Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0043352 (xerostomia)
 4,250 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Seventeen idiopathic parkinsonian patients ranging between 47 and 75 years of age were included in this study to investigate the effect and tolerance of lisuride on PD. The duration of this simple clinical study, which had no control group was 12 weeks. There was 50% relief in disability scores and ADL in 13 patients in the first group in the combined therapy for 12 weeks with lisuride added to L-DOPA plus benserazide (p < 0.01). Optimal lisuride doses added to L-DOPA plus benserazide varied between 0.1 and 0.8 mg (mean 0.5 +/- 0.2 mg). With the addition of lisuride to treatment, the L-DOPA plus benserazide dose was reduced in 6 of 13 by 38%. Monotherapy with lisuride resulted in 56% to 57% improvement in disability scores and 47% in relief in ADL. Dry mouth, nausea, weakness, postural hypotension, and headache were the most frequently encountered side effects of lisuride. These adverse effects disappeared in 3 or 4 days, depending on a slight decrease and following increase in the dose of lisuride and/or the development of tolerance. Not only will such a combined therapy contribute to the reduction of the end-of-dose inadequacies, on-off phenomena, wearing off, peak-dose dyskinesias, and similar motor fluctuations, it may also play a prophylactic role in their prevention or delay.
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PMID:A study on the effect and tolerance of lisuride on Parkinson's disease. 861 74

The classic centrally acting antihypertensives such as clonidine, guanfacine and alpha-methyl-DOPA (via its active metabolite alpha-methyl-noradrenaline) induce peripheral sympathoinhibition and a fall in blood pressure as a result of alpha2-adrenoceptor stimulation in the brain stem. These drugs have lost much of their clinical importance because of their unfavourable side-effects (sedation, dry mouth, impotence), which are also mediated by alpha2-adrenoceptors, although in other anatomical regions. Moxonidine and rilmenidine are the examples of a new class of centrally acting antihypertensives, which cause peripheral sympathoinhibition mediated by imidazoline (I1)-receptors in the rostral ventromedulla (RVLM). Their side-effect profile appears to be better than that of clonidine and alpha-methyl-DOPA, probably because of a weaker affinity for alpha2-adrenoceptors. The mode of action, haemodynamic profile, antihypertensive efficacy and adverse reactions of the classic and newer centrally acting antihypertensives are the subject of the present survey. Attention is also paid to other therapeutic applications of centrally acting antihypertensives, such as congestive heart failure and the metabolic syndrome.
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PMID:Centrally acting antihypertensive drugs. Present and future. 1042 8