Mechanisms behind arterial hypertension

An increase in vasoconstrictive activity

The sympathetic nervous system.

This system plays a key role in regulating vascular tonus. This system is involved in regulating the cardiac system and peripheral vascular resistance which are two of the major defining components of arterial pressure.


Noradrenaline, released from adrenergic synapses causes arterial and venal constriction through the activation of the postsynaptic receptors alfa1 and alfa2. As a consequence, the arterial pressure rises. On the other hand, the activation of beta2 postsynaptic receptors is associated with a reduction of vascular tonus, hence the lowering of arterial pressure.

The renal theory through the renin-angiotensin system

As a consequence of reduced renal blood flow (due to an ischemia of some sort), the cells of the juxtaglomerular apparatus produce a proteolytic enzyme; renin. Renin acts on angiotensinogen (an alfa2 globulin which is synthesized in the liver) and cleaves a decapeptide to release angiotensin 1.

The angiotensin-converting enzyme (ACE) found in the lungs converts angiotensin 1 to angiotensin 2. Angiotensin 2 is an octapeptide which has vasoconstrictive effects 4 to 10 times more powerful than adrenaline or noradrenaline.

This induces the release of aldosterone from the adrenal gland, causing the retention of sodium and the increase in arterial pressure. Angiotensin 2 is also a sympathetic, central and peripheral nervous system stimulator, therefore making the release of noradrenaline easier. With age, the secretion of renin is lowered in all individuals, whether or not they suffer from hypertensive disease.

This shows that the retention of sodium is accompanied by the progressive decrease of functional nephrons (lowered kidney function, of which the nephron is its functional unit, which makes up renal tissue).

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The effects of the sympathetic nervous system over the blood vessels are mediated via adrenaline, which is mainly produced from the medulla of the adrenal glands, and noradrenaline, which is released from the sympathetic nerve endings into the synaptic space.

Patients suffering from arterial hypertension experience an increase in sympathetic activity and a lowering of vagal activity. In patients suffering from sustained arterial hypertension, neurogenic factors affect the increase in peripheral vascular resistance perhaps through stimulating higher sensitivity of arterioles to the firing of the alfa receptors.

In elderly patients with stable arterial hypertension, the cardiac output is no longer elevated and the effects of the sympathetic nervous system are no longer present. 

Arterial hypertension may also be accompanied by damage sustained by the beta-adrenergic receptors. Younger patients suffering from threshold arterial hypertension often exhibit an increase in heart rate and output, which belie the involvement of the beta-adrenergic receptors.

Adrenaline also contributes to the emergence of a condition such as arterial hypertension. The plasma levels of this hormone are often elevated in patients suffering from threshold or moderated arterial hypertension.  

During very severe psychological trauma, the cerebral cortex becomes excited, and due to the extremity of the excitation, the cortex can no longer respond and becomes inhibited. As a consequence of this, the subcortical centers evade the control of the cortex and in conjunction with vasomotor centers become anarchic.

In this way, they transmit their impulses using the sympathetic system to the endocrine glands, the kidneys and the smooth muscle of the arterioles.  

Increase in vasodilation

The kallikrein-kinin system.

This system works in association with kininogen and forms bradykinin. Bradykinin causes the release of the endothelial-derived relaxing factor and of prostacyclin with vasodilatory properties.

Arterial natriuretic peptide.

This factor bears diuretic, natriuretic and vasodilatory properties. This factor is synthesized and secreted by the cardiac muscle cells in the walls of the atria of the heart.


The vasodilatory function of the prostaglandins is evident in their inhibitory effects on the vasoconstrictor properties of angiotensin II and noradrenaline.

Sodium retention in the kidneys

The retention of salt in the organism is one of the main mechanisms which dictates the development of arterial hypertension.
This is mediated via three mechanisms:

  • Sodium traps water, keeping the water from being lost in urine, and hence causing an increase in blood volume. 
  • Sodium becomes trapped in the vessel walls and as a consequence, the vessel walls begin taking in more water.
    The walls become thicker, therefore narrowing the lumen of the vessels, hence causing an increase in vascular resistance to blood flux and an increase in arterial pressure.  
  • Sodium and water cause an increased sensitivity of arterial walls to vasopressin and other related substances.
    These substances cause the arteries to contract and increase peripheral resistance. 

The increase of insulin in the blood

Hypertensive patients often exhibit hyperinsulinemia, which causes an increase in blood pressure through the re-absorption of sodium from the kidneys and the stimulation of the sympathetic of the nervous system.  

Damaging the endothelium

Many vasoactive substances are produced by the endothelium. Some of the most important substances include nitric oxide, also known as the endothelial-derived relaxing factor, which has vasodilatory properties.

The main role of nitric oxide is related to the fact that acetylcholine has vasoconstrictive properties in cases of endothelium damage. Damage to the endothelium occurs in patients suffering from arterial hypertension because the vasodilatory response to acetylcholine is lacking.  

Cell membrane disorders

It is theorized that in primary hypertension the sodium pump which affects the intake of sodium into the cell is damaged. In these conditions, the sodium gradient between the intracellular and extracellular environment is disrupted.

As a consequence, this condition causes an increase in the exchange of sodium for calcium, which leads to the buildup of calcium inside the cell. This has vasoconstrictive properties. This disorder seems to have an inheritable component.  

Medically Reviewed by a doctor on 26 Mar 2018
Medical Author: Dr. med. Diana Hysi