Diastolic blood pressure (DBP) is the second, or lower, number in a blood pressure reading, representing the force exerted on artery walls when the heart relaxes and refills with blood between beats. An elevated DBP signals that the body’s vascular system is maintaining an abnormally high resting pressure. While high systolic pressure is often more concerning for older adults, a rise in DBP is a significant marker of future cardiovascular risk, especially for individuals under the age of 50. Understanding the underlying mechanisms driving this elevation is necessary to address the various factors that cause it.
Understanding the Mechanics of Diastolic Pressure
The primary physiological factor determining diastolic blood pressure is the total resistance within the smallest blood vessels, known as the peripheral vascular resistance (PVR). This resistance is controlled mainly by the state of the arterioles, which are the tiny resistance vessels leading into the capillaries. When these arterioles narrow, a process called vasoconstriction, the flow of blood is restricted, creating a backup of pressure in the larger arteries during the heart’s relaxation phase.
The elasticity of the large arteries, such as the aorta, also plays a role in maintaining DBP through the Windkessel effect, where these vessels recoil to propel blood forward during diastole. However, a rise in DBP is predominantly driven by increased PVR, reflecting a widespread tightening of the peripheral arterioles. This is distinct from the stiffness of large arteries, which tends to increase systolic pressure. Therefore, DBP elevation signals a mechanical problem in the microcirculation, where increased tone in the resistance vessels is impeding blood runoff.
Primary Lifestyle and Dietary Factors
A diet high in sodium is a significant contributor to DBP elevation through both fluid dynamics and direct vascular effects. Excessive salt intake causes the body to retain more water, leading to an expanded blood volume. This increased fluid volume raises the overall pressure within the circulatory system. High sodium levels also directly increase the contraction of smooth muscle cells in the arteriole walls, which promotes vasoconstriction and a higher PVR.
Chronic stress activates the sympathetic nervous system, the body’s “fight-or-flight” response, which causes repeated surges of vasoconstricting hormones like adrenaline and cortisol. These hormones trigger the narrowing of arterioles, acutely increasing peripheral resistance and spiking DBP. Chronic activation of this hormonal cascade can lead to structural changes in the blood vessels and contribute to sustained hypertension.
Obesity and excess weight raise DBP by increasing the body’s overall demand for blood circulation. The heart must pump blood to a greater volume of tissue, resulting in an expanded blood volume and increased cardiac output. This condition often involves an increase in sympathetic nervous system tone and inflammatory factors, which promote microvascular dysfunction and structural remodeling, ultimately raising PVR.
A lack of regular physical activity or a sedentary lifestyle independently contributes to higher DBP, even when controlling for body weight. Prolonged sitting causes a measurable decline in endothelial function, particularly in the arteries of the lower limbs. Regular activity, in contrast, promotes vascular conditioning that helps maintain the appropriate vasodilatory tone and reduces peripheral resistance.
Excessive alcohol consumption, particularly chronic heavy drinking, consistently increases DBP over time by stimulating the sympathetic nervous system and elevating stress hormones like cortisol and renin. Alcohol can also cause endothelial injury and inflammation, which impairs the ability of blood vessels to regulate their tone. While a large dose of alcohol may cause a temporary drop in blood pressure, a rebound effect occurs later that results in a net increase in DBP.
Secondary Disease States and Medications
Obstructive Sleep Apnea (OSA) is a frequent cause of elevated DBP. Repeated episodes of hypoxia and arousal during sleep trigger persistent overactivity of the sympathetic nervous system. This sustained sympathetic outflow causes chronic vasoconstriction and an increase in peripheral vascular resistance, keeping DBP elevated throughout the night and the day.
Chronic kidney disease elevates DBP primarily through the dysregulation of the Renin-Angiotensin-Aldosterone System (RAAS). Impaired kidney function leads to the overactivation of this hormonal system, generating high levels of Angiotensin II, a powerful vasoconstrictor. Angiotensin II directly increases systemic vascular resistance, and it also stimulates the release of Aldosterone, which promotes the retention of sodium and water, further expanding blood volume and raising pressure.
Several common medications can cause DBP elevation as a side effect. Nonsteroidal Anti-inflammatory Drugs (NSAIDs) inhibit the production of vasodilatory prostaglandins. This inhibition leads to unopposed vasoconstriction and increased peripheral vascular resistance, along with an increased tendency for sodium and water retention. Similarly, corticosteroids can raise blood pressure due to their mineralocorticoid effects, leading to fluid retention and higher blood volume.