How does the pathophysiology of hypertension (high blood pressure) differ between essential hypertension and secondary hypertension?
Hypertension, or high blood pressure, is a chronic condition that affects the force of blood against the artery walls. It can lead to serious complications such as heart disease, stroke, and kidney damage. Hypertension can be classified into two types: essential hypertension and secondary hypertension.
Essential hypertension, also known as primary or idiopathic hypertension, is the most common type of hypertension. It accounts for about 90-95% of all cases. The exact cause of essential hypertension is unknown, but it is influenced by genetic and environmental factors. Some of the risk factors for essential hypertension include:
– Age: Blood pressure tends to increase with age as the arteries become stiffer and narrower.
– Race: African Americans are more likely to develop essential hypertension than other races.
– Family history: Having a close relative with high blood pressure increases the likelihood of developing it.
– Obesity: Excess body weight puts more strain on the heart and blood vessels.
– Physical inactivity: Lack of exercise reduces the elasticity and efficiency of the blood vessels.
– Smoking: Tobacco use damages the lining of the arteries and increases blood pressure.
– Alcohol: Excessive alcohol consumption raises blood pressure and interferes with blood pressure medications.
– Diet: Eating too much salt, processed foods, saturated fats, and cholesterol can increase blood pressure.
– Stress: Chronic stress can activate the sympathetic nervous system, which increases heart rate and blood pressure.
Essential hypertension usually develops gradually over many years and does not have any specific symptoms. It can only be detected by regular blood pressure measurements.
Secondary hypertension, on the other hand, is caused by an identifiable underlying condition that affects the kidneys, arteries, heart, or endocrine system. It accounts for about 5-10% of all cases. Some of the causes of secondary hypertension include:
– Chronic kidney disease: Reduced kidney function can impair the regulation of fluid and electrolyte balance, leading to increased blood volume and pressure.
– Renal artery stenosis: Narrowing of the arteries that supply blood to the kidneys can reduce renal blood flow and trigger the renin-angiotensin-aldosterone system (RAAS), which increases sodium and water retention and vasoconstriction.
– Coarctation of the aorta: A congenital defect that causes a narrowing of the aorta, the main artery that carries blood from the heart to the body. This creates a pressure gradient between the upper and lower body parts, resulting in high blood pressure in the upper body and low blood pressure in the lower body.
– Pheochromocytoma: A rare tumor that produces excess catecholamines (adrenaline and noradrenaline), which stimulate the sympathetic nervous system and increase heart rate and blood pressure.
– Cushing’s syndrome: A condition that causes excess cortisol production by the adrenal glands or exogenous administration of glucocorticoids. Cortisol has multiple effects on blood pressure, such as increasing sodium and water retention, enhancing vascular reactivity, and stimulating the RAAS.
– Hyperaldosteronism: A condition that causes excess aldosterone production by the adrenal glands or exogenous administration of mineralocorticoids. Aldosterone increases sodium and water retention and potassium excretion, leading to increased blood volume and pressure.
– Hyperthyroidism: A condition that causes excess thyroid hormone production by the thyroid gland or exogenous administration of thyroid hormones. Thyroid hormones increase cardiac output, heart rate, and peripheral vasodilation, leading to increased blood pressure.
Secondary hypertension usually develops suddenly and may have symptoms related to the underlying condition, such as headache, palpitations, sweating, fatigue, or abdominal pain. It can be diagnosed by identifying the cause through laboratory tests, imaging studies, or biopsy.
The pathophysiology of hypertension differs between essential hypertension and secondary hypertension in terms of the mechanisms involved in increasing blood pressure. Essential hypertension is mainly due to increased peripheral resistance caused by structural and functional changes in small arteries and arterioles. These changes include hypertrophy (thickening) of smooth muscle cells, fibrosis (scarring) of connective tissue, inflammation (swelling) of endothelial cells, and reduced production of nitric oxide (a vasodilator). These changes are influenced by genetic factors that affect various pathways involved in vascular tone regulation, such as angiotensin II receptors, calcium channels, sodium-potassium pumps, endothelin receptors, etc. Environmental factors such as diet, stress, smoking, etc., can also modulate these pathways through hormonal or neural mechanisms.
Secondary hypertension is mainly due to increased cardiac output or increased blood volume caused by disorders that affect the kidneys, arteries, heart, or endocrine system. These disorders alter the normal feedback mechanisms that regulate blood pressure by affecting various hormones or enzymes involved in fluid and electrolyte balance (such as renin, angiotensin II, aldosterone), vascular tone (such as catecholamines, cortisol, thyroid hormones), or cardiac function (such as aortic pressure, cardiac output).
References:
– High blood pressure (hypertension) – Symptoms & causes – Mayo Clinic. https://www.mayoclinic.org/diseases-conditions/high-blood-pressure/symptoms-causes/syc-20373410
– Pathophysiology of hypertension – Wikipedia. https://en.wikipedia.org/wiki/Pathophysiology_of_hypertension
– Hypertension – World Health Organization (WHO). https://www.who.int/news-room/fact-sheets/detail/hypertension
