pituitrin and Constipation

Enuresis was historically viewed as a primarily psychiatric disorder, but this understanding has changed dramatically since the end of the last century, when it became clear that somatic factors, such as nocturnal polyuria as a result of vasopressin deficiency, nocturnal detrusor overactivity and high arousal thresholds, all play a crucial role in enuresis pathogenesis. It has also become clear that enuresis is inherited in the majority of cases, although the correlation between genotype and enuretic phenotype is not straightforward. The standard view of enuresis as being the result of either (i) nocturnal polyuria and high arousal thresholds; or (ii) nocturnal detrusor overactivity and high arousal thresholds has become well-established, but further research now complicates the picture. First, psychological/psychiatric problems are overrepresented in enuresis, and might in a minority of cases have a causal or aggravating role. Second, nocturnal polyuria is not always linked to vasopressin deficiency. Third, nocturnal detrusor overactivity is in itself pathogenetically heterogeneous, and could be linked to constipation. Fourth, the sleep of enuretic children might be "deep," but possibly also disturbed (by obstructed airways or a distended or contracting bladder). These children might have high arousal thresholds because of the enuresis instead of the other way around. The same might possibly be said about nocturnal polyuria. Taking these new insights into account, a new model of enuresis pathogenesis is presented, which is more complicated but hopefully also more true than the standard consensus.

Topics: Adult; Antidiuretic Agents; Arousal; Central Nervous System; Child; Constipation; Deamino Arginine Vasopressin; Enuresis; Humans; Polyuria; Sleep; Urinary Bladder, Overactive; Vasopressins

Topics: Abdomen; Autonomic Nervous System; Axons; Constipation; Cranial Nerves; Depression; Diabetic Neuropathies; Drug Interactions; Hallucinations; Humans; Hyponatremia; Hypotension, Orthostatic; Intestinal Obstruction; Muscular Atrophy; Nervous System Diseases; Neural Conduction; Norepinephrine; Pain; Paresthesia; Parkinson Disease; Peripheral Nervous System Diseases; Seizures; Vasopressins; Vincristine

The effects of vasopressin on colonic motility were investigated in 6 healthy subjects and 10 patients with chronic idiopathic constipation. Recordings of the colonic myoelectric spiking activity were performed by means of 50-cm long silastic tube, equipped with four bipolar ring electrodes fixed at 10-cm intervals, which was introduced by flexible colonoscopy into the left colon. Tracing were obtained for 1 h in the fasting state and for another hour after an intramuscular injection of a pharmacological dose of vasopressin (0.3 U/kg). The different types of spike bursts generated by the colonic smooth muscle were compared before and after vasopressin injection. In both controls and patients, the tracing showed (i) rhythmic stationary spike bursts (RSB) that were seen at only one electrode site; and (ii) sporadic bursts that were either propagating over all four electrodes (SPB) or nonpropagating (SNPB). Injection of vasopressin in controls was followed for 30 min by a significant increase in the number of propagating bursts from 2.7 +/- 0.6 (mean +/- SEM) to 5.2 +/- 1.4 bursts (p less than 0.05); RSB and SNPB were not altered by vasopressin. In the constipated patients, the number of propagating bursts during the control period was significantly lower (0.8 +/- 0.2 bursts/30 min) than in the volunteers (p less than 0.05). After vasopressin, there was a significant increase to 3.6 +/- 0.8 bursts/30 min (p less than 0.001); RSB and SNPB also did not show significant alteration after vasopressin. Finally, 4 out of the 10 patients passed stools during the recording session.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Chronic Disease; Colon; Constipation; Electromyography; Electrophysiology; Female; Gastrointestinal Motility; Humans; Male; Peristalsis; Vasopressins