Abnormal regulation of adrenal angiotensin II receptors in spontaneously hypertensive rats.
The aldosterone response to angiotensin II is blunted in spontaneously hypertensive rats (SHR). To determine whether this blunting is due to a defect in angiotensin II receptors, we assessed angiotensin II binding to intact adrenal glomerulosa cells in SHR and normotensive Wistar-Kyoto rats (WKY) that had been fed high or low sodium diets before sacrifice. In rats on high salt intake, we observed no difference between the two strains in either receptor affinity (Kd = 1.0-1.2 nM) or binding capacity (36,000-38,000 receptors/cell). When sodium-restricted, WKY increased receptor content more than fourfold to 167,000 sites/cell. SHR increased receptor number to only 103,000 sites/cell, which was significantly (p less than 0.01) less than the WKY increase. The cause of the abnormal receptor regulation remains unclear. Two known receptor regulators, the plasma angiotensin II level and the state of potassium balance, were similar in the two strains. Our results suggest that the blunted aldosterone response to angiotensin previously reported in SHR is due to abnormal angiotensin receptor up-regulation in the adrenal gland in response to sodium restriction.[1]References
- Abnormal regulation of adrenal angiotensin II receptors in spontaneously hypertensive rats. Bradshaw, B., Moore, T.J. Hypertension (1988) [Pubmed]
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