A case of adrenal tumor producing ll-deoxycorticosterone, 18-hydroxy-ll-deoxycorticoste-rone and aldosterone is reported. A 55-year-old womanhad hypertension, hypokalemia, low plasma renin activity and an adrenal tumor. The plasma level ofaldosterone was normal, and the levels of ll-deoxycorticosterone and 18-hydroxy-ll-deoxycorticosterone were extremely high. After the tumor removal, the plasma level of aldosterone decreased and plasma levels of ll-deoxycorticosterone and 18-hydroxy-ll-deoxycorticosterone were normalized. The tumor was benign adenoma and the production of steroid hormones was under control ofadrenocorticotropic hormone. The enzyme activity of 21-hydroxylation in the tumor was elevated and that of ll(3-hydroxylation was decreased compared with the adjacent tissue.
A premenopausal female patient presented with acute myocardial infarction of 3 different coronary vessels at different times within 1 year. These events were caused not by restenotic lesions after balloon angioplasty but by new lesions, which were successfully treated by primary angioplasty. Although she had a history of hypertension, type IIB hyperlipidemia, and diabetes, they had been well-controlled on medication. An elevated serum lipoprotein(a) level may have played a role in this rapid angiographic progression.
1. Sarcoplasmic reticulum (SR) in small resistance arteries plays a role in the regulation of the cytosolic free calcium concentration by sequestration of calcium from cytoplasm.2. To examine the contribution of calcium (CaZ+) sequestration by the SHR to both contraction and relaxation in young spontaneously hypertensive rats (SHR), we measured evoked tension before and after depletion of SR Ca2+ stores in the rings of the first branch of superior mesenteric artery in 5 week old SHR and age-matched Wistar-Kyoto (WKY) rats. Contractile responses were induced by 40 mmol/L potassium and 10 mmol/L caffeine before and after the treatment with ryanodine or thapsigargin, which depletes SR calcium stores.3. The magnitude of potassium-induced contraction was almost the same in both strains. 4. Ryanodine and thapsigargin did not affect the resting tension and almost decreased caffeine-induced contraction in both strains.
5.After the treatment with ryanodine or thapsigargin, the magnitude and the rate of potassium-induced contraction were augmented greatly in SHR, but not in WKY. 6. The relative relaxation rate after exposure of potassium was significantly slowed in SHR by ryanodine or thapsigargin, but only slightly in WKY.7. These results suggest that Ca2+ sequestration by the SR in SHR was greater than in WKY. Therefore, it is concluded that SR plays an important role in preventing the development of hypertension in SHR via a buffering effect on the elevation of cytosolic free CaZ+.
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