This explanation is supported by the observation that hypertension in stroke-prone spontaneously hypertensive rats is partially ameliorated by chronic (more than 8 weeks long) administration of arundic acid59, by histological observation of astrogliosis in spontaneously hypertensive rats49 and by the observations that the functional properties of astrocytes isolated from spontaneously hypertensive rats, especially the responsiveness of these astrocytes to angiotensin II, are different from those of normotensive Wistar rats59–62. The gene discussed is AGT; the disease is Hypertension.