Lateral parabrachial nucleus and serotonergic mechanisms in the control of salt appetite in rats

The nucleus of the solitary tract (NTS) is the primary site of the cardiovascular afferent information about arterial blood pressure and volume. The NTS projects to areas in the central nervous system involved in cardiovascular regulation and hydroelectrolyte balance, such as the anteroventral third ventricle region and the lateral parabrachial nucleus. The aim of the present study was to investigate the effects of electrolytic lesion of the commissural NTS on water and 0.3 M NaCl intake and the cardiovascular responses to subcutaneous injection of isoproterenol. Male Holtzman rats weighing 280 to 320 g were submitted to sham lesion or electrolytic lesion of the commissural NTS (N = 6-15/group). The sham-lesioned rats had the electrode placed along the same coordinates, except that no current was passed. Water intake induced by subcutaneous isoproterenol (30 µg/kg body weight) significantly increased in chronic (15 days) commissural NTS-lesioned rats (to 2.4 ± 0.2 vs sham: 1.9 ± 0.2 mL 100 g body weight -1 60 min -1 ). Isoproterenol did not induce any sodium intake in sham or in commissural NTS-lesioned rats. The isoproterenol-induced hypotension (sham: -27 ± 4 vs commissural NTS-lesioned rats: -22 ± 4 mmHg/20 min) and tachycardia (sham: 168 ± 10 vs commissural NTS: 144 ± 24 bpm/20 min) were not different between groups. The present results suggest that the commissural NTS is part of an inhibitory neural pathway involved in the control of water intake induced by subcutaneous isoproterenol, and that the overdrinking observed in lesioned rats is not the result of a cardiovascular imbalance in these animals.

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Lesions of the commissural subnucleus of the nucleus of the solitary tract increase isoproterenol-induced water intake

Blanch

Freiria-Oliveira

Colombari

et al. 2007

“…Fluid intake was determined over 2 h at 30-min intervals. In this situation, the effect of the ANG-converting enzyme inhibitor captopril increases plasma levels of ANG I available to the circumventricular organs of the lamina terminalis, probably the SFO, in which the local conversion to ANG II occurs, leading to the stimulation of water intake and of sodium appetite (4,(23)(24)(25). Sodium preference was calculated according to the following formula: volume of 0.3 M NaCl intake/ volume of 0.3 M NaCl intake + volume of water intake.…”

Section: Methodsmentioning

confidence: 99%

Effect of electrolytic lesion of the dorsal raphe nucleus on water intake and sodium appetite

Olivares

Costa-e-Sousa

Cavalcante-Lima

et al. 2003

The present study determined the effect of an electrolytic lesion of the dorsal raphe nucleus (DRN) on water intake and sodium appetite. Male Wistar rats weighing 290-320 g with a lesion of the DRN (L-DRN), performed two days before experiments and confirmed by histology at the end of the experiments, presented increased sensitivity to the dehydration induced by fluid deprivation. The cumulative water intake of L-DRN rats reached 23.3 ± 1.9 ml (a 79% increase, N = 9) while sham-lesioned rats (SL-DRN) did not exceed 13.0 ± 1.0 ml (N = 11, P < 0.0001) after 5 h. The L-DRN rats treated with isoproterenol (300 µg kg -1 ml -1 , sc) exhibited an increase in water intake that persisted throughout the experimental period (L-DRN, 15.7 ± 1.47 ml, N = 9 vs SL-DRN, 9.3 ± 1.8 ml, N = 11, P < 0.05). The L-DRN rats also showed an increased spontaneous sodium appetite during the entire period of assessment. The intake of 0.3 M NaCl after 12, 24, 36 and 72 h by the L-DRN rats was always higher than 20.2 ± 4.45 ml (N = 10), while the intake by SL-DRN was always lower than 2.45 ± 0.86 ml (N = 10, P < 0.00001). Sodium-and water-depleted L-DRN rats also exhibited an increased sodium appetite (13.9 ± 2.0 ml, N = 11) compared to SL-DRN (4.6 ± 0.64 ml, N = 11) after 120 min of observation (P < 0.02). The sodium preference of L-DRN rats in both conditions was always higher than that of SL-DRN rats. These results suggest that electrolytic lesion of the DRN overcomes a tonic inhibitory component of sodium appetite. Correspondence

“…Furthermore, aldosterone release activated by ANG II during (15), in spite of the controversy on whether central or systemic ANG II is important for saline intake (15,(33)(34)(35)(36). Finally, the unloading of volume receptors probably removes the inhibition that hindbrain structures exert on water and saline intake (16,37,38). Every mechanism so far tested ( Table 1) that induces water and saline intake is inhibited by clonidine.…”

Section: Water Intakementioning

confidence: 99%

Multifactorial control of water and saline intake: role of <FONT FACE=Symbol>a</font>2-adrenoceptors

Deluca¹,

Menani²

1997

Water and saline intake is controlled by several mechanisms activated during dehydration. Some mechanisms, such as the production of angiotensin II and unloading of cardiovascular receptors, activate both behaviors, while others, such as the increase in blood osmolality or sodium concentration, activate water, but inhibit saline intake. Aldosterone probably activates only saline intake. Clonidine, an α 2 -adrenergic agonist, inhibits water and saline intake induced by these mechanisms. One model to describe the interactions between these multiple mechanisms is a wire-block diagram, where the brain circuit that controls each intake is represented by a summing point of its respective inhibiting and activating factors. The α 2 -adrenoceptors constitute an inhibitory factor common to both summing points.