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High Blood Pressure & Diabetes - A Positive Feedback Loop

How diabetes and high blood pressure feed one another

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Updated February 22, 2008

Diabetes and high blood pressure are related diseases that feed one another and tend to get worse with time. In biological terms, the relationship between diabetes and high blood pressure is a type of positive feedback loop, where one step causes a second step and that second step “feeds back” to cause more of the first step.

The most well-studied example of the self-reinforcing relationship between diabetes and high blood pressure takes place in the kidneys. The kidneys are the body’s most important long-term blood pressure regulator. By balancing the amount of salt and potassium in the body, the kidneys ultimately control how much fluid is excreted as urine. This fluid regulating function helps modulate long-term blood pressure by physically controlling how much liquid is present in the blood vessels. Carrying out this function depends on a constant flow of blood across delicate capillary structures known as glomeruli (singular: glomerulus). The glomeruli are the filtering units of the kidney.

The high blood sugar levels associated with diabetes damage capillaries, including those that comprise the glomeruli. Through a complex series of steps, excess blood sugar actually causes the walls of capillaries to thicken and, in some cases, degrade entirely. While the precise mechanisms underlying this process are too complicated to discuss in detail, the end result is that the glomeruli become thicker, and are tricked into thinking that they aren’t receiving enough blood. As a result, the kidneys respond by raising blood pressure to restore “normal” blood flow through the glomeruli. Because they have been damaged, the glomeruli essentially require a permanent increase in blood pressure in order to continue filtering the blood. As time goes on, continued exposure to elevated sugar damages the glomeruli more, leading to ever increasing blood pressures as the kidneys try to correct the situation.

These elevated blood pressures have widespread effects on the other organ systems of the body, including the muscles and insulin secreting areas of the pancreas. In the muscles, higher pressure causes blood vessels to contract. As a result, less blood flows through the large muscle areas of the body. This leads to a decrease in the size of muscle cells and a decrease in the amount of sugar that those cells absorb from the blood. Because less sugar is being absorbed from the blood, the level of free sugar in the blood rises. This free sugar ultimately makes its way to the kidneys, where it contributes to further glomerular damage. Altered blood flow through the pancreas, as a result of autoregulation, can also lead to a decrease in insulin production, raising the blood sugar even higher.

Because diabetes and high blood pressure are so strongly self-reinforcing, it is vitally important to maintain tight control of both blood sugar and blood pressure. Even modest elevations of either in patients suffering from both diseases can quickly lead to an exaggerated amount (an “amplified” amount) of damage. This is the primary reason that treatment goals for blood sugar are more rigorous in the setting of high blood pressure and treatment goals for blood pressure are more rigorous in the setting of diabetes.

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Sources:

Tight blood pressure control and risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 38. UK Prospective Diabetes Study Group. BMJ 1998; 317:703.

K/DOQI Clinical Practice Guidelines and Clinical Practice recommendations for diabetes and chronic kidney disease. Am J Kidney Dis 2007; 49(Suppl 2):S17.

Jafar, TH, Stark, PC, Schmid, CH, et al. Progression of chronic kidney disease: the role of blood pressure control, proteinuria, and angiotensin-converting enzyme inhibition: a patient-level meta-analysis. Ann Intern Med 2003; 139:244.

Buse, JB, Ginsberg, HN, Bakris, GL, et al. Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association. Circulation 2007; 115:114.

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