particularly with BPH
* remember parasympathetic carried via vagus!

b) symptoms associated with sympathetic blockade:
1. sexual dysfunction
2. orthostatic hypotension

THIS IS WHY WE NO LONGER USE GANGLION BLOCKERS TO TREAT HTN

100

Adrenergic neuron blockers used to treat HTN

1. drugs depleting NE stores in the adrenergic nerve terminal (reserpine)
2. Drugs depleting & blocking the release of stored NE (guanethidine)
3. both lead to decrease in SNS activity-->decrease in BP
4. compensatory response = salt retention

101

Reserpine

drugs depleting NE stores in the adrenergic nerve terminal

1. Reserpine blocks the vesicular uptake & storage of biogenic amines
2. by interfering w an uptake mechanism (vesicular membrane associated transporter-VMAT) -->depletion of NE, serotonin & dopamine
3. both very effective as antihypertensive, but has more toxicities
4. Reserpine READILY CROSSES BBB-->depletion of cerebral amine stores-->sedation, mental depression & parkinsonism symptoms

102

Guanethidine

Drugs depleting & blocking the release of stored NE

1. Inhibits the release of NE from sympathetic nerve endings
2. guanethidine is transported across the nerve membrane by the same mechanism that transports NE (NET)
--->uptake is essential for the drug's action
3. Once it has entered the nerve it's concentrated in transmitter vesicles, where it replaces NE-->causes gradual depletion of NE stores

103

ADR of reserpine

mental depression

104

ADR of guanethidine

1. orthostatic hypotension (bc lost sympathetic regulation)
2. sexual dysfunction (bc loss of sympathetic effects)
3. diarrhea (unopposed PNS activity)
4. If used with cocaine & TCAs--> can BLOCK the effect of guanethidine bc G uses the catecholamine repute pump that is inhibited by cocaine & TCAs!

105

Hypertensive Emergency/Crisis Causes

1. ingestion of tyramine-rich goods in patients taking MAOIs (use labetalol)
2. pre-eclampsia
3. Recreational drug use (cocaine, amphetamines)-->need to use alpha and beta blockers)
4. Pheochromocytoma (massive release of endogenous catecholamines)
5. Thyrotoxicosis (hyperthyroidism)
6. sudden withdrawal of beta blockers, clonidine

106

Symptoms of thyrotoxicosis (hyperthyroidism)

-Sudden weight loss, even when your appetite and the amount and type of food you eat remain the same or even increase
-Rapid heartbeat (tachycardia) — commonly more than 100 beats a minute — irregular heartbeat (arrhythmia) or pounding of your heart (palpitations)
-Increased appetite
-Nervousness, anxiety and irritability
-Tremor — usually a fine trembling in your hands and fingers
-Sweating
-Changes in menstrual patterns
-Increased sensitivity to heat
-Changes in bowel patterns, especially more frequent bowel movements
-An enlarged thyroid gland (goiter), which may appear as a swelling at the base of your neck
-Fatigue, muscle weakness
-Difficulty sleeping
-Skin thinning
-Fine, brittle hair

107

Symptoms of pheochromocytoma

-episodic and sudden onset of severe headaches.
sweating.
-abdominal pain.
-hypertension (high blood pressure) which may be resistant to conventional medications.
-rapid heart rate.
-irritability and anxiety.

108

symptoms of pre-eclampsia

1. High BP
2. Protein in urine

109

Drugs used to treat Hypertensive Emergencies

1. Parenteral antihypertensive medications are used to lower BP RAPIDLY
2. MC used drug to treat = Sodium Nitroprusside
Also used:
-fenoldopam
-nitroglycerine
-labetalol
-calcium channel blockers
-diazoxide
-hydralazine

110

MC drug used to treat hypertensive emergencies

Sodium Nitroprusside

111

Drug used to manage intraoperative & postoperative hypertension

Esmolol

112

Drugs used to treat angina pectoris & contraindicated drugs

Used: 1. beta blockers, CCB
Contraindicated: direct vasodilators

113

Drugs contraindicated to treat bradycardia, heart block, sick sinus syndrome

1. beta blockers. labetalol, verapamil, diltiazem

114

ADR associated with clonidine & methyldopa

CNS: sedation & drowsiness (up to 50%); nightmares; decreased REM sleep (up to 40% with clonidine)

Cardio: Clonidine--> can cause hypertensive crisis when drug is withdrawn, may --> tachycardia, sweating, nausea, tremor, restlessness, apprehension & can be life threatening

GI: xerostomia (clonidine up to 50%, methyldopa up to 10%, centrally mediated

Other Symptoms:
sexual dysfunction
skin eruption
+ coombs test w methyldopa (up to 30% w long-term therapy)
hemolytic anemia occurs in 1-5% of cases with methyldopa

115

Stimulation of alpha 2 adrenoreceptors results in

1. DECREASES sympathetic outflow & INCREASES vagal outflow
2. stimulation of alpha 2 receptors on NE terminals DECREASES NE release

116

What effect will reserpine have on the content of NE within the nerve terminal? Why?

1. the consequence of reserpine = that dopamine & any NE present in the cytoplasm are decimated by MAO-->so the vesicular content of NE falls
2. bc of the depletion of NE in adrenergic nerves--> fall in BP & a pictures of PNS dominance with nasal stuffiness & diarrhea
3. bc of the central depletion of amines patient s may complain of
a) depression--due to depletion of dopamine
b) Parkinsonism
c) galactorrhea