Sodium appetite and thirst in cattle subjected to dehydration

1989 ◽  
Vol 257 (5) ◽  
pp. R1212-R1218 ◽  
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger

Cows having free access to water (hydrated) or deprived of water for 26.5 h (dehydrated) were infused for 3 h with angiotensin II or captopril solutions intravenously (iv) or intracerebroventricularly (icv) beginning 1 h before access to 0.3 M NaHCO3/NaCl solution for 2 h. The results agree with the results of the experiments with the same agents and doses in Na-deficient cows. Only iv infusion of angiotensin II stimulated Na appetite and only icv infusion of angiotensin II stimulated thirst. Therefore, barriers to the penetration of angiotensin II in the brain determined the particular site of action and elicited response. Dehydration did not stimulate Na appetite and, as shown previously, Na deficiency did not stimulate thirst, but both behaviors seem to be influenced by angiotensin-related mechanisms in the brain. The inability of iv angiotensin II to stimulate Na appetite in hydrated cows might be explained by the lack of a response caused by, and common to, Na deficiency and dehydration, e.g., upregulation of angiotensin II receptors, or reduced extracellular fluid volume.

1988 ◽  
Vol 255 (2) ◽  
pp. R205-R211 ◽  
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger

Cows depleted of Na by loss of saliva from a parotid fistula for 46 h had an avid appetite for Na solution. They drank 21.0 +/- 1.6 liter of 0.3 M NaHCO3-NaCl solution during 2 h of access but little or no water during that time. Solutions of angiotensin II or captopril were infused for 3 h intravenously or into a lateral ventricle (intracerebroventricular) beginning 1 h before access to Na solution. Intravenous angiotensin II increased Na intake (to 26.8 +/- 2.9 liter, P less than 0.01) but did not alter water intake. Intracerebroventricular angiotensin II increased water intake but did not alter Na intake. Intravenous captopril reduced Na intake (to 11.0 +/- 2.1 liter, P less than 0.001) and concurrent intravenous angiotensin II prevented the reduction but concurrent intracerebroventricular angiotensin II did not. Intracerebroventricular captopril did not alter Na or water intake. Intravenous captopril reduced to zero the water intake during the hour before Na access, and concurrent intravenous angiotensin II prevented that reduction also. The dipsogenic action of intracerebroventricular angiotensin II was potentiated by intravenous captopril. The results of these experiments suggest that if angiotensin II receptors involved in the mechanism regulating Na appetite are in the brain, they are accessible only from the blood, e.g., in circumventricular organs. Thirst was inhibited by reduction of angiotensin II in blood but was stimulated only by angiotensin II acting inside the blood-brain barrier.


1978 ◽  
Vol 55 (1) ◽  
pp. 81-87 ◽  
Author(s):  
A. J. Mourant

1. Rats with indwelling aortic and right atrial cannulae were maintained on a sodium-free diet before and after renal arterial constriction combined with contralateral nephrectomy. Control animals underwent the same protocol except that non-constricting clips were used. 2. Plasma volumes in the salt-deprived animals were lower than previously determined values in animals with free access to sodium. After clipping plasma volume increased in the hypertensive animals. Extracellular fluid volume was increased equally in both normotensive and hypertensive animals on the second postoperative day only. 3. Before clipping and contralateral nephrectomy plasma angiotensin II values were higher than normal. After the operation angiotensin II concentrations fell to normal over a period of 14 days without significant differences between experimental and control groups. 4. It is concluded that high blood pressure after clipping may be in part maintained by increases in plasma volume. However, the results strongly suggest that other renal mechanisms are likely to be of major pathogenic importance.


1995 ◽  
Vol 268 (6) ◽  
pp. R1401-R1405 ◽  
Author(s):  
M. el Ghissassi ◽  
S. N. Thornton ◽  
S. Nicolaidis

The angiotensin receptor specificity, with respect to fluid intake, of the organum cavum prelamina terminalis (OCPLT), a recently discovered discrete forebrain structure with high sensitivity to angiotensin II (ANG II), was investigated. ANG II (10 ng) microinjected into the OCPLT significantly increased water consumption but did not induce intake of a hypertonic (3%) NaCl solution. Losartan, an ANG II type 1 (AT1) receptor-specific antagonist, produced dose-related (1-100 ng) inhibition of ANG II-induced drinking. The ANG II type 2 receptor-specific antagonist CGP-42112A was ineffective. Intake of the 3% NaCl solution in response to microinjection of either of the antagonists into the OCPLT was never observed. These findings suggest that water intake produced by microinjection of ANG II into the OCPLT is mediated by AT1 receptors uniquely and that, in contrast to other regions of the brain, these receptors do not induce salt intake when stimulated by ANG II.


