Essential Hypertension

The majority of people diagnosed with essential hypertension will have no obvious cause for their high blood pressure. This form of hypertension is often only discovered during a routine check up by a licensed medical practitioner. There is no definitive cause for essential hypertension but it is thought to include genetic, nervous system, and hormone factors.

The key feature in all patients with essential hypertension is an increase in resistance to blood flow through blood vessels. Scientists are investigating the mechanism of salt, the nervous system, and hormones specific to water balance on blood flow resistance.

Essential Hypertension

Salt Balance
Dietary salt, especially in preprepared food dishes is a likely culprit causing essential hypertension. Impaired kidney excretion of salt may be one of the first changes in the development of essential hypertension. Salt retention then causes increased blood volume and a subsequent increase in the heart’s work rate to circulate this increased volume. Total body salt is correlated with blood pressure in patients with essential hypertension. As salt levels rise, so does the person’s blood pressure.

The Nervous System
Blood vessel size and the heart’s work rate are partly controlled, subconsciously, by the nervous system. The sympathetic nervous system exerts its effect via specific neurotransmitters acting at these sites. Studies find that patients with essential hypertension tend to have hypersensitivity to these neurotransmitters resulting in exaggerated responses. Younger people with essential hypertension also tend to have higher resting plasma neurotransmitter levels than age-matched, normotensive controls.

Hormonal Causes of Essential Hypertension
The main hormone system controlling water balance and blood pressure is the renin-angiotensin-aldosterone system. Renin is released from the kidney into the blood where it then acts on angiotensinogen, to release angiotensin I. This is then converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II is a powerful vasoconstrictor and is therefore capable of inducing hypertension if renin release is unregulated. However, only a small proportion of patients with essential hypertension have raised plasma renin levels so this is not a pure causal relationship. However, many patients with essential hypertension do respond positively to treatment by drugs called ACE inhibitors which work to reduce the function of ACE.