The kidneys play a central role in the long-term control of arterial pressure by regulating
sodium balance and extracellular fluid volume. The renin-angiotensin system is important in the regulation of the arterial pressure through its chronic effects on the pressure natriuresis relationship. Under physiologic conditions,
angiotensin II (Ang II) is important in causing the long-term relationship between arterial pressure and
sodium excretion to be very steep, so that minimal changes in arterial pressure are necessary to maintain
sodium balance in response to variations in
sodium intake. An inability to suppress Ang II formation in response to increases in
sodium intake can lead to
salt-sensitive
hypertension. Excess formation of Ang II, such as in
renovascular hypertension, causes the pressure natriuresis relationship to be shifted to higher arterial pressures so that higher arterial pressures are necessary to maintain
sodium balance. Ang II decreases pressure natriuresis by enhancing tubular reabsorption and/or reducing glomerular filtration. Because Ang II does not decrease glomerular filtration in most circumstances, the
sodium retaining actions of Ang II are usually caused by increased tubular reabsorption. However, there are a number of pathophysiologic conditions where Ang II interacts with various local autocrine and paracrine factors (such as
nitric oxide [NO],
eicosanoids,
adenosine, and
superoxide) to influence glomerular filtration rate. Ang II enhances tubular reabsorption either indirectly, through
aldosterone stimulation, via alterations in renal hemodynamics (physical factors or medullary blood flow), or by directly enhancing tubular
sodium transport. Converting
enzyme inhibitors or Ang II receptor antagonists improve pressure natriuresis and are very effective in the treatment of various forms of
hypertension associated with normal or enhanced activity of the renin-angiotensin system.