Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The suppression of heart rate variation reflects cardiac autonomic nervous dysfunction and is known to be associated with a poor prognosis or sudden death in diabetic patients. We investigated consecutive changes in the heart rate variation in 51 alcoholics using the coefficient of variation of R-R interval (CVRR). To correct for age effects, a ratio of CVRR to the standard predicted value (CVP) was calculated. On the whole, CVRR/CVP was suppressed on admission and on the 7th day of abstinence and increased on the 30th day. However, alcoholics could be divided into two groups by their CVRR/CVP on the 30th day: one group with transient autonomic dysfunction whose CVRR/CVP was more than 0.8 (n = 32), and the other group with persistent autonomic dysfunction whose CVRR/CVP was less than 0.8 (n = 19). Withdrawal hypertension occurred more frequently (63% vs. 19%) and mean systolic pressure (159 +/- 24 mmHg vs. 138 +/- 17 mmHg) was higher in the latter group than in the former, suggesting that persistent autonomic damage might, at least in part, contribute to withdrawal hypertension. To investigate further the relationship between the persistent autonomic damage and other complications, the CVRR/CVP on the 30th day of abstinence was analyzed in an additional 85 alcoholics (total n = 136). Persistent suppression of the CVRR/CVP was more frequently found in alcoholics with leg paresthesia (64%, n = 22), the Wernicke-Korsakoff syndrome (73%, n = 11), or diabetes mellitus (69%, n = 68), than in alcoholics without these complications (31%, n = 35).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired autonomic nervous system in alcoholics assessed by heart rate variation. 166 63

Studies were undertaken to investigate the role of the CNS in withdrawal hypertension caused by abrupt cessation of long-term clonidine treatment. The studies were conducted on male wistar rats receiving clonidine, 100 micrograms/kg subcutaneously twice daily for seven days. Withdrawal hypertension occurred 16 to 18 hours following the last injection of clonidine. Pressor responses to posterior hypothalamic stimulation were significantly potentiated in the rats undergoing clonidine withdrawal, and the depressor response to a single injection of 10 micrograms of clonidine into the lateral cerebral ventricle was significantly attenuated in these animals. Studies on pithed rats demonstrated that destruction of the CNS eliminated the withdrawal hypertension. These data suggest that alpha-adrenoreceptors in the nucleus tractus solitarius play an important role in the normal maintenance of blood pressure, and a decrease in sensitivity of these receptors could result in the development of a hypertensive state.
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PMID:Central alpha-adrenergic control of blood pressure. Effects of clonidine withdrawal. 629 8