Biological half-life and organ distribution of [3H]8-arginine-vasopressin in the rat

Janáky, Tamás; László, F; Sirokmán, F.; Morgat, J. L.

doi:10.1677/joe.0.0930295

Cited by 40 publications

(19 citation statements)

References 16 publications

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“…Moreover, we discovered that intravenously injected bicuculline (GABA A receptor antagonist) lowered the plasma levels of AVP and oxytocin in these animals. There was a difference in the measured time course of the effects that is likely explained by the differences between the half-lives of these hormones in the blood (AVP, 2-17 min vs oxytocin, 1-2 min; Janáky et al, 1982;Gimpl and Fahrenholz, 2001). The absence of bicuculline-induced release of AVP and oxytocin in control rats might be attributable to that the amount of bicuculline injected (2 mg/kg body weight: subconvulsive dose) was too small to remove significantly the strong GABAergic inhibition.…”

Section: Discussionmentioning

confidence: 99%

Chronic Hyperosmotic Stress Converts GABAergic Inhibition into Excitation in Vasopressin and Oxytocin Neurons in the Rat

Kim¹,

Kim²,

Kim³

et al. 2011

J. Neurosci.

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In mammals, the increased secretion of arginine-vasopressin (AVP) (antidiuretic hormone) and oxytocin (natriuretic hormone) is a key physiological response to hyperosmotic stress. In this study, we examined whether chronic hyperosmotic stress weakens GABA A receptor-mediated synaptic inhibition in rat hypothalamic magnocellular neurosecretory cells (MNCs) secreting these hormones. Gramicidin-perforated recordings of MNCs in acute hypothalamic slices prepared from control rats and ones subjected to the chronic hyperosmotic stress revealed that this challenge not only attenuated the GABAergic inhibition but actually converted it into excitation. The hyperosmotic stress caused a profound depolarizing shift in the reversal potential of GABAergic response (E GABA ) in MNCs. This E GABA shift was associated with increased expression of NaϪ cotransporter 1 (NKCC1) in MNCs and was blocked by the NKCC inhibitor bumetanide as well as by decreasing NKCC activity through a reduction of extracellular sodium. Blocking central oxytocin receptors during the hyperosmotic stress prevented the switch to GABAergic excitation. Finally, intravenous injection of the GABA A receptor antagonist bicuculline lowered the plasma levels of AVP and oxytocin in rats under the chronic hyperosmotic stress. We conclude that the GABAergic responses of MNCs switch between inhibition and excitation in response to physiological needs through the regulation of transmembrane Cl Ϫ gradients.

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Section: Discussionmentioning

confidence: 99%

Chronic Hyperosmotic Stress Converts GABAergic Inhibition into Excitation in Vasopressin and Oxytocin Neurons in the Rat

Kim¹,

Kim²,

Kim³

et al. 2011

J. Neurosci.

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“…This time course is consistent with the half-life of vasopressin of a few minutes. [41][42][43] On the other hand, based on the rapid time course, the initial immediate fall is likely because of sympathetic withdrawal. This conclusion is supported by the studies in animals in which both the vasopressin and sympathetic inputs were blocked, because decreasing forebrain OSM had no further effect on BP.…”

Section: Discussionmentioning

confidence: 99%

Central Action of Increased Osmolality to Support Blood Pressure in Deoxycorticosterone Acetate–Salt Rats

