Observation of Energy and Baseline Dependent Reactor Antineutrino Disappearance in the RENO Experiment.

The RENO experiment has analyzed about 500 live days of data to observe an energy dependent disappearance of reactor ν[over ¯]_{e} by comparing their prompt signal spectra measured in two identical near and far detectors. In the period between August of 2011 and January of 2013, the far (near) detector observed 31 541 (290 775) electron antineutrino candidate events with a background fraction of 4.9% (2.8%). The measured prompt spectra show an excess of reactor ν[over ¯]_{e} around 5 MeV relative to the prediction from a most commonly used model. A clear energy and baseline dependent disappearance of reactor ν[over ¯]_{e} is observed in the deficit of the observed number of ν[over ¯]_{e}. Based on the measured far-to-near ratio of prompt spectra, we obtain sin^{2}2θ_{13}=0.082±0.009(stat)±0.006(syst) and |Δm_{ee}^{2}|=[2.62_{-0.23}^{+0.21}(stat)_{-0.13}^{+0.12}(syst)]×10^{-3} eV^{2}.

Forebrain lesions that disrupt water homeostasis do not eliminate the sodium appetite of sodium deficiency in sheep.

Brain structures located within the anterior wall of the third brain ventricle (subfornical organ, median preoptic nucleus and organum vasculosum of the lamina terminalis) are known to be involved in thirst as well as other aspects of body fluid and electrolyte balance. The present studies evaluated the role of these structures in the Na appetite of mildly or moderately Na-depleted sheep (sheep with a parotid fistula deprived of Na solution for 22 or 46 h). In addition, the role of these structures was tested in mildly Na-depleted sheep in which the Na appetite was enhanced by decreasing cerebrospinal fluid and brain extracellular fluid Na concentration (i.e., i.c.v. infusion of hypertonic saccharide solution) or was decreased by systemic infusion of hypertonic saline. The results indicated that sheep with lesions which reduced or eliminated daily water intake or water intake in response to hypertonicity of body fluids had, in all situations tested, appropriate changes in Na appetite (i.e., similar to their prelesion changes). Thus, the present experiments demonstrated that the brain areas involved in thirst as well as other aspects of body fluid and electrolyte balance are anatomically different from those involved in regulating Na appetite.

Renal denervation does not prevent dehydration-induced natriuresis in sheep.

Normal sheep or sheep in which the renal nerves had been extirpated were deprived of water for 2 days in order to determine whether changes in renal nerve activity contribute to natriuresis during water deprivation. Both groups of sheep showed a considerable natriuresis throughout the period of water deprivation and increases in plasma osmolality and plasma Na concentration. Renal denervation, as indicated by the absence of catecholamine fluorescence in kidney sections, was extensive. Previous experiments have suggested cerebral involvement in the induction of dehydration-induced natriuresis. The present results indicate that the efferent pathway mediating this cerebral influence on renal sodium excretion does not involve the renal nerves, suggesting a hormonal mechanism as the likely pathway.

Volume influences on thirst and vasopressin secretion in dehydrated sheep.

The contribution of extracellular fluid volume (ECFV) to water consumption and plasma vasopressin concentration (PAVP) after water deprivation for 52 h was examined in sheep. Intravenous infusion of isotonic NaCl, equivalent to either estimated ECFV loss or total body water loss, significantly reduced water intake by 37% when water was offered 3 h after infusion but not when water was offered 1 h after infusion. Plasma osmolality (POsm) was reduced after 3 h. Infusion of 200 mM NaCl, which maintained POsm, decreased water consumption by the same degree as isotonic NaCl infusion. Thus large decreases in POsm had no effect on water intake in this experimental protocol. Lack of inhibition of drinking 1 h after infusion suggests that the decrease observed after 3 h may have been mediated by receptors in the interstitial fluid (ISF) compartment and not the intravascular compartment. PAVP was reduced 3 h after infusion of NaCl but not at 1 or 2 h after infusion. POsm was also decreased at 3 h. Thus reduction of PAVP by NaCl infusion may have been caused by either ISF or intracellular fluid volume expansion.

Ablation of subfornical organ does not prevent angiotensin-induced water drinking in sheep.

