Convulsive and hypothermic effects of vasopressin in the brain of the rat

Kasting, Norman W.; Veale, W. L.; Cooper, K. E.

doi:10.1139/y80-054

Cited by 130 publications

(33 citation statements)

References 18 publications

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“…This could possibly be attributable to a higher body temperature. To our knowledge, absolute measurements of body temperature in LE and DI rats are not available, but VP is known to play a role in the control of basal body temperature (46)(47)(48) and to be antipyretic (49)(50)(51). Moreover, heat dissipation is impaired in humans with DI (52).…”

Section: Discussionmentioning

confidence: 99%

Vasopressin contributes to hyperfiltration, albuminuria, and renal hypertrophy in diabetes mellitus: Study in vasopressin-deficient Brattleboro rats

Bardoux

Martin

Ahloulay

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

127

108

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Diabetic nephropathy represents a major complication of diabetes mellitus (DM), and the origin of this complication is poorly understood. Vasopressin (VP), which is elevated in type I and type II DM, has been shown to increase glomerular filtration rate in normal rats and to contribute to progression of chronic renal failure in 5͞6 nephrectomized rats. The present study was thus designed to evaluate whether VP contributes to the renal disorders of DM. Renal function was compared in Brattleboro rats with diabetes insipidus (DI) lacking VP and in normal Long-Evans (LE) rats, with or without streptozotocin-induced DM. Blood and urine were collected after 2 and 4 weeks of DM, and creatinine clearance, urinary glucose and albumin excretion, and kidney weight were measured. Plasma glucose increased 3-fold in DM rats of both strains, but glucose excretion was Ϸ40% lower in DI-DM than in LE-DM, suggesting less intense metabolic disorders. Creatinine clearance increased significantly in LE-DM (P < 0.01) but failed to increase in DI-DM. Urinary albumin excretion more than doubled in LE-DM but rose by only 34% in DI-DM rats (P < 0.05). Kidney hypertrophy was also less intense in DI-DM than in LE-DM (P < 0.001). These results suggest that VP plays a critical role in diabetic hyperfiltration and albuminuria induced by DM. This hormone thus seems to be an additional risk factor for diabetic nephropathy and, thus, a potential target for prevention and͞or therapeutic intervention.One of the major complications of diabetes mellitus (DM) is a progressive nephropathy that develops in about one-third of patients within 10-20 years after the onset of the disease and leads in most cases to end stage renal failure (1). This represents a major problem of public health because a large fraction of dialysis requirements is attributable to DM nephropathy. Although a number of studies have already been devoted to this problem, the factors contributing to diabetic nephropathy are not yet fully identified.A characteristic feature observed in diabetic patients is an elevation of plasma vasopressin (VP), well documented in both type I and type II DM (2-5). This elevation also occurs in animal models of DM, whether experimental or genetically determined (6, 7). Several studies have investigated the possible factors responsible for this increase in VP secretion (3,6,8,9). But they did not succeed in identifying the responsible stimulus for this increase. They revealed a resetting of the osmostat in diabetics but concluded that hyperglycemia was not responsible for this resetting because increasing plasma glucose and osmolality by intravenous infusion of hypertonic dextrose produced no increase in plasma vasopressin in diabetics or in healthy controls (8).Little attention has been given to the possible functional consequences of the rise in plasma VP. To our knowledge, the possible contribution of VP to the renal complications of DM has never been investigated in spite of several previous findings suggesting that this hormone represents a ...

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Section: Discussionmentioning

confidence: 99%

Vasopressin contributes to hyperfiltration, albuminuria, and renal hypertrophy in diabetes mellitus: Study in vasopressin-deficient Brattleboro rats

Bardoux

Martin

Ahloulay

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

127

108

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“…The hypothermic effect of LVP administered peripherally has been largely attributed to the baroreflexive suppression of nonshivering thermogenesis (456). AVP has also been reported to work as an endogenous antipyretic molecule in the CNS (243,263,368). The AVP-induced reduction in body temperature is caused partly by a reduction in the metabolic rate associated with the suppression of the lipid metabolism (243,395).…”

Section: Water Homeostasis and Thermoregulationmentioning

confidence: 99%

Vasopressin V1a and V1b Receptors: From Molecules to Physiological Systems

Koshimizu

Nakamura

Egashira

et al. 2012

Physiological Reviews

314

297

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The neurohypophysial hormone arginine vasopressin (AVP) is essential for a wide range of physiological functions, including water reabsorption, cardiovascular homeostasis, hormone secretion, and social behavior. These and other actions of AVP are mediated by at least three distinct receptor subtypes: V1a, V1b, and V2. Although the antidiuretic action of AVP and V2 receptor in renal distal tubules and collecting ducts is relatively well understood, recent years have seen an increasing understanding of the physiological roles of V1a and V1b receptors. The V1a receptor is originally found in the vascular smooth muscle and the V1b receptor in the anterior pituitary. Deletion of V1a or V1b receptor genes in mice revealed that the contributions of these receptors extend far beyond cardiovascular or hormone-secreting functions. Together with extensively developed pharmacological tools, genetically altered rodent models have advanced the understanding of a variety of AVP systems. Our report reviews the findings in this important field by covering a wide range of research, from the molecular physiology of V1a and V1b receptors to studies on whole animals, including gene knockout/knockdown studies.

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“…A great many papers have addressed the effects of vasopressin on centrally regulated functions such as learning and memory (De Wied 1969), cardiovascular regulation (Versteeg et al 1983), thermoregulation (Kasting 1989), and motor behaviors (Kasting et al 1980). Many of these studies involved injecting vasopressin or its anal ogs into the ventricles or into areas that do not necessarily receive vasopressin-ir fibers.…”

Section: Nonreproductive Functionsmentioning

confidence: 99%