1986 ◽  
Vol 251 (4) ◽  
pp. R690-R699 ◽  
Author(s):  
R. S. Weisinger ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
A. F. Muller ◽  
E. Tarjan

The effect of both intravenous (iv; 24 micrograms/h) and intracerebroventricular (ivt; 3.8 micrograms/h) infusion over 1-2 days of angiotensin II (ANG II) on Na intake of both Na-replete and -deplete sheep (i.e., 22 h loss of parotid saliva) was observed. In Na-replete sheep with continuous access to water and 2-h daily access to 0.5 M NaCl solution, both iv and ivt ANG II caused an increase in Na intake. The increase in Na intake caused by iv or ivt ANG II was preceded by a Na deficit due to increased urinary Na excretion. The increase in Na intake was eliminated by the continuous return of urine. In Na-deplete sheep with continuous access to water and 2-h daily access to 0.6 M NaHCO3 solution, iv ANG II caused no change in Na loss but a small increase in Na intake during the 1st day of infusion. The ivt ANG II caused no change in Na loss or in Na intake. The iv ANG II caused a small and inconsistent increase in water intake in Na-replete sheep but did not cause any change in water intake of Na-deplete sheep. The ivt ANG II caused a large increase in water intake in both Na-replete and -deplete sheep. In both Na-replete and -deplete sheep, iv ANG II did not alter cerebrospinal fluid or plasma [Na] or osmolality but decreased plasma [K]. The ivt ANG II decreased both cerebrospinal fluid and plasma [Na] and osmolality. The results of the present experiments are consistent with the proposition that the ANG II-induced Na appetite in sheep is largely due to an ANG II-induced Na loss preceding the development of appetite.


1960 ◽  
Vol 199 (1) ◽  
pp. 22-24 ◽  
Author(s):  
Libby F. Titlebaum ◽  
John L. Falk ◽  
Jean Mayer

Groups of normal rats and animals with diabetes insipidus were tested on their relative acceptance and rejection of various concentrations of NaCl solution. Rats with diabetes inspidus drank more than normal rats in the hypotonic range. Their acceptance was maximal at a lower solution concentration than in the case of normal animals and relative rejection began at concentrations where normals ingested maximally. The results are discussed in relation to such factors in the internal environment as serum sodium level and extracellular fluid volume.


2013 ◽  
Vol 2013 ◽  
pp. 1-22 ◽  
Author(s):  
Courtney Premer ◽  
Courtney Lamondin ◽  
Ann Mitzey ◽  
Robert C. Speth ◽  
Mark S. Brownfield

Angiotensin II increases blood pressure and stimulates thirst and sodium appetite in the brain. It also stimulates secretion of aldosterone from the adrenal zona glomerulosa and epinephrine from the adrenal medulla. The rat has 3 subtypes of angiotensin II receptors:AT1a,AT1b, and AT2. mRNAs for all three subtypes occur in the adrenal and brain. To immunohistochemically differentiate these receptor subtypes, rabbits were immunized with C-terminal fragments of these subtypes to generate receptor subtype-specific antibodies. Immunofluorescence revealedAT1aand AT2receptors in adrenal zona glomerulosa and medulla.AT1bimmunofluorescence was present in the zona glomerulosa, but not the medulla. Ultrastructural immunogold labeling for theAT1areceptor in glomerulosa and medullary cells localized it to plasma membrane, endocytic vesicles, multivesicular bodies, and the nucleus.AT1band AT2, but notAT1a, immunofluorescence was observed in the anterior pituitary. Stellate cells wereAT1bpositive while ovoid cells were AT2positive. In the brain, neurons wereAT1a,AT1b, and AT2positive, but glia was onlyAT1bpositive. Highest levels ofAT1a,AT1b, and AT2receptor immunofluorescence were in the subfornical organ, median eminence, area postrema, paraventricular nucleus, and solitary tract nucleus. These studies complement those employing different techniques to characterize Ang II receptors.


Physiology ◽  
2004 ◽  
Vol 19 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Michael J. McKinley ◽  
Alan Kim Johnson

Thirst is important for maintaining body fluid homeostasis and may arise from deficits in either intracellular or extracellular fluid volume. Neural signals arising from osmotic and hormonal influences on the lamina terminalis may be integrated within the brain, with afferent information relayed from intrathoracic baroreceptors via the hindbrain to generate thirst.


1984 ◽  
Vol 247 (2) ◽  
pp. R356-R365 ◽  
Author(s):  
K. E. Moe ◽  
M. L. Weiss ◽  
A. N. Epstein

Angiotensin II and aldosterone increase in response to sodium deficiency to promote sodium and water conservation. In addition, they may act synergistically to arouse a sodium appetite. If so, then blockade of endogenous angiotensin should decrease the appetite. In experiments reported here, captopril (SQ 14,225) was given peripherally to rats to block conversion of angiotensin I to angiotensin II. It both enhanced and suppressed sodium depletion-induced sodium appetite. The appetite was suppressed when captopril was given in high doses, which block conversion centrally as well as peripherally. The same doses of captopril had no effect on urinary sodium excretion or on sodium appetite aroused by mineralocorticoid treatment. Low doses, which block conversion only in the periphery, enhanced salt intake elicited by depletion, and the enhancement was abolished by captopril given directly into the brain. Therefore the enhancement was probably due to a captopril-induced increase of peripheral angiotensin I, which gained access to the brain and was converted there to angiotensin II.


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