O'Donaughy

Brooks

2006

Hypertension

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Abstract-To test the hypothesis that increased osmolality contributes to hypertension in deoxycorticosterone acetate (DOCA)-salt-hypertensive rats by acting in the brain, DOCA-salt and Sham-salt rats were instrumented with bilateral, nonoccluding intracarotid and femoral catheters. Two weeks prior, rats were uninephrectomized and received subcutaneous implants with or without DOCA (65 mg) and began drinking salt water (1% NaCl and 0.2% KCl). DOCA-salt rats (nϭ28) exhibited elevated blood pressure (159Ϯ4 mm Hg; PϽ0.05) and heart rate (392Ϯ10 bpm; PϽ0.05) compared with Sham-salt animals (nϭ5; blood pressure: 107Ϯ5 mm Hg; heart rate: 355Ϯ10 bpm). Bilateral intracarotid infusion of hypotonic fluid (osmolality: Ϸ40 mOsm/L), which lowers osmolality of blood to the brain by Ϸ2%, rapidly decreased blood pressure in DOCA-salt rats (Ϫ22Ϯ4 mm Hg after 15 minutes; PϽ0.05; nϭ7) but not Sham-salt rats (2Ϯ2 mm Hg; nϭ5). Hypotonic fluid infused intravenously did not lower blood pressure (0Ϯ2 mm Hg) in DOCA-salt rats (nϭ7). In DOCA-salt rats pretreated with a V 1 vasopressin antagonist (Manning compound, 5 g, IV), intracarotid hypotonic infusion still decreased blood pressure (Ϫ10Ϯ3 mm Hg; PϽ0.05; nϭ9), but the response was smaller (PϽ0.05). Finally, in DOCA-salt rats (nϭ4) pretreated with the V 1 antagonist and the ganglionic blocker hexamethonium, decreasing osmolality of blood to the brain did not reduce blood pressure. These data indicate that, in DOCA-salt rats, hypertonicity acts in the brain to support blood pressure, in part by stimulating vasopressin secretion and in part by stimulating another rapidly reversible mechanism, likely the sympathetic nervous system. Key Words: hypertension, sodium-dependent Ⅲ central nervous system Ⅲ hypertension, mineralocorticoid Ⅲ sodium Ⅲ sympathetic nervous system Ⅲ vasopressin I ncreasing evidence supports a role for body fluid osmolality (OSM) in the regulation of blood pressure (BP) and sympathetic nerve activity (for reviews see References 1,2 ). Acute increases in OSM rapidly elevate BP and sympathetic nerve activity to specific beds, 3-5 and more chronic increases in plasma OSM, such as during water deprivation, seem to sustain this rapid sympathoexcitation. 6 Moreover, recent studies suggest that increased OSM contributes to sympathoexcitation in at least one model of salt-sensitive hypertension, the deoxycorticosterone-treated rat consuming excess salt (DOCA-salt) rat. More specifically, DOCA-salt rats exhibit hypertension and elevated OSM and/or NaCl levels, 7-10 and normalization of OSM results in profound decreases in BP and lumbar sympathetic nerve activity. 8 However, the site at which OSM is sensed to trigger sustained sympathoexcitation in DOCA-salt rats has not been identified.Osmoreceptors are present in numerous organs, including the liver, kidney, and brain, but significant indirect evidence implicates the brain in this action. First, forebrain circumventricular organs contain osmoreceptors that are exquisitely sensitive to minute changes in OSM. 11 Second, forebrain...

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“…In se lecting a method of central AVP treatment, we wanted a system which would provide access of the peptide (AVP) to brain (sep tal) receptors. Since vasopressin does not cross the blood-brain barrier to enter the nervous system in any significant amount [37] and has only a half-life in the circulation of about 3 min [38] we elected to use the miniaturized controlled-delivery Accurel devices which, when implanted in the lateral ventricle of the rat brain (adjacent to the septum) produced a constant enhance ment of AVP levels in the CSF for at least one week [29],…”

Section: Discussionmentioning

confidence: 99%

Regulation of Vasopressin Receptors and Phosphoinositide Hydrolysis in the Septum of Heterozygous and Homozygous Brattleboro Rats

et al. 1989

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Accurel polypropylene mini-devices, loaded with arginine vasopressin (AVP) and implanted in the lateral cerebral ventricle were used to centrally treat heterozygous (HE) and homozygous (HO) Brattleboro (BB) rats. After 1 week of treatment, the concentration of AVP receptors in the HO-BB rat septum decreased from 19.4 ± 2.6 to 12.4 ± 1.1 fmol/mg protein, but remained unchanged in the HE-BB rat (10.7 ± 0.8 and 7.0 ± 1.1 fmol/mg protein). In the HO-BB rat the [Η]-AVP equilibrium dissociation constant (K_D) of the septal AVP receptor decreased following AVP treatment (from 4.17 ± 0.7 to 1.97 ± 0.3 nM) compared to that of control animals. This decrease in receptor number following AVP treatment was accompanied by a decrease in the postreceptor response to AVP as measured by the AVP-stimulation of [³H]-inositol-1-phosphate (IP₁) accumulation (22.0 ± 6.1%) when compared to untreated animals (54.3 ± 8.3%). This apparent AVP-induced down-regulation was not due to occupancy of the binding sites by AVP since preincubation of the tissue at 37 °C for 60 min (which was able to cause near-complete dissociation of the hormone-receptor complex) did not result in an increased number of binding sites upon reexposure to [³H]-AVP. This study thus provides evidence for the homologous down-regulation and desensitization in terms of [³H]-IP₁ accumulation (phosphoinositide hydrolysis) of AVP receptors in the septum of the BB rat.

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Biological half-life and organ distribution of [3H]8-arginine-vasopressin in the rat

Cited by 40 publications

References 16 publications

Chronic Hyperosmotic Stress Converts GABAergic Inhibition into Excitation in Vasopressin and Oxytocin Neurons in the Rat

Chronic Hyperosmotic Stress Converts GABAergic Inhibition into Excitation in Vasopressin and Oxytocin Neurons in the Rat

Central Action of Increased Osmolality to Support Blood Pressure in Deoxycorticosterone Acetate–Salt Rats

Regulation of Vasopressin Receptors and Phosphoinositide Hydrolysis in the Septum of Heterozygous and Homozygous Brattleboro Rats

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