¶ … Hypertension
Essential hypertension or primary hypertension is a highly complex disorder. There are various factors modulating BP or blood pressure in order for adequate tissue perfusion to occur. These include:
Vascular reactivity
Vascular caliber
Humoral mediators
Circulating blood volume
Blood viscosity
Blood vessel elasticity
Cardiac output
Neural stimulation
History of high blood pressure in family
Ethnic background
Aside from these factors, the natural course of primary hypertension is progression from infrequent or occasional to established or frequent hypertension. There is a long, asymptomatic, and invariable period when the persistent hypertension then progresses into complicated hypertension. This means there will be target organ damage to the small arteries and aorta, retina, heart, kidneys, and central nervous system.
The journey to primary hypertension begins with prehypertension from ages 10-30 years. The transition to early hypertension occurs from ages 20-40 years. During this phase peripheral resistance is noticeable. After this stage is established hypertension and this occurs from 30-50 years leading to the last phase, complicated hypertension from ages 40-60 years.
There are various factors that influence BP regulation. Arterial BP can be considered a product of peripheral vascular resistance and cardiac output. Factors that affect cardiac output include renal function, sodium intake, and mineralocorticoids. Peripheral vascular resistance is reliant on humoral factors, the sympathetic nervous system, and local autoregulation. The effects produced by the sympathetic nervous systems are done so via the vasodilator beta effect or vasoconstrictor alpha effect.
Hypertension is an all too common disease, affecting millions. However, research states essential hypertension comes from the body's inability to excrete excess sodium via the kidneys. "Essential hypertension develops when the kidneys become unable to excrete the amount of sodium ingested, unless blood pressure is increased ... shift of the pressure natriuresis relationship toward abnormally high pressure levels is a pathophysiological characteristic of essential hypertension" (Bolivar, 2013, p. 2). While there are several factors that can lead to this, what makes essential hypertension its namesake is when there is no known cause for the hypertension.
Essential hypertension or primary hypertension often has no clearly defined aetiology. While the latest research suggests renal problems as a cause, from a practical standpoint, it is best defined as a level of blood pressure that when treated to lower blood pressure, provides major clinical benefits. The level of positive results changes from patient to patient, depending on absolute cardiovascular risk. Hypertension itself is defined as great than or equal to 140/90 mmHg.
The pathogenesis of primary hypertension has three common causes. They are genetic predisposition, disturbances in neurohumoral control mechanisms and vascular structure, an environmental and lifestyle influences. The first one, genetic predisposition means blood pressure can run in families. Many studies found a consistent level of correlation among first-degree relatives. Meaning, if one relative is found to have deviations from norm BP, then the first-degree relative will also deviate on average by +2 mmHg.
Environmental and lifestyle influences also contribute to a higher prevalence of hypertension, especially in economically developing countries. The "Western" diet of fast food and high salt foods contributes to not only obesity, but also high blood pressure. In terms of pathophysiology, there is appears to be a distinctive find in primary hypertension. That is an inappropriate increase in peripheral vascular resistance, as mentioned earlier, in relation to cardiac output.
What this means is the small arteries or arterioles have been remodeled and are characterized by higher media/lumen ration. There is also a stiffening of large conduit arteries like the aorta influencing the progression and development of hypertension, particularly systolic hypertension (MacGregor & Kaplan, 2010, p. 134). Hypertensions also leads to decreased nitric oxide production and endothelial dysfunction. This could be a consequence of hypertension more so than anything else.
Vascular reactivity or cardiovascular reactivity is commonly understood as a reflection of the physiologic changes of a person's heart from resting/baseline state to a kind of psychological/physical stressor or challenge. An exaggerated cardiovascular response typically indicates hypertension or some other coronary heart disease. Vascular caliber concerns the interactions among the frictional drag produced by the stream, as well as the sensitivity of endothelial cells to such a force. If the drag force put on the endothelial cells reaches a critical set-point, these the cells remain at rest with respect to the factors affecting caliber. Increases in the flow rate also increases the drag, appearing to induce the endothelium to produce a signal triggering relaxation of the subjacent...
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