Abstract-Chronic treatment of saline-drmkmg stroke-prone spontaneously hypertensive rats (SHRSP) with agents that interfere with the formation or actions of angotensm II (Ang II) prevents the development of stroke and renal vascular damage Ang II, m addltlon to its direct vascular effects, stimulates the synthesis and release of aldosteroneTo assess the role of aldosterone m the development of pathologc changes m these rats, we implanted time-release pellets containing 200 mg of the mmeralocortlcold receptor antagomst, spu-onolactone, mto 14 SHRSP at 7 5 weeks of age Eight SHRSP httermates received placebo pellets Over the period of study (3 to 4 weeks), systolic blood pressure (SBP) (PRA) and aldosterone as independent nsk factors for heart attack and stroke ' They found that among the patients who developed strokes and myocardlal mfarctlons, all had normal or high PRA, and aldosterone secretlon Previous studies by our group and others have provided expenmental evidence to support a role for the renm-angotensm-aldosterone system (RAAS) m the development of vascular qury, as angotensm converting enzyme (ACE) mhlbltors2-6 and Ang II receptor antagonlsts7-9 prevented the development of stroke and malignant nephrosclerosls m SHRSP Since these studies were conducted m salt-loaded SHRSP, which respond to these agents with nummal blood pressure lowermg, they provided evidence for a pathophyslolog& role for Ang II m the development of vascular lesions of malignant nephrosclerosls independent of severely elevated blood pressure Consistent with a role for Ang II was the finding that SHRSP display a paradoxical increase m PRA with rime, despite continued salt-loading 3 9,'" Although Ang II stimulates the synthesis and release of aldosterone," " m addmon to its direct vascular actions, a role for mmeralocortlcolds m the pathology of SHRSP
Cultured skin fibroblasts derived from Alzheimer disease patients fail to express the 1.6-kilobase (kb) mRNA and the corresponding 40-kDa form of (2'-5')oligoadenylate (2-5A) synthetase when exposed to interferon. In addition, the 3.6-kb mRNA, which is present in normal fibroblasts, is barely detectable in the Alzheimer disease counterpart. The deficiency of the 2-5A synthetase 1.6-kb mRNA and its corresponding protein is not related to an impairment of interferon receptors but most probably represents an alteration in the expression of the 2-5A synthetase gene. The data have potential implications for the diagnosis of Alzheimer disease and demonstrate that the absence of a specific form of 2-5A synthetase is linked to a disease state.
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