Stress and High Blood Pressure

 Stress and High Blood Pressure

Stress and High Blood Pressure

All of us must have seen persons suffering from high blood pressure in our surroundings. At times, high blood pressure can affect the comparatively lower age group people either. Have you ever questioned him on how he gets his blood pressure increased? Researchers have discovered the truth that stress can have an influence to produce high blood pressure. It also makes worse the situation in the existing hypertensive (people with high blood pressure) patients. Stress activates the secretion of stress hormones in our bodies. The stress hormones identified are adrenaline, dopamine, and cortisol. All of these hormones have straight role-playing activities in increasing blood pressure.

Adrenaline has got an act of positive modulator over the α-receptors present in numerous tissues in our body. The intervention of α- receptors in the mechanism of our body is like this –

The prejunctional α2-receptors help to help inhibit neuronal Ca2+ channels and, reduce the availability of intracellular Ca2+ by decreasing cAMP (cyclic Amino Mono Phosphate) production. After that, the neurotransmitter (adrenaline and noradrenaline) secretion is also diminished. Hyperpolarization mediated by the activation of K+ channels may also take place.

In smooth muscles of our body as well as the vascular muscles contain a lot of α-receptors. The contraction of muscles takes place by the action of the α1 receptors. The activated G protein amplifies IP3/DAG production. After that, there is the recruitment of Ca2+ from the intracellular organelle. The bulk of the Ca2+ comes from intracellular mitochondria. Ca2+ triggers the Calmodulin-dependent Myosin light chain kinase (it is an enzyme present in the striated and smooth muscles). This enzyme facilitates the phosphorylation of myosin fiber. It helps the contraction of the Actin-Myosin complex. In this way, the whole muscle fiber is contracted. The α2 receptors which are vasoconstrictors in nature increase Ca2+ influx without the utilization of IP3 most likely.

Glucocorticoid hormones inhibit capillary permeability. It also maintains the muscular tones of the arterioles and contractility of the myocardium (heart muscle). They have a lenient and pressor action of Adrenaline and Angiotensin. They also play a permissive role in the formation of high blood pressure to occur. The chief mineralocorticoid action is an augmentation in the Sodium reabsorption from the distal convoluted tubule in the nephron of the kidney. There is a relative increase in the excretion of Potassium and hydrogen ions. If there is a high level of mineralocorticoid, as in the cases of stress, the maximal tubular reabsorptive capacity for Sodium is increased. In turn, this high level of Sodium brings water from the distal convoluted tubules of the kidney (reabsorption). The total blood volume is increased and it helps in the formation of high blood pressure.

The peripherally formed Dopamine (DA) is responsible for the increase in the heart rate in amount to its action on β-adrenergic receptors. Though Dopamine stimulates adrenergic receptors of blood vessels too, a major increase in blood pressure is not seen. It affects more in younger people more because they have a more active adrenal gland which is capable to secrete stress hormones on a bigger scale as compared to aged persons.

So, it is obvious that stress has a direct triggering effect on hormone production and consequently, high blood pressure. If stress can be withdrawn, all the stress hormone levels will be back to their normal level and the blood pressure will be normal too.