Hypertension (HTN), commonly known as high blood pressure, induces pathological changes throughout the cardiovascular system, particularly in the body’s arteries. One reason that arteries suffer a disproportionate amount of damage stems from the basic anatomy of the human circulatory system. The left ventricle of the heart generates far more contractile force than the heart’s other chambers. The arterial system constitutes the high pressure side of circulation; consequently, when the left ventricle ejects blood into the aorta, its walls are exposed to a surge of pressure with each heart beat. In chronically elevated blood pressure, the large arteries can accommodate the stronger pressure waves due to their thick walls; smaller arteries, however, undergo the pathological process known as atherosclerosis. More on that in a moment.
Years of research have revealed that the heart is only part of the story. It seems that the sympathetic nervous system, the kidneys, smooth muscle, and endothelial cells lining the blood vessels all contribute to the dysregulation of vascular tone culminating in hypertension. Surprisingly, the cause/s of 90% of HTN cases remain obscure. Risk factors include family history, obesity, smoking, and, in some cases, excessive sodium intake. Regardless of the etiology of HTN, its chronic effects are well understood.
Medium sized arteries: Atherosclerosis
These arteries seem to be the blood vessels most prone to developing atherosclerosis. In the popular press, this term is defined as “hardening of the arteries”, a largely accurate description. Basically, when arterial walls are subject to chronically elevated pressure, cells called fibroblasts proliferate within the intimal layer of the arterial wall, a process called intimal thickening. Comorbid conditions like high cholesterol and diabetes further accelerate atherosclerosis. Over time, the lumen of these vessels becomes progressively narrower, impairing blood flow in many parts of the body, such as the lower extremities as well as the coronary arteries supplying the heart muscle and the carotid arteries, which supply blood to the brain. Not surprisingly, this sets the stage for heart attacks and strokes, two of the leading causes of death in the Western world today. Poor circulation in the legs and feet is, of course, a set up for gangrene and amputation.
Small arteries and capillaries: Retinal damage and Lacunar infarcts
Hypertensive damage to small vessels is observed most readily in the retina. Chronic HTN wreaks havoc on the retinal vessels. Ophthalmologists have coined descriptive terms for these pathological changes including cotton wool spots, copper wires, and proliferative retinopathy, most often seen in diabetics.
In addition to retinal damage and blindness, a second consequence of long standing HTN on small blood vessels is a phenomenon called lacunar infarcts. These can be thought of as microvascular ruptures or ministrokes, which often occur in a region of the brain called the basal ganglia. Lacunar infarcts can produce distinct motor deficits including expressive aphasia, or difficulty with motor control of speech.
Kidney damage – Chronic Kidney Disease
No discussion of HTN induced vascular damage would be complete without mentioning chronic kidney disease. Long standing HTN causes irreversible damage to the renal glomeruli. Over the course of several years, the protein network surrounding the glomerular blood vessels, called the basement membrane, becomes scarred with collagen and other fibrotic debris. The rate of blood filtration through the kidneys, called the glomerular filtration rate or GFR, declines as the nephrons gradually lose their ability to filter plasma into urine. Kidney failure ensues when 75% or so of the renal nephrons become non-functional.
Unfortunately, the kidneys respond to this decline in GFR by activating a protein called angiotensin. This protein raises blood pressure in three ways: 1) direct vasoconstriction; 2) production of the hormone aldosterone, which causes sodium retention; 3) activating hypothalamic neurons responsible for triggering the sensation of thirst. This creates a vicious cycle in which the failing kidneys hasten their own demise by continually raising arterial blood pressure. Ultimately, patients with chronic renal failure require dialysis or a kidney transplant to remain alive.
