Systemic Arterial Pressure - Long-term Regulation

  • While changes to the Systemic Vascular Resistance (SVR) can transiently affect the systemic arterial pressure, arterial pressures tend to return to their original baseline within hours even if the changes to SVR are maintained. A variety of empirical studies have demonstrated that long-term control of the systemic arterial pressure over timescales of days, weeks, and months is principally regulated by the kidneys and is not dependent on changes to the systemic vasculature. The capacity of the kidneys to control arterial pressure depends on their ability to modify the extracellular fluid (ECF) volume which in a healthy individual determines the total blood volume. We first discuss how kidneys can control the extracellular fluid volume and subsequently describe how ECF volume is connected to systemic arterial pressures in healthy and pathologic contexts. The concepts discussed here heavily depend on a sound understanding of renal physiology; consequently, it may be worthwhile to revisit this page after reading through the Renal Physiology section.
Renal Volume Regulation
  • The kidneys respond to changes in systemic arterial pressure by modifying their urinary excretion of sodium and water. When arterial pressures are elevated, renal urinary excretion of sodium and water increases; conversely, when arterial pressures are deficient, renal urinary excretion of sodium and water decreases. The mechanisms which connect changes in arterial pressures to renal urinary excretion of salt and water are described more fully in ECF volume regulation and principally rely on mechanisms pressure natriuresis and the RAAS System. Nevertheless, this relationship between systemic arterial pressures and renal urinary excretion is largely independent of the SVR; consequently, whether or not the SVR is high or low, the kidneys will respond as described above by matching their urinary excretion to the effective systemic arterial pressure
  • As described more fully in ECF volume regulation the capacity of the kidneys to regulate urinary salt and water excretion allows these organs to regulate the total ECF volume which, as discussed below, is a major determinant of systemic arterial pressure in healthy individuals. Taken together, the relationship between arterial pressure, renal salt and water excretion, and ECF volume resembles a negative feedback control circuit in which changes to arterial pressure modulate renal sodium and water excretion which in turn affect ECF volume and thus modulate arterial pressure. Once again, this negative feedback appears to act completely independently of the SVR and explains why changes to the SVR can only affect arterial pressures transiently.
  • While a rapid increase in SVR will immediately boost the blood pressure, the kidneys will respond by progressively excreting salt and water, thus reducing the ECF volume and thus causing a slow decline in arterial pressure. Conversely, while a rapid decrease in SVR will immediately reduce the blood pressure, the kidneys will respond by retaining more salt and water than that ingested, thus increasing the ECF volume and thus causing a slow increase in the arterial pressure
ECF Volume and Arterial Pressure
  • Overview
    • In healthy individuals the total volume of the extracellular fluid is proportional to the systemic arterial pressure. Although this may appear to be an intuitive relationship, the physiological mechanism by which these two variables are linked is rather complex and is described below. However, in a variety of disease states the connection between ECF Volume and arterial pressure is deranged which can lead to increases in ECF volume without proportional enhancements of systemic arterial pressure.
  • Healthy State
    • In healthy individuals, increases in ECF volume result in a proportional increase in the total blood volume. As described in our discussion of the vascular function curve, an increase in total blood volume will enhance the "Mean Systemic Pressure" which in turn increases the venous return and thus the cardiac preload. Courtesy of the Frank-Starling Relationship, increased preload on the heart will enhance the cardiac output. Finally, as discussed in systemic arterial pressure regulation, an increased cardiac output will boost the systemic arterial pressure so long as the SVR remains constant. In this way, an increase in ECF volume results in an increase in the arterial pressure; conversely, a decrease in ECF volume will yield a decline in arterial pressure.
  • Diseased State
    • In certain disease states, increases in ECF volume does not result in proportional increases in the total blood volume. This occurs in contexts of deranged Starling Forces in which fluid leaks out of the vasculature and thus does not contribute to the total blood volume but instead contributes to states of generalized edema, peripheral edema, or ascites. In such cases, the renal mechanisms of long-term arterial pressure regulation in fact exacerbate these edematous states. This occurs because the kidneys continue to resorb salt and water in an attempt to boost the systemic arterial pressure; however, instead of contributing to correcting the deficient arterial pressure, the additional fluid volume simply ends up in the interstitial fluid and thus aggravates the edema. Frequently, such edematous states are corrected by using diuretics, which modulate renal physiology in such a way that the kidneys excrete large volumes of salt and water, thus decreasing the ineffective additional ECF volume and correcting the edema