The subfornical organ (SFO) and surrounding periventricular tissue were ablated in sheep. Such a lesion did not significantly reduce water drinking in response to intracarotid, intravenous, or intracerebroventricular infusions of [Val5]angiotensin II amide (ANG II) but caused reduced intake of water in response to intracarotid infusion of hypertonic saline. The dipsogenic response of these sheep to water deprivation for 3 days was similar to that of normal sheep subjected to water deprivation. Although the results are not conclusive in excluding the SFO from having a role in ANG II-induced drinking, they show that there are receptors outside the SFO sensitive to blood-borne ANG II that are involved in water drinking in sheep. The results also show that tissue in the SFO or its surroundings may be involved in drinking caused by acute hypertonicity.

Augmented plasma renin levels in dehydrated sheep with periventricular lesions.

Ablation of tissue in the midline anterior wall of the third ventricle (AV3V) of sheep did not consistently alter baseline plasma renin concentration (PRC) in water replete animals, but caused a greatly augmented increase in PRC in response to water deprivation. PRC might increase in these sheep in order to maintain blood pressure, however it is possible that a central inhibitory influence on renal renin release, operative during dehydration, is disrupted by AV3V-lesions.

Natriuresis induced by arginine vasopressin infusion in sheep.

The aim of this study was to investigate whether arginine vasopressin (AVP) is natriuretic in sheep at plasma concentrations comparable to those induced by water deprivation. AVP was infused intravenously at 0.1, 0.2, and 0.5 microgram/h for 24-48 h in sheep allowed free access to water. Infusion of AVP at 0.1 microgram/h did not alter renal Na output, whereas infusion of AVP at both 0.2 and 0.5 microgram/h significantly increased daily output of Na in urine. Significant natriuresis did not occur until 3.5 h after the start of AVP infusion at 0.2 microgram/h. Plasma AVP levels induced by these infusions were 9.8 +/- 1.6 (0.1 microgram/h AVP), 21.9 +/- 7.7 (0.2 microgram/h AVP), and 32.5 +/- 9.0 pg/ml (0.5 microgram/h AVP) after 24 h. These concentrations are within the range found in sheep deprived of water for 3 days. Hypophysectomy abolished increases in plasma AVP concentration but not natriuresis in response to water deprivation. This suggests that increased plasma AVP concentration does not play an essential role in the mechanisms subserving dehydration-induced natriuresis.

The anterior wall of the third cerebral ventricle and homeostatic responses to dehydration.

Within the anterior wall of the third cerebral ventricle, structures are found which have been implicated in the regulation of fluid and electrolyte balance. These structures include the subfornical organ (SFO), preoptic medianus nucleus (PMN) and the organum vasculosum of the lamina terminalis (OVLT). In sheep, the OVLT rises from the ventricular floor over the optic chiasma and occupies most of the midline ventricular wall up to the level of anterior commissure. It contains a plexus of blood vessels at its base which possess fenestrated endothelial cells, and appears to lack ependyma. The SFO of sheep bulges into the third ventricle above the anterior commissure and the PMN is situated between the SFO and OVLT, surrounding the rostral edge of the midline anterior commissure. Like most mammals, water deprivation in sheep results in hypertonicity of body fluids, thirst and graded increase in plasma concentration of vasopressin (AVP). Dehydration also causes a natriuresis in these animals. In sheep with combined ablation of OVLT/PMN tissue, the volume of water drunk, the increases in plasma vasopressin (AVP) level, and the natriuresis in response to dehydration were considerably attenuated, and extreme hypernatremia resulted. Additionally, ablation of OVLT/PMN tissue almost abolished water drinking and AVP secretion in response to systemic infusion of hypertonic NaCl, but did not diminish AVP secretion in response to haemorrhage. In other animals, the OVLT and PMN were individually ablated. While partial osmoregulatory deficits were observed in each case, these deficits were smaller than those observed with combined OVLT/PMN ablation. In contrast to these results, the homeostatic responses to dehydration were not diminished in sheep with combined SFO/PMN lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral involvement in dehydration-induced natriuresis.

Water deprivation caused daily urinary Na output to more than double in normal sheep, but caused no increase in Na excretion in sheep (A3VL-sheep) in which the anterior third ventricle wall had been ablated. Dehydrated A3VL-sheep exhibited a much greater degree of hypernatremia than dehydrated normal sheep, although water losses were similar in both groups. We postulate that the natriuresis induced by dehydration is a cerebrally mediated homeostatic response.