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RECAP: what is blood pressure and how is it regulated?

Blood pressure is the pressure exerted by the blood on the blood vessels.

Blood Pressure Regulation:

SHORT TERM: via neural systems, eg. baroreceptors

LONG TERM: via hormones and Na+ balance, eg. ECFV, degree of vasoconstriction


How can high blood pressure arise?

- an increase in ECFV
- an increase in vasoconstrictor agents
- a reduction in vasodilator agents


What are the two types of hypertension?

PRIMARY HYPERTENSION ( >90% of cases): has an unknown cause

SECONDARY HYPERTENSION (~10% of cases): has an identifiable cause

Some causes of hypertension:
- renal diseases (eg. glomerulonephritis, diabetic nephropathy)
- vascular causes (eg. renal artery stenosis)
- hormonal abnormalities (eg. Conn's syndrome, Cushing's syndrome, phaeochromocytoma)
- drugs (eg. contraceptive pill)
- pregnancy (eg. pre-eclampsia)
- monogenic genetic diseases (eg. Liddle's)


Describe essential hypertension ( >90% of cases).

It has a prevalence in urban-based populations (~20%).

Genetic predisposition and environmental factors are proposed to cause essential hypertension through many mechanisms:
- increased sympathetic nervous system (SNS)
- increased renin-angiotensin-aldosterone system (RAAS)
- obesity/ insulin resistance
- endothelial dysfunction
- defects in vascular smooth muscle contraction
- defects in renal Na handling, increased salt intake
- age
- ethnicity (eg. it's more common in Afro-Caribbean groups)


Why do we need to treat hypertension?

A reduction in blood pressure levels reduces the relative risk of consequences:
- a 5 mmHg drop in diastolic BP for 5 years
- reduces the chances of strokes by 42%
- reduces the chances of heart attacks by 16%
- reduces the vascular mortality by 21%


What are the goals of anti-hypertensive treatment?

The goals of anti-hypertensive treatment:
- adequate blood pressure control ( <140/90 mmHg), to alter the relative risk
- prevention of organ damage
- controlling other cardiovascular risk factors


What are the three main treatment pathways for hypertension?

- non-pharmacological (eg. lifestyle modifications)
- pharmacological treatment
- surgical treatment (eg. Conn's Syndrome)


List some non-pharmacological treatments for hypertension (ie. lifestyle changes)?

- quit smoking (if applicable)
- weight control
- eat less salt
- regular exercise
- reduce alcohol intake
- behavioural therapies


List some pharmacological treatments for hypertension (ie.drugs)?

- major classes of antihypertensive drugs
- ACE inhibitors
- Angiotensin II receptor blockers
- diuretics
- drugs acting on the sympathetic nervous system
- vasodilators


What are some side effects of ACE inhibitors (caused by the decreased Angiotensin II effects)?

- cough (common) - due to bradykinin breakdown (con-compliance issue)

- angioedema (rare) - due to bradykinin breakdown (very serious, prevents breathing)


What are some side effects of ACE inhibitors and AT1 receptor blockers?

- hyperkalaemia (opposite to loop and thiazide diuretics) - this is due to decreased aldosterone, which leads to decreased Na reabsorption and hence decreased K excretion

- contraindicated in pregnancy - foetal problems

- contraindicated in renal stenosis - decreased efferent renal arteriole constriction, which decreases the pressure gradient across the Bowman's capsule, which leads to decreased GFR


Describe diuretics.

They increase sodium and water excretion. This reduced blood volume, which reduces CO, which reduces BP.

There are different types, such as loop diuretics, thiazides and potassium-sparing diuretics.

Some of their major side-effects are:
- hypokalaemia (with loop and thiazide, but not K-sparing)
- lipid abnormalities
- glucose intolerance/ hyperglycaemia (decreased insulin release)


What are the consequences of sympathetic nerve stimulation of the CVS?

β1 - increase HR and contractility, which increases CO, which increases BP

α1 - vasoconstriction, which increases TRP, which increases BP


How would you decrease sympathetic activity?

CNS: α2 adrenoreceptor agonists (eg. Clonidine, used in hypertensive crisis)

Ganglion blockers: NIC blockers (eg. Trimethapan, used in hypertensive crisis)

Synaptci blockade (eg. Reserpine, an old antihypertensive)


List some adrenoceptor blockers.

α1 blockers: cause the relaxation of vascular smooth muscle, eg. prazosin (used in hypertensive crisis)

β1 blockers: cause a reduction in CO and renin release (eg. atenolol)


Describe K channel openers as vasodilators.

Examples of K channel openers would be Minoxidil and Diazoxide.

When the K channel opens, there is a K efflux from the cells. This causes vascular smooth muscle hyperpolarisation. This leads to a reduction in VGCC activity, which leads to a reduction in [Ca]i.
This leads to less MLCK activity, which leads to increased relaxation, thus we have vasodilation.


Describe voltage-dependant Ca2+ channel blockers as vasodilators.

Examples of voltage-dependent Ca2+ channel blockers are dihydropyridines (such as Amlodipine). It is more vascularly selective.

They block voltage-gated Ca2+ channel activity in vascular smooth muscle cells. This causes a reduction in [Ca]i. This leads to less MLCK activity, which leads to increased relaxation, thus we have vasodilation.


What issues do you need to consider in selecting the drug therapy?

- essential vs. secondary hypertension
- evidence of efficacy
- side effects of the drugs
- drug interactions
- co-existing diseases
- quality of life
- economic considerations

, among others ...

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