Activation of kidney-directed neurons in the lamina terminalis by alterations in body fluid balance

2001 ◽  
Vol 281 (5) ◽  
pp. R1637-R1646 ◽  
Author(s):  
D. J. Sly ◽  
M. J. McKinley ◽  
B. J. Oldfield

This study was undertaken to determine if neurons in the lamina terminalis, previously identified as projecting to the kidney (35), were responsive to alterations in stimuli associated with fluid balance homeostasis. Neurons in the lamina terminalis projecting to the kidney were identified by the retrograde transynaptic transport of Bartha's strain of pseudorabies virus in anesthetized rats. Rats were also exposed to 24-h water deprivation, intravenous hypertonic saline, or intracerebroventricular ANG II. To determine if “kidney-directed” neurons were activated following each stimulus, brain sections that included the lamina terminalis were examined immunohistochemically for viral antigen and Fos protein. With the exception of ANG II in the subfornical organ, all regions of the lamina terminalis contained neurons that were significantly activated by water deprivation, hypertonic saline, and ANG II. These results provide evidence for a neural substrate, which may underpin some of the effects of hypertonic saline and ANG II on renal function thought to be mediated through the lamina terminalis.

2011 ◽  
Vol 1383 ◽  
pp. 179-186 ◽  
Author(s):  
Rie Asami ◽  
Kentaro Ono ◽  
Osamu Nakanishi ◽  
Kiyotoshi Inenaga

2000 ◽  
Vol 279 (5) ◽  
pp. R1827-R1833 ◽  
Author(s):  
C. N. May ◽  
R. M. McAllen ◽  
M. J. McKinley

The lamina terminalis is situated in the anterior wall of the third ventricle and plays a major role in fluid and electrolyte homeostasis and cardiovascular regulation. The present study examined whether the effects of intracerebroventricular infusion of hypertonic saline and ANG II on renal sympathetic nerve activity (RSNA) were mediated by the lamina terminalis. In control, conscious sheep ( n = 5), intracerebroventricular infusions of 0.6 M NaCl (1 ml/h for 20 min) and ANG II (10 nmol/h for 30 min) increased mean arterial pressure (MAP) by 6 ± 1 ( P < 0.001) and 14 ± 3 mmHg ( P < 0.001) and inhibited RSNA by 80 ± 6 ( P < 0.001) and 89 ± 7% ( P < 0.001), respectively. Both treatments reduced plasma renin concentration (PRC). Intracerebroventricular infusion of artificial cerebrospinal fluid (1 ml/h for 30 min) had no effect. In conscious sheep with lesions of the lamina terminalis ( n = 6), all of the responses to intracerebroventricular hypertonic saline and ANG II were abolished. In conclusion, the effects of intracerebroventricular hypertonic saline and ANG II on RSNA, PRC, and MAP depend on the integrity of the lamina terminalis, indicating that this site plays an essential role in coordinating the homeostatic responses to changes in brain Na+ concentration.


1986 ◽  
Vol 250 (6) ◽  
pp. R1052-R1059 ◽  
Author(s):  
M. J. McKinley ◽  
D. A. Denton ◽  
R. G. Park ◽  
R. S. Weisinger

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.


Author(s):  
Neil E. Rowland

Thirst is a specific and compelling sensation, often arising from internal signals of dehydration but modulated by many environmental variables. There are several historical landmarks in the study of thirst and drinking behavior. The basic physiology of body fluid balance is important, in particular the mechanisms that conserve fluid loss. The transduction of fluid deficits can be discussed in relation to osmotic pressure (osmoreceptors) and volume (baroreceptors). Other relevant issues include the neurobiological mechanisms by which these signals are transformed to intracellular and extracellular dehydration thirsts, respectively, including the prominent role of structures along the lamina terminalis. Other considerations are the integration of signals from natural dehydration conditions, including water deprivation, thermoregulatory fluid loss, and thirst associated with eating dry food. These mechanisms should also be considered within a broader theoretical framework of organization of motivated behavior based on incentive salience.


2005 ◽  
Vol 37 (Supplement) ◽  
pp. S104???S105
Author(s):  
Simone D. Henkin ◽  
M??rcio Martins Silveira ◽  
Henrique Lannerhirt ◽  
Fl??via Meyer ◽  
Luis Fernando Martins Kruel

2014 ◽  
Vol 9 (4) ◽  
pp. 689-694 ◽  
Author(s):  
Javier Abian-Vicen ◽  
Adrián Castanedo ◽  
Pablo Abian ◽  
Cristina Gonzalez-Millan ◽  
Juan José Salinero ◽  
...  

The aim was to analyze the influence of competitive round on muscle strength, body-fluid balance, and renal function in elite badminton players during a real competition. Body mass, jump height during a countermovement jump, handgrip force, and urine samples were obtained from 13 elite badminton players (6 men and 7 women) before and after the 2nd-round and quarterfinal matches of the national Spanish badminton championship. Sweat rate was determined by using prematch-to-postmatch body-mass change and by weighing individually labeled fluid bottles. Sweat rates were 1.04 ± 0.62 and 0.98 ± 0.43 L/h, while rehydration rate was 0.69 ± 0.26 and 0.91 ± 0.52 L/h for the 2nd round and quarterfinals, respectively. Thus, dehydration was 0.47% ± 1.03% after the 2nd round and 0.23% ± 0.43% after the quarterfinals. There were no differences in prematch-to-postmatch jump height, but jump height was reduced from 37.51 ± 8.83 cm after the 2nd-round game to 34.82 ± 7.37 cm after the quarterfinals (P < .05). No significant differences were found in handgrip force when comparing prepost matches or rounds, although there were significant differences between dominant and nondominant hands (P < .05). The succession of rounds caused the appearance of proteinuria, hematuria, glycosuria, and higher nitrite and ketone concentrations in urine. Rehydration patterns during a real badminton competition were effective to prevent dehydration. A badminton match did not affect jump height or handgrip force, but jump height was progressively reduced by the competitive round. Badminton players’ renal responses reflected diminished renal flux due to the high-intensity nature of this racket sport.


1994 ◽  
Vol 55 (1) ◽  
pp. 163-167 ◽  
Author(s):  
Tetsuya Yoshida ◽  
Tadashi Okuno ◽  
Takashi Kawabata ◽  
Taketoshi Morimoto

1996 ◽  
Vol 28 (Supplement) ◽  
pp. 157
Author(s):  
R. Soler ◽  
M. A. Rivera ◽  
A. Rivera-Brown ◽  
W. R. Frontera ◽  
E. Lopategui

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