Water intake elicited by injections of angiotensin II into preoptic area of rats

1981 ◽  
Vol 240 (1) ◽  
pp. R70-R74 ◽  
Author(s):  
D. B. Richardson ◽  
G. J. Mogenson

Drinking in response to unilateral injections of angiotensin II (AII) into the preoptic area is relatively weak and a relatively high dose of AII is required. A comparison was made of the drinking elicited by bilateral and unilateral injections of AII. Reliable drinking was observed when 5 X 10(-12) mol of AII in 0.2 microliter was injected bilaterally into the preoptic area, and in some animals when the dose of AII was 0.5 X 10(-12) mol in 0.2 microliter. The volumes of water intake were significantly larger with bilateral injections compared to unilateral injections. By injection of tritiated AII to elicit drinking and subsequent autoradiographic analysis of brain sections, it was shown that the injections were confined to the preoptic region and did not reach the cerebral ventricles. The results suggest that 1) bilateral injections may be more appropriate for comparing the preoptic region with other putative angiotensin receptive sites, 2) there is a greater responsiveness of the preoptic region to bilateral as compared with unilateral injections, and 3) the AII receptive area is diffusely represented in the region of the medial preoptic nucleus.

1992 ◽  
Vol 262 (2) ◽  
pp. R204-R210
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger

Cows that were normally hydrated or deprived of water were given intravenous or intracerebroventricular (icv) infusions of angiotensin I converting-enzyme inhibitors (CEI) or angiotensin II antagonists. Normally hydrated Na-deficient cows increased water intake in a dose-related manner in response to icv infusion of angiotensin I (n = 5). The response to 3 micrograms/h angiotensin I was abolished by concurrent icv infusion of the CEI captopril at 3 mg/h but not by intravenous infusion of captopril at 120 mg/h, which reduced Na appetite (n = 5). The icv infusion of captopril at 12 mg/h did not reduce the water intake of cows that were water restricted for 26.5 h (n = 4) or water restricted and Na deficient (n = 4). The icv infusion of the more lipophilic CEI ramipril at 3 mg/h (n = 7) did not reduce the water intake of normally hydrated or dehydrated cows but reduced the "need-free" intake of Na solution by dehydrated cows. The icv infusion of the nonpeptide antagonist Du Pont 753 at 3 mg/h (n = 7) reduced water intake in dehydrated cows. The results indicate that brain angiotensin may be involved in thirst in cattle. The data suggest that this brain angiotensin II may be formed by a pathway that does not include converting enzyme and that is sited inside the blood brain barrier, possibly in the median preoptic nucleus.


1984 ◽  
Vol 100 (2) ◽  
pp. 183-NP ◽  
Author(s):  
J. Kucharczyk

ABSTRACT Water intake elicited by microinjection of the hormone angiotensin-II into the preoptic region of cyclic female rats was significantly less on days of vaginal oestrus than at dioestrus or metoestrus, whereas the drinking of 2·7% NaCl solution, to which rats also had access, did not vary with the cycle. Administration of the same dose of angiotensin-II to the subfornical organ and the lateral cerebral ventricles induced drinking at all stages of the oestrous cycle, but the volumes of water or 2·7% NaCl ingested did not vary with the cycle. Water intake after subcutaneous injection of isoprenaline, a β-adrenergic agonist which causes increased angiotensin biosynthesis, varied cyclically with the stage of the oestrous cycle. On the other hand, water and 2·7% NaCl intakes induced by intraperitoneal injection of hypertonic NaCl (a cellular stimulus of thirst) or by 24-h water deprivation (which dehydrates both the extracellular and cellular body fluid compartments) did not differ significantly at the various stages of the oestrous cycle. The finding that fluctuations in angiotensin- and isoprenaline-induced water intake parallel the changes in spontaneous 24-h drinking suggests that the preoptic region may play an important role in the maintenance of extracellular fluid balance in synchrony with the oestrous cycle. J. Endocr. (1984) 100, 183–188


1980 ◽  
Vol 87 (1) ◽  
pp. 109-112 ◽  
Author(s):  
D. B. AVRITH ◽  
M. J. WISELKA ◽  
J. T. FITZSIMONS

Rats given free access to food, water and 2·7% NaCl and injected with either renin or angiotensin II into the preoptic area showed an immediate increase in water intake followed by an increase in intake of 2·7% NaCl. The rats continued to drink the hypertonic NaCl solution throughout the test session of 18 h. Intracranial injections of the dipsogen, carbachol, caused thirst but no sodium appetite. Bilateral adrenalectomy had no effect on either the initial water intake or the delayed intake of NaCl that was induced by intracranial injections of renin or angiotensin II. However, the increased water intake during the 18 h after the administration of renin was reduced to normal levels in adrenalectomized rats. Similar results were obtained with hypophysectomized rats. These results demonstrated that the delayed sodium appetite induced by renin or angiotensin II is not secondary to the stimulation of release of hormones from the pituitary gland or adrenal cortex.


1988 ◽  
Vol 254 (1) ◽  
pp. R69-R74 ◽  
Author(s):  
M. D. Evered ◽  
M. M. Robinson ◽  
P. A. Rose

To investigate the relationship between angiotensin II (ANG II) and mean arterial pressure (MAP) in the control of drinking in rats, we infused ANG II intravenously at constant rates (either 50 or 100 ng.kg-1.min-1 for 90 min) and varied MAP by intravenous injections of diazoxide (5-20 mg/kg). Rats were pretreated with captopril to block the endogenous synthesis of ANG II. When given alone, low and high doses of ANG II increased MAP approximately 30 and 50 mmHg, respectively. The low but not the high dose significantly increased water intake above control levels. Both doses caused such a large diuresis and natriuresis that the net effect was fluid loss. Reducing MAP toward normal greatly increased the drinking response to the high but not the low dose of ANG II and reduced the urinary solute and water loss to both doses. These results support the hypothesis that water intake and net fluid gain are inhibited when MAP is above normal. When MAP was reduced below normal in rats given constant infusions of ANG II the amount of water drunk and net fluid gain was proportional to the dose of ANG II but not the dose of diazoxide, the degree of hypotension, or urinary losses. This is consistent with previous reports that ANG II is essential for the drinking response to hypotension. Furthermore, it demonstrates that ANG II is not merely permissive but probably the signal controlling water intake when arterial pressure is reduced below normal.


1987 ◽  
Vol 54 (1) ◽  
pp. 13-17 ◽  
Author(s):  
Giancarlo Panzica ◽  
Carla Viglietti‐Panzica ◽  
Maria Grazia Fiori ◽  
Maurizio Calcagni ◽  
Giancarlo Anselmetti ◽  
...  

1993 ◽  
Vol 13 (3) ◽  
pp. 233-245 ◽  
Author(s):  
Takaya Sato ◽  
Masami Niwa ◽  
Akihiko Himeno ◽  
Keisuke Tsutsumi ◽  
Tsugio Amemiya

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