Research ideas about Hypertension by Faizan Malik

(Following article contains research ideas about the possible causes of Hypertension and are contributed by Faizan Malik. He is one of the most talented students of Hajvery University having a very good research mind.)

Primary and Secondary Hypertension

A. Primary or “Essential” Hypertension

1. Etiology – unknown

2. Accounts for approximately 90% of hypertension

3. Onset typically in the fifth or sixth decade of life

4. Strong family history – 70-80% positive family history

a. If hypertension is present in both parents, risk of hypertension in off-spring is increased by 250%

b. BP correlations are stronger among parent and child than between spouses, suggesting that environmental factors are less important than genetic ones

c. Certain races (e.g. African Americans) are at much higher risk of hypertension

B. Secondary Hypertension

1. Identifiable underlying cause:

a. kidney disease

b. renal artery stenosis

c. hyperaldosteronism

d. pheochromocytoma

2. Represents approximately 10% of all hypertension

3. Has specific therapy, and is potentially curable

4. Often distinguishable from essential hypertension on clinical grounds

C. Approaches to understand potential mechanisms of hypertension

1. Identify demographics – unusual to see new-onset of essential hypertension in children or the elderly, family history of essential hypertension, race.

2. Identify co-morbid conditions – i.e. RAS is an extension of peripheral vascular disease

Role of the kidney in systemic hypertension

A. Evidence

1. With progressive loss of kidney function, virtually 100% of patients become hypertensive

2. Chronic kidney disease is the most common cause of secondary hypertension

3. Hypertension frequently improved or “cured” with hemodialysis.

Hypothesis I –

Kidney failure leads to impaired sodium excretion, resulting in expansion of the ECF, volume overload, and subsequent systemic hypertension.

1. Evidence supporting Hypothesis I

a. Blood volume correlates with systemic blood pressure in patients with advanced kidney disease.

b. Systemic hypertension due to kidney disease frequently responds to maneuvers that reduce ECF volume:

i. sodium restriction

ii. diuretics

iii. ultrafiltration (part of dialysis)

2. Mechanism of hypertension

a. Despite clear-cut volume expansion, cardiac output is near normal. Hypertension is primarily due to an increase in SVR.

b. Suggests abnormal vasoregulation, possibly related to SNS and RAAS.

Hypothesis II –

Impaired kidney sodium excretion is necessary to sustain all forms of hypertension.

a. Small changes in systemic BP should lead to marked changes in sodium excretion rates by the kidney

b. In normals, increased sodium intake leads to ECF expansion, increased CO and BP, increased kidney Na+ excretion, and normalization of hemodynamics.

c. Hypertension must be associated with resetting of this mechanism at a higher blood pressure. Although both normotensive and hypertensive patients are in a steady state (intake = output), the hypertensive patients achieve this balance at a higher blood pressure.

d. With increased dietary Na+, the hypertensive patients increase BP to a greater extent.

Conclusions:

The kidney plays an essential role in modulating systemic blood pressure by adjusting kidney sodium excretion rate (pressure natriuresis phenomena). Sustained systemic hypertension is believed to necessitate a disturbance of this phenomenon, resulting in impaired sodium excretion. Modulation of sodium intake and kidney sodium excretion (diuretics) effectively reduces blood pressure in the majority of patients.

Author (and for further ideas):

Faizan Malik, (e-mail: thinking_science@ymail.com), Batch-IV, Pharmacy Deptt., Hajvery University, Lahore, Pakistan


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