Intracerebroventricular losartan inhibits postprandial drinking in sheep

1997 ◽  
Vol 272 (4) ◽  
pp. R1055-R1059 ◽  
Author(s):  
M. Mathai ◽  
M. D. Evered ◽  
M. J. McKinley
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Food Intake ◽  
Water Intake ◽  
Fluid Balance ◽  
Intravenous Infusion ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
Drinking Response ◽  
Dependent Mechanism

We investigated the contribution of brain angiotensinergic mechanisms to postprandial drinking in sheep. Sheep in fluid balance were given 0.8 kg chaff for 30 min, and water intake was measured for the next hour. Intracerebroventricular infusion of the AT1 type angiotensin II (ANG II) receptor blocker losartan (1 mg/h) reduced postprandial drinking by approximately 70% (n = 7, P < 0.01) but did not affect food intake. The same losartan dose given intravenously had little or no effect on prandial drinking. Feeding increased Na+ concentrations in plasma and cerebrospinal fluid (CSF; n = 5, P < 0.05). Intracerebroventricular losartan (1 mg/h) inhibited the drinking responses to intracarotid infusion of ANG II (0.8 microg/min for 30 min, n = 4, P < 0.01) and to intracerebroventricular infusion of 0.5 M NaCl (1 ml/h for 1 h, n = 5, P < 0.05) but had no effect on drinking responses to intravenous infusion of 4 M NaCl (1.3 ml/min for 30 min). These findings indicate that a brain ANG II-dependent mechanism is involved in postprandial drinking in sheep. They suggest also that the mechanism by which increasing CSF Na+ causes thirst involves brain ANG II and is different from the mechanism subserving the drinking response to changes in blood Na+.

Angiotensin and Na appetite of sheep

1986 ◽  
Vol 251 (4) ◽  
pp. R690-R699 ◽  
Author(s):  
R. S. Weisinger ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
A. F. Muller ◽  
E. Tarjan
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Ang Ii ◽  
Nacl Solution ◽  
Parotid Saliva ◽  
Continuous Access ◽  
Access To Water

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.

Effect of intravenous angiotensin II on Fos distribution and drinking behavior in rabbits

1997 ◽  
Vol 272 (5) ◽  
pp. R1515-R1524 ◽  
Author(s):  
E. Badoer ◽  
D. McKinlay
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Intravenous Infusion ◽  
Drinking Behavior ◽  
Ventrolateral Medulla ◽  
Lamina Terminalis ◽  
Ang Ii ◽  
Solitary Tract ◽  
Cell Nuclei ◽  
Drinking Response

We investigated the effect of intravenous infusion of angiotensin II (ANG II, 40 ng.kg-1.min-1) on the distribution of Fos in the subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), and the medulla of the conscious rabbit. ANG II elicited significant increases in the number of Fos-positive cell nuclei in the SFO and OVLT (15- and 10-fold, respectively). Raising blood pressure with phenylephrine did not elicit Fos in these nuclei. These nuclei are believed to be responsible for the dipsogenic actions of ANG II; however, ANG II was not dipsogenic. When blood pressure was held at preinfusion levels by the coadministration of sodium nitroprus-side and ANG II, the rabbits did not drink but Fos production in the lamina terminalis was elevated. In the medulla, ANG II did not significantly increase Fos production in the nucleus of the solitary tract (NTS) or ventrolateral medulla (VLM). However, with the coadministration of sodium nitroprusside, there were marked increases in the NTS and VLM. The results suggest that neurons in the SFO and OVLT are either not involved in the dipsogenic pathways or there is disruption further downstream in the central pathways that would normally mediate a drinking response to ANG II.

Intracerebroventricular infusion of angiotensin II increases water and ethanol intake in rats

1999 ◽  
Vol 277 (1) ◽  
pp. R162-R172 ◽  
Author(s):  
R. S. Weisinger ◽  
J. R. Blair-West ◽  
P. Burns ◽  
D. A. Denton
Keyword(s):  
Angiotensin Ii ◽  
Direct Effect ◽  
Water Intake ◽  
Indirect Effect ◽  
Taste Preference ◽  
Ethanol Solution ◽  
Ethanol Intake ◽  
Ang Ii ◽  
Intracerebroventricular Infusion ◽  
Stimulation Of

The influence of prolonged ingestion of ethanol on stimulation of water or ethanol intake by intracerebroventricular infusion of ANG II was evaluated in rats. Animals were maintained for 5–6 mo with either 10% ethanol solution or water as their only source of fluid. In both groups of rats, infusion of ANG II caused a large increase in water intake (7-fold) and a lesser increase in 10% ethanol intake (2-fold). The effect of ANG II on the volume of ethanol solution ingested, however, was inversely related to the concentration of the ethanol solution. As the concentration of ethanol solution was decreased, frequency and duration of drinking bouts increased. The intake of sweetened 10% ethanol solution or commercially produced wine during infusion of ANG II was similar to the intake of 10% ethanol and not related to taste preference. In conclusion, chronic consumption of ethanol solution did not appear to adversely effect ANG II stimulation of water intake. The intake of ethanol solution during infusion of ANG II was inhibited by a direct effect of ingested ethanol and/or by indirect effect from metabolized ethanol.

