The role of angiotensin II in the central regulation of feed intake in sheep

2001 ◽  
Vol 81 (2) ◽  
pp. 215-221 ◽  
Author(s):  
Katsunori Sunagawa ◽  
Richard S. Weisinger ◽  
Michael J. McKinley ◽  
Brett S. Purcell ◽  
Craig Thomson ◽  
...  

The objective was to determine the role of Angiotensin II (ANG) in the central regulation of feed intake by ruminants. As a control treatment, artificial cerebrospinal fluid (CSF) was given (over a period of 98.5 h) as a continuous intracerebroventricular (ICV) infusion (0.2 mL h–1) into the lateral ventricle of ewes (n = 5). Approximately 9 d later, the infusion was repeated with the same ewes, but the CSF contained ANG (25 g μL–1). The ewes were fed dried alfalfa chaff for 2 h once daily and both water and a 0.5 M NaCl solution were available ad libitum (except that water intake was restricted on the first day of ANG infusion). Infusion of ANG resulted in severe thirst that persisted when water intake was restricted to an amount equal to voluntary intake during the control infusion. Furthermore, when ewes had ad libitum access to water, consumption during ANG infusion was 1.4 to 2.8-fold greater than that during CSF infusion (P < 0.01). Compared with CSF infusion, ANG infusion decreased eating rates by an average of 46.5% (range, 31.8–62.6%; P < 0.01) and feed intake by 25.0% (5.4–48.1%; P < 0.01), and increased salt intake by 273.8% (124.0–417.6%; P < 0.01). We concluded that ANG produced thirst sensations in the brain, resulting in excessive water intake that caused ruminal distension and significantly reduced feed intake. Key words: Angiotensin, brain, thirst, feed intake, sheep

1983 ◽  
Vol 244 (2) ◽  
pp. R244-R248 ◽  
Author(s):  
C. C. Barney ◽  
R. M. Threatte ◽  
M. J. Fregly

The role of angiotensin II in the control of water intake following deprivation of water for varying lengths of time was studied. Male rats were deprived of water for 0, 12, 24, 36, or 48 h. Water intakes were measured with and without pretreatment with the angiotensin I-converting enzyme inhibitor, captopril (50 mg/kg, ip). Captopril had no significant effect on water intake following either 0 or 12 h of water deprivation. However, captopril significantly attenuated water intake following 24-48 h of water deprivation with the magnitude of the attenuation increasing as the length of the period of water deprivation increased. Plasma renin activity was significantly increased over control levels after 24-48 h of water deprivation but not after 12 h of water deprivation. Plasma renin activity tended to increase as the length of the water-deprivation period increased. Serum osmolality and sodium concentration were significantly increased over control levels following 12-48 h of water deprivation. Serum osmolality and sodium concentration failed to show any further increases with increasing length of water deprivation beyond the increases following 12 h of water deprivation. The data indicate that the water intake of water-deprived rats can be divided into an angiotensin II-dependent component and angiotensin II-independent component. The angiotensin II-independent component appears to be more important in the early stages of water deprivation whereas the angiotensin II-dependent component becomes more important as the length of the water-deprivation period increases.


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.


1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.


1981 ◽  
Vol 241 (5) ◽  
pp. F525-F531
Author(s):  
F. H. Leenen ◽  
W. de Jong

In two-kidney one-clip hypertensive rats we evaluated the effect of water restriction on the development and maintenance of severe hypertension (systemic blood pressure 200-230 mmHg). After application of renal arterial clips in rats allowed access to water for 1 or 2 h daily, BP stabilized at 180-190 mmHg. No increase in water intake occurred and plasma renin activity(PRA) (measured before the drinking period) was significantly below the levels observed in ad libitum-drinking hypertensive rats. In rats administered 4 ml water/100 g body weight twice daily by gavage, development of hypertension was more clearly suppressed. Blood pressure increased slowly and reached levels of only 150-170 mmHg. Furthermore, PRA was significantly lower in this group compared with ad libitum-drinking hypertensive animals. In rats with established (4-5 wk) renal hypertension, restriction of water intake to 1 or 2 h daily resulted in a rapid decrease in BP of about 30 mmHg. Daily administration of Pitressin tannate to hypertensive rats allowed free access to water induced a similar decrease in BP as well as suppression of PRA. These results indicate that the hypotensive effect of water restriction in the two-kidney one-clip hypertensive rat model may be mediated, at least in part, through elevated circulating levels of vasopressin that subsequently inhibit renin release.


