1.A colony of stroke-prone spontaneously hypertensive rats has been developed by selective breeding.2. These animals developed severe hypertension early in life, the magnitude of the hypertension being closely related to the incidence of stroke.3. No evidence was obtained of any humoral factor responsible for strokes.4. Local factors predisposing to stroke were a scanty arterial supply with characteristic recurrent branching of long and large arteries, together with increased vascular permeability, angio-necrosis, and formation of microaneurysms. 5. Strokes could be prevented by adequate antihypertensive therapy from an early age.
The angiotensin II (AII) antagonist [Sar1-Ala8]AII (Saralasin) was injected into the brain ventricles (IVT) and intravenously (IV) in five different types of hypertensive unanesthetized rats. Renal hypertension was studied 16-22 days after kidney clipping. Intravenous infusions of cumulative doses (0.1-100 microgram/kg per min) and IVT injections (5-40 microgram) of Saralasin did not change mean arterial pressure (MAP) in controls and in one-clip, one-kidney Goldblatt hypertension, whereas MAP decreased in one-clip, two-kidney Goldblatt hypertension following IV and IVT Saralasin. In two-clip, two kidney hypertensive rats, IVT Saralasin decreased MAP but was ineffective when infused IV. Both IV and IVT Saralasin increased MAP in DOC hypertension. In spontaneously hypertensive (SH) rats, IV Saralasin increased MAP; IVT injection decreased MAP. The effect of IVT Saralasin in SH rats persisted 15-20 h after nephrectomy. We conclude that plasma AII may contribute to peripheral and central mechanisms of blood pressure regulation. The dissociation of the effects of IV and IVT Saralasin and the persistance of blood pressure decrease in nephrectomized SH rats following IVT Saralasin further support a role for locally formed brain angiotensin.
Morphological changes in astrocytes have been studied in the primary motor cortex of persons dying with or without amyotrophic lateral sclerosis (ALS). Glial fibrillary acidic protein (GFAP) and S-100 protein were used as immunohistochemical markers for reactive astroglia. In 12 brains of individuals without neurological disease glial cells showing moderate immunoreactivity for both GFAP and S-100 protein were uniformly distributed in the primary motor cortex in the upper regions of layer I and layer II. In 8 of 11 ALS cases, intensely immunoreactive cells were additionally found to occur and were scattered irregularly, mostly in layers II and III, but occasionally in layers IV and V. Clusters of these intensely positive cells occurred in patches about 200-400 micron in diameter, each containing about 6 to greater than 20 such cells. GFAP-positive astrocytes were seen in some of the 36 brains from persons with neurological problems other than ALS but the pattern was different. The abnormal appearance of clusters of positive astrocytes of the primary motor cortex may be intimately associated with the ALS disease process.
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