Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Improvement in the efficacy of newer antihypertensive agents has resulted in consideration of the side effects of drug therapy. Impairment of memory function resulting from antihypertensive therapy has been clinically suspected. This observation has been supported by a study in which the effects of methyldopa and propranolol on memory function were reported. Recently, memory function has been assessed in a group of patients treated with either a beta-blocker (atenolol) or an angiotensin-converting enzyme inhibitor (enalapril) in a randomised, observer-blind study in moderate essential hypertension. The patients were assessed, on placebo and after 16 weeks of treatment on active therapy, by use of a series of 4 memory function tests related to everyday life. In the hypertension study group, 13 received atenolol and 12 received enalapril. Similar reduction of diastolic pressure occurred in both groups, but systolic pressure was significantly reduced in the enalapril group (p less than 0.05). In the atenolol group memory performance scores were consistently lower than in the placebo phase in 9 of 28 estimates of memory function. In the enalapril group there were no significant changes. The study indicated that atenolol might produce mild memory impairment, whereas enalapril was devoid of any measurable effect on memory function.
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PMID:Memory function--effects of different antihypertensive drugs. 306 88

Stroke-prone spontaneously hypertensive rats (SHRSP) are the best model for essential hypertension and stroke. In this study, one investigated whether SHRSP might be a useful animal model for vascular dementia. An impairment of learning-memory function was found in SHRSP. A disturbance in circadian rhythm after stroke in SHRSP was clarified. Desynchronization of light and dark alternation cycles and abnormal rhythm were also demonstrated. These observations point to the possibility that the decreased passive avoidance response observed in SHRSP might be similar to the phenomenon of memory impairment in patients with vascular dementia. The behavioral changes in ambulation in SHRSP, including the desynchronization between light and dark alternation cycles and the abnormal rhythm before death, might correspond to the behavioral changes associated with the delirium-state observed in patients with dementia. Cerebral cortex levels of acetylcholine and choline in SHRSP decreased significantly as compared with the Wistar Kyoto rats (WKY) control group. Hippocampal levels of acetylcholine and choline in SHRSP decreased significantly as compared with those in WKY. Moreover, a correlation between passive avoidance response latency and hippocampal acetylcholine levels was observed. These findings suggest that decreased acetylcholine levels in both the cerebral cortex and the hippocampus may be related to the impairment of learning-memory function and abnormal behavior. In SHRSP, increases in blood viscosity, hematocrit and fibrinogen might produce the formation of thrombus and induce cerebral infarction. Some histopathological findings caused by cerebrovascular disorder in human brain very similar to those observed in the SHRSP brain. On the other hand, so called 'senile changes' were detected only in the human case, and not observed in the SHRSP.
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PMID:Pathogenesis of vascular dementia in stroke-prone spontaneously hypertensive rats. 1109 Sep 55