1975 ◽  
Vol 228 (5) ◽  
pp. 1293-1297 ◽  
Author(s):  
M van Gemert ◽  
M Miller ◽  
RJ Carey ◽  
AM Moses

Studies were carried out in the rat to detemine if hypothalamic lesions which caused polydipsia and polyuria had their effect mediated through an alteration of the ability of the neurohypophyseal system to release ADH. Rats with medial preoptic lesions hadincreased water intake while on ad libitum access to water and slightly impaired ability to conserve water following dehydration, but with no impairment of urine-concentrating ability. These were associated with an increase in plasma osmolality both during ad libitum fluid intake and after dehydration. Urinary ADH excretion was at leastas great as in shamoperated controls during ad libitum water intake, but failed to increase during dehydration in spite of a marked increase in plasma osmolality. Pituitary ADH content did not differ from control animals either during ad libitum water intake of after dehydration. Animals with lesions in the lateral preoptic and septal areas did not differ from control animals during ad libitum fluid intake and after dehydration even though lateral preoptic lesions produced polydipsia. In all animals, lesions were remote from the supraoptic nuclei, which showed no histological evidence of damage. It is concluded thatareas of the central nervous system away from the supraoptic nuclei are involved in the regulation of both water intake and ADH release.


1981 ◽  
Vol 240 (1) ◽  
pp. R75-R80 ◽  
Author(s):  
M. C. Lee ◽  
T. N. Thrasher ◽  
D. J. Ramsay

The role of the renin-angiotensin system in drinking induced by water deprivation and caval ligation was assessed by infusion of saralasin into the lateral ventricles of rats. This technique was first validated by demonstrating its capability to specifically antagonize drinking to both systemic and central angiotensin II. However, neither the latency to drink nor the amount of water consumed following 24- or 30-h water deprivation was affected by saralasin. Furthermore, saralasin had no significant effect on the recovery of blood pressure or on the water intake following ligation of the abdominal vena cava. These observations suggest that the renin-angiotensin system alone does not play an essential role in the control of drinking following water deprivation or caval ligation in rats.


1978 ◽  
Vol 90 (3) ◽  
pp. 641-642
Author(s):  
M. Singh ◽  
T. More

Yellowing of wool as a function of physiological stress caused by nutritional deficiency in the feed of sheep (Das, 1965) though not confirmed by subsequent studies (Singh et al. 1977) evoked interest in the role of physiological stress in causing canary staining of wool. Restricted water intake as is generally the case with sheep in arid or even semiarid regions during summer, imposes considerable physiological stress. Furthermore, canary coloration is thought to be a sequel to an adaptive mechanism to hot and humid conditions in Indian sheep which have a greater reliance on cutaneous evaporation for dissipating body heat (Acharaya & Singh, 1976). It was, therefore, decided to study the influence, if any, of restricting access to water on the canary coloration of wool (non-scourable yellow coloration of the autumn clip) in the stain-susceptible Chokla sheep


1995 ◽  
Vol 37 (5) ◽  
pp. 463-466 ◽  
Author(s):  
Silas Pereira Barbosa ◽  
Juliana Irani Fratucci de Gobbi ◽  
Luciana Zilioli ◽  
Luiz Antonio de Arruda Camargo ◽  
Wilson Abrão Saad ◽  
...  

Author(s):  
Belete Kuraz ◽  
Adugna Tolera ◽  
Aster Abebe

Background: Mineral deficiencies are considered to be one of the nutritional constraints to sheep performance. An experiment was conducted to evaluate the role of bole soil on feed intake, live weight change and carcass characteristics of Arsi-Bale sheep fed natural grass hay and concentrate supplement and its cost-benefit analysis of bole soil supplementation. Result: Total DM, OM, CP, NDF, ADF intake and ADL were higher (p less than 0.0001) for T3 than for T1, T2 and T4. Final weight, body weight change, average daily gain and feed conversion efficiency were greater (p less than 0.0001) for T3 and T2 than for T1 and T4. There were no differences (p greater than 0.05) between T3 and T2 whereas T4 was greater than T1 in these variables. Slaughter weight (SW) was heavier (p less than 0.0001) for treatment two and treatment three than for treatment four and treatment one, hot carcass weight, foreleg weight and dressing percentage on empty body weight basis were greater (p less than 0.0001) for T3 and T2 than for T1and T4. Conclusion: Bole soil supplementation had potentially highest effect on feed intake, live weight change and carcass characteristics of Arsi-Bale sheep than non-supplemented groups. The present study also revealed that supplementation of minerals improved the total weight gain of sheep over the control treatment.


1989 ◽  
Vol 257 (2) ◽  
pp. R383-R387 ◽  
Author(s):  
J. L. Miner ◽  
M. A. Della-Fera ◽  
J. A. Paterson ◽  
C. A. Baile

We compared the effects of neuropeptide Y (NPY) injected into the lateral ventricle (LV) and periphery (ip in rats; iv in sheep) on feed and water intake. In sated rats, a bolus injection of 1.18 or 2.35 nmol of NPY administered LV, but not ip, increased (P less than 0.05) feed intake on average of 809% within 30 min of injection. In sated sheep, an LV bolus injection of 2.35 nmol of NPY increased feed intake by 154% within 30 min. Similar doses of human pancreatic polypeptide and peptide YY were less orexigenic than NPY in sheep. After 24 h, cumulative feed intakes were similar among control and peptide treatments. Intravenous injection of 2.35 nmol NPY did not increase feed intake in sheep. Water intake was stimulated (P less than 0.05) by NPY (LV injection) in both the presence and absence of feed. We propose that NPY is involved in the central regulation of consummatory behavior in sheep.


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