INCREASED DENSITY OF RENAL AMYLIN BINDING-SITES IN EXPERIMENTAL-HYPERTENSION

High-affinity binding sites for the pancreatic p-cell hormone amylin h ave been reported in the kidney, and it has been postulated that these sites may be involved in the genesis of hypertension. In the present study, we have used in vivo injection of I-125-amylin and in vitro aut oradiographic techniques to assess renal amylin binding in both a gene tic and a surgically induced model of hypertension. In the spontaneous ly hypertensive rat (SHR) at 6 weeks of age, before the rise in systol ic blood pressure, there was a 36% increase in density of amylin bindi ng compared with their normotensive counterpart, the Wistar-Kyoto rat (WKY). In SHR, there was a further increase in the density of amylin b inding (to 53% greater) as the systolic blood pressure rose between 6 and 12 weeks of age. Histological examination of kidneys from SHR at 1 2 weeks of age evealed staining for a brush border glycoprotein, norma lly restricted to the proximal tubules, extending from the urinary pol e into half of the epithelial lining of the glomerular capsule. In con trast io WKY, these cells also bound I-125-amylin with high density in SHR. II;. a rat model of renal ablation and hypertension, systolic bl ood pressure correlated with the den sity of I-125-amylin binding in t he renal cortex (r=.54, P=.003, n=28). The changes in amylin binding r eported here suggest a possible role for this peptide and/or activatio n of its receptor in the genesis as well as the maintenance of hyperte nsion.