Role of thromboxane receptors in the dipsogenic response to central angiotensin II

2002 ◽  
Vol 282 (3) ◽  
pp. R865-R869 ◽  
Author(s):  
Chagriya Kitiyakara ◽  
William J. Welch ◽  
Joseph G. Verbalis ◽  
Christopher S. Wilcox
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Ang Ii ◽  
Tp Receptor ◽  
Drinking Response ◽  
Tp Receptors ◽  
Thromboxane Receptors ◽  
Prostaglandin H ◽  
The Brain

Central angiotensin II (ANG II) regulates thirst. Because thromboxane A2-prostaglandin H2 (TP) receptors are expressed in the brain and mediate some of the effects of ANG II in the vasculature, we investigated the hypothesis that TP receptors mediate the drinking response to intracerebroventricular (icv) injections of ANG II. Pretreatment with the specific TP-receptor antagonist ifetroban (Ifet) decreased water intake with 50 ng/kg icv ANG II (ANG II + Veh, 7.2 ± 0.7 ml vs. ANG II + Ifet, 2.8 ± 0.8 ml; n = 5 rats; P < 0.001) but had no effect on water intake induced by hypertonic saline (NaCl + Veh, 8.4 ± 1.1 ml vs. NaCl + Ifet, 8.9 ± 1.8 ml; n = 5 rats; P = not significant). Administration of 0.6 μg/kg icv of the TP-receptor agonist U-46,619 did not induce drinking when given alone but did increase the dipsogenic response to a near-threshold dose of 15 ng/kg icv ANG II (ANG II + Veh, 1.1 ± 0.7 vs. ANG II + U-46,619, 4.5 ± 0.9 ml; n = 5 rats; P < 0.01). We conclude that central TP receptors contribute to the dipsogenic response to ANG II.

Role of brain angiotensin II in thirst and sodium appetite of sheep

1997 ◽  
Vol 273 (1) ◽  
pp. R187-R196 ◽  
Author(s):  
R. S. Weisinger ◽  
J. R. Blair-West ◽  
D. A. Denton ◽  
E. Tarjan
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Water Intake ◽  
Neural System ◽  
At1 Receptor ◽  
Hypertonic Solution ◽  
Ang Ii ◽  
Sodium Appetite ◽  
Intracerebroventricular Infusion

The contribution of brain angiotensin II (ANG II) to thirst and Na+ appetite of sheep was evaluated. Thirst was stimulated by water deprivation, intracarotid or intracerebroventricular infusion of ANG II, or intracarotid or intracerebroventricular infusion of hypertonic solution. Intracerebroventricular infusion, over 1-3 h, of the ANG II type 1 (AT1) receptor antagonist, losartan, decreased or abolished water intake caused by all of the stimuli tested. Intracerebroventricular infusion of ZD-7155, another AT1-receptor antagonist, blocked ANG II-induced water intake. Neither losartan nor ZD-7155 infused intracerebroventricularly altered the Na+ appetite of Na(+)-depleted sheep. Intracerebroventricular infusion of losartan over 3 h, however, did block the increase in water intake and the decrease in Na+ intake caused by intracerebroventricular infusion of hypertonic NaCl in Na(+)-depleted sheep. Intracerebroventricular infusion of the ANG II type 2 (AT2) receptor antagonist, PD-123319, over 1-3 h, did not alter ANG II-induced water intake or Na+ depletion-induced Na+ intake. These results are consistent with the proposition that brain ANG II, working via AT1 receptors, is involved in the neural system controlling some aspects of physiological thirst and Na+ appetite. A role for AT2 receptors in physiological thirst or Na+ appetite is not supported by the present results.

