Key result
Sodium loading increased renal cortical AT(1) receptor binding measured by PET compared with sodium deprivation in dogs, inversely correlating with renin-angiotensin system activity.
Does not support clinical use of renal PET AT1 imaging; leaves open its role in human hypertension research.
Increased sodium intake and enhanced sodium sensitivity are implicated in the pathogenesis of hypertension and in the control of a major regulator of BP, the type 1 angiotensin receptor (AT(1) receptor). An in vivo technique to study changes of renal AT(1) receptors by dietary sodium was developed that uses positron emission tomography (PET). PET revealed that renal cortical AT(1) receptor binding was increased in sodium-loaded compared with sodium-deprived dogs, which correlated with ex vivo estimations of AT(1) receptor numbers. Plasma renin activity, angiotensin II, and aldosterone were inversely related to changes in AT(1) receptor binding. These results demonstrate, for the first time in vivo, that the renal AT(1) receptor is inversely related to the activity of the renin angiotensin system, which may provide a compensatory mechanism to prevent inappropriate fluctuations in arterial BP. The ability to measure AT(1) receptor binding in vivo has potential significance for clinical studies of AT(1) receptors, because PET is a noninvasive imaging technique that is readily applicable in humans.
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Szabó et al. (2001) studied this question. Sodium loading vs. Sodium deprivation was evaluated on Renal cortical AT(1) receptor binding. Sodium loading increased renal cortical AT(1) receptor binding measured by PET compared with sodium deprivation in dogs, inversely correlating with renin-angiotensin system activity.
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