Unilateral renovascular hypertension in rats. Measurements of medullary granules, juxtaglomerular granularity and cellularity, and areas of adrenal zones.
To produce hypertension, the left renal artery was clipped in 20 rats. Six rats had a sham operation. After 4 months, some of the rats showed only a moderate increase in blood pressure, and a second clipping of the same artery was performed. When hypertension became severe in some of the rats, 2 to 4 weeks later, all rats were sacrificed. The "clipped" rats were divided into four groups depending on whether they had little change in blood pressure, acute hypertension, chronic hypertension, or chronic and superimposed acute hypertension. The average adrenal weights were increased in the two groups with acute hypertension. The area of the adrenal glomerular zone was increased in all three groups with hypertension. The groups with acute hypertension also showed increases in the combined areas of (1) the medullary and androgenic zones and possibly (2) the fascicular and reticular zones. The granules of the left juxtaglomerular apparatus were greatly increased in the group with acute hypertension, but were only slightly elevated in the group with chronic hypertension and the group with chronic and superimposed acute hypertension. An increased juxtaglomerular cellularity in the clipped kidney correlated best with hypertension. Renal medullary granular counts were decreased in the right and left kidneys of all clipped groups whether or not they had hypertension, but no changes were found in the amount of medullary interstitial space. The above results are consistent with the evidence in acute unilateral renovascular hypertension with the opposite kidney intact that the clipped kidney is responsible initially via a renin-angiotensin-aldosterone mechanism, with participation by the major adrenal zones. In chronic hypertension some other mechanisms, with participation by the major adrenal zones. In chronic hypertension some other mechanisms, which seem to be related to juxtaglomerular cellularity in the clipped kidney, are operating. Other evidence suggests that such mechanisms may depend on sodium retention, volume expansion, and increased sensitivity to vasoconstrictors.
D000208:Acute Disease; D000311:Adrenal Glands / Q000473:pathology*; D000818:Animals; D001835:Body Weight; D002452:Cell Count; D002908:Chronic Disease; D004195:Disease Models, Animal; D005260:Female; D006977:Hypertension, Renal / Q000209:etiology / Q000473:pathology*; D007238:Infarction; D007606:Juxtaglomerular Apparatus / Q000473:pathology; D007668:Kidney / Q000473:pathology*; D007672:Kidney Cortex / Q000098:blood supply; D007679:Kidney Medulla / Q000098:blood supply; D051381:Rats; D012078:Renal Artery Obstruction