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PubMed · 1609254

Monosymptomatic bedwetting.

J C Djurhuus·J P Nørgaard·S Rittig
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Abstract

An update of the pathogenesis and treatment of monosymptomatic bedwetting is presented. This frequently occurring entity seems to have a multifactorial pathogenesis incorporating arousal disturbances and disturbances to the circadian rhythm of diuresis modulating hormones. It has recently been substantiated that the bladder reservoir function in monosymptomatic bedwetting is normal. This is further underlined by the fact that treatment of instability of the bladder has proven futile. In a substantial part of the monosymptomatic bedwetters the changes in circadian rhythm of antidiuretic hormone can be counteracted by desmopressin diacetate (DDAVP), which abolishes the symptom in more than 2/3 of the patients. Monitoring circadian rhythms of arginine vasopressin (AVP) and treatment with DDAVP have led to increased understanding of the pathogenesis of monosymptomatic bedwetting and opened new fields of investigation.

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Arginine VasopressinChildCircadian RhythmDeamino Arginine VasopressinEnuresisFemaleHumansMaleMental DisordersPolyuriaSleep Wake DisordersUrinary Bladder DiseasesJournal ArticleReview

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J C Djurhuus, J P Nørgaard, S Rittig. 1992. Monosymptomatic bedwetting.. https://pubmed.ncbi.nlm.nih.gov/1609254/

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BACKGROUND: Arginine vasopressin (AVP) has recently been demonstrated as an alternative in the treatment of severe refractory vasodilatation in coronary artery bypass grafting. However, AVP may be a spasmogen for graft spasm. We compared the in vitro antispastic effect among calcium-channel antagonists (nifedipine, diltiazem, and verapamil), nitroglycerin, and the highly selective AVP (V1) receptor antagonist [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin. METHODS: Human internal mammary artery segments (n = 218) were studied in organ baths. The inhibitory effects of the above vasodilators on AVP-mediated contraction were studied in two ways: relaxation with AVP precontraction and depression of the AVP-induced contraction after pretreatment with vasodilators. RESULTS: All three calcium-channel antagonists caused limited relaxation (18.3%+/-5.4% for nifedipine, n = 11; 22.2%+/-3.8% for verapamil, n = 10; and 26.2%+/-7.5% for diltiazem, n = 9). The plasma concentration of calcium-channel antagonists had no significant depression effect on the AVP-induced contraction. In contrast, [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin caused full (100%, n = 11) and nitroglycerin caused nearly full (93%+/-3%, n = 10) relaxation. Pretreatment with [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin (10(-8), 10(-7), or 10(-6) mol/L, respectively) significantly increased the effective concentration for 50% of the AVP-induced contraction (10(-8.6)+/-10(0.1) mol/L, p = 0.009; 10(-7.8)+/-10(0.07) mol/L, p = 0.000; or 10(-6.9)+/-10(0.11) mol/L, p = 0.000 versus the control, 10(-9.24)+/-10(0.16) mol/L). However, nitroglycerin only slightly depressed the AVP-induced contraction. CONCLUSIONS: [1-Deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin may provide specific antispastic effect in either prophylaxis or treatment of the AVP-related vasospasm in the internal mammary artery. Nitroglycerin may be effective in treatment but has little effect on prophylaxis. Use of calcium-channel antagonists may have little benefit in AVP-related vasospasm.

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