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At least 523 records · Page 29Linked to original sources
PubMed1999

Metoprine-induced thirst and diuresis in Wistar rats.

In the present study, the renal responses to metoprine, a histamine-N-methyltransferase inhibitor, were studied in conscious rats. Metoprine (10-20 mg kg(-1)) or vehicle were administered i.p. to male Wistar rats and the effects were followed for the subsequent 24 h. It was found that as early as 3 h after the drug administration metoprine 20 mg kg(-1) had increased water consumption and urine flow approximately 6-8-fold. The treatment decreased urine osmolality and increased free water clearance, but caused no change in plasma renin activity or plasma vasopressin concentration. In addition, a metoprine-induced elevation in the systolic blood pressure was observed during the first few hours of the experiment. During the nocturnal period of the study, glomerular filtration rate and the excretion of electrolytes did not increase in metoprine-treated rats as they did in control rats. A decrease in the release of atrial natriuretic peptide was also found. The present results show that inhibition of histamine catabolism by metoprine causes massive changes in renal functions. It seems to promote water excretion by the kidneys but, on the other hand, to reduce the excretion of electrolytes. Although the exact mechanisms, especially the role of increased blood pressure and nocturnal suppression of atrial natriuretic peptide, require further clarification, the present data suggest that renin-angiotensin system and vasopressin were not involved in these renal responses to metoprine.

Animals↗
PubMed1985

Lack of thirst, osmoreceptor dysfunction, early puberty and abnormally aggressive behaviour in two boys.

Two unrelated boys (C.C. 13 years; J.W. 18 years) presenting with early puberty and episodes of aggressive behaviour were found to have hypernatraemia and hypodipsia. Plasma vasopressin (AVP) levels were inappropriately low in relation to plasma osmolality, but the patients did not have diabetes insipidus since 24 h urinary volumes were less than 1 litre and the maximal urinary osmolality was 1232 in C.C. and 950 in J.W. Plasma renin activity was elevated (greater than 2000 mg AI/1/h) although aldosterone concentrations were normal. Excretion of a water load (20 ml/kg) was delayed, but plasma renin and aldosterone fell with increased naturesis. An infusion of 0.85 mol/l saline produced a rise in AVP in C.C. but not in J.W. Insulin and hypotension resulted in the release of AVP in both boys suggesting a selective defect of osmoreceptor function. Hyperprolactinaemia and an exaggerated PRL response to TRH were also noted but no intracranial lesion was demonstrable on CT scan. These boys appear to have a hypothalamic syndrome with early puberty, hyperprolactinaemia, hypodipsia and osmoreceptor dysfunction which may be associated with aggressive behaviour.

Adolescent↗
PubMed1996

The neuronal role of angiotensin II in thirst, sodium appetite, cognition and memory.

Within the past two decades, a great deal has been learnt about the renin-angiotensin system in the brain. The renin-angiotensin system is one of the best-studied enzyme-neuropeptide systems in the brain. The diversity of localization of this peptide throughout the brain has implied a variety of potential functions. Besides its classical role in the regulation of blood pressure and body-fluid homeostasis, it has more subtle functions involving complex mechanisms such as learning and memory. The profound effects on behaviour produced by angiotensin are of broad interest to neuroscientists. The mechanisms of action differ depending on whether angiotensin is locally synthesized and whether regulation is governed by neural or metabolic inputs impinging on the neurones. Its central action is mediated through peptidergic receptors present on neurones. The description of the receptor subtypes AT1 and AT2 for angiotensin II and the development of non-peptidic specific angiotensin receptor subtype antagonists have opened a new area in this field of research. The AT1 site, which preferentially binds to angiotensin II and angiotensin III, appears to mediate the classical angiotensin functions concerned with maintenance of blood pressure and body-fluid control. In addition, most of the behavioural effects described so far are linked with AT1, although so-called psychotropic effects are presumed to be mediated by receptor systems other than the known specific angiotensin receptors. In fact, evidence for the existence of such receptors with high-affinity binding has been reported. The central action of angiotensin II mediated by AT2 is as yet unclear. Most reports concerning this receptor subtype suggest a role in differentiation and development, since the number of binding sites is higher in fetal and young rats than in adults. Furthermore, the neuronal effect of angiotensin II in the inferior olivary nucleus which is blocked specifically by AT2 antagonists suggests an involvement in motor control. Over the next few years we should find answers to many of the questions currently unanswered about angiotensin function and, given the rapid progress in research on this neuropeptide, it may serve as a model for the action of peptides on neuronal function in general.

Angiotensin II↗
PubMed1971

Induction of hypovolaemia by thirst-inducing doses of renin or angiotensin II.

1. Intravenous injection of five Goldblatt units (Gbl.U) of renin, or intravenous infusion of 2.5 mug of angiotensin into nephrectomized rats decreased plasma volume by 22 +/- 2% (calculated from the increase of the haematocrit) or by 14 +/- 2% (calculated from the increase in protein concentration) within 2 minutes. Fifteen minutes and 60 min after injection or infusion, the plasma volume (calculated from both parameters) was still 10% lower than initially.2. The initial discrepancy between haematocrit values and plasma protein concentration was neither due to mobilization of red blood cells (r.b.c.) from the spleen, nor to an increase in r.b.c. volume.3. The observed decrease in plasma volume was large enough to explain the drinking response to renin and angiotensin. Renin may thus induce or aggravate hypovolaemia rather than signalling its occurrence to hypothalamic receptors.

Angiotensin II↗
PubMed1983

Central control of vasopressin release and thirst.

The effects of changes in the composition and/or the volume of the extracellular fluid on central receptors involved in the regulation of water balance are discussed. A review of results obtained in adults is given, followed by a discussion of possible roles for vasopressin during the neonatal period.

Angiotensin II↗