Angiotensin II regulates oxygen consumption

2002 ◽  
Vol 282 (2) ◽  
pp. R445-R453 ◽  
Author(s):  
Lisa Cassis ◽  
Marc Helton ◽  
Vicki English ◽  
Gerome Burke
Keyword(s):  
Body Weight ◽  
Oxygen Consumption ◽  
Angiotensin Ii ◽  
Food Intake ◽  
Energy Expenditure ◽  
Water Intake ◽  
Systolic Pressure ◽  
Ang Ii ◽  
Exposure Energy ◽  
Rebound Increase

Previous studies demonstrated that angiotensin II (ANG II) decreases body weight. This study examined whether ANG II regulates body weight through energy expenditure. Acute ANG II administration decreased oxygen consumption. To determine whether this effect was maintained, rats were infused with ANG II or saline for 14 days. Oxygen consumption was transiently decreased on day 1 of ANG II infusion; however, body weight and food intake were reduced for 14 days. In pair-feeding studies, reductions in food intake accounted for 63% of the effect of ANG II on body weight but did not influence systolic pressure, water intake, or oxygen consumption. With 28 days of ANG II infusion, differences in body weight between ANG II and control rats were of greater magnitude. An initial decrease in oxygen consumption was followed by a rebound increase. Coadministration of losartan prevented the effect of ANG II on body weight, food intake, blood pressure, and water intake. However, losartan only partially prevented ANG II reductions in oxygen consumption. These results demonstrate that ANG II transiently decreases oxygen consumption through mechanisms unrelated to food intake. With chronic ANG II exposure, energy expenditure may contribute to sustained reductions in body weight.

Effect of arterial pressure on drinking and urinary responses to angiotensin II

1988 ◽  
Vol 254 (1) ◽  
pp. R69-R74 ◽  
Author(s):  
M. D. Evered ◽  
M. M. Robinson ◽  
P. A. Rose
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Water Intake ◽  
Fluid Loss ◽  
High Dose ◽  
Ang Ii ◽  
Intravenous Injections ◽  
Drinking Response ◽  
High Doses ◽  
The Relationship

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.

Involvement of angiotensin II in water intake of genetically polydipsic mice

1991 ◽  
Vol 260 (6) ◽  
pp. R1152-R1158 ◽  
Author(s):  
T. Katafuchi ◽  
Y. Hattori ◽  
I. Nagatomo ◽  
K. Koizumi ◽  
E. Silverstein
Keyword(s):  
Angiotensin Ii ◽  
Food Intake ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Dark Period ◽  
Plasma Renin ◽  
Ang Ii ◽  
Arterial Blood ◽  
Daily Water Intake ◽  
Reduced Drinking

The involvement of angiotensin II (ANG II) in the genetic polydipsia of the STR/N strain of mice was investigated. Daily water intake of the polydipsic inbred STR/N of both sexes ranged between five and eight times that of nonpolydipsic controls: STR/1N, a mutant of the STR/N, and Swiss-Webster (S/W) mice. Nevertheless the diurnal pattern of drinking was maintained in the STR/N. There was no difference in daily food intake, arterial blood pressure, and plasma renin activity among the three groups. Drinking responses to 48 h of water deprivation were not significantly different between the polydipsic mice and their control groups. Captopril, an angiotensin I converting-enzyme inhibitor, injected subcutaneously just before the dark period, reduced drinking for 6 h in the polydipsic strain only. Food intake of all three groups of mice was not affected. Similarly the ANG II antagonist saralasin, [Sar1,-Ile8]ANG II, injected into the lateral cerebroventricle just before the dark period, significantly reduced water intake for 6 h after injection in the polydipsic mice only. Intracerebroventricular injection of ANG II increased drinking in the nondeprived controls but not in the polydipsic mice. These findings suggest that the polydipsia in the STR/N mice may involve, at least in part, the ANG II system in the brain.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

1993 ◽  
Vol 265 (3) ◽  
pp. R591-R595 ◽  
Author(s):  
R. L. Thunhorst ◽  
S. J. Lewis ◽  
A. K. Johnson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Arterial Blood Pressure ◽  
Water Intake ◽  
Enzyme Inhibitor ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Arterial Blood ◽  
Endogenous Formation

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.

scholarly journals Brain Prostaglandin D2 Increases Neurogenic Pressor Activity and Mean Arterial Pressure in Angiotensin II-Salt Hypertensive Rats

Hypertension ◽  
2019 ◽  
Vol 74 (6) ◽  
pp. 1499-1506 ◽  
Author(s):  
Ninitha Asirvatham-Jeyaraj ◽  
A. Daniel Jones ◽  
Robert Burnett ◽  
Gregory D. Fink
Keyword(s):  
Cerebrospinal Fluid ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Developmental Stage ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
Salt Hypertension ◽  
Pressor Activity

This study tested whether brain L-PGDS (lipocalin-type prostaglandin [PG] D synthase), through prostanoid signaling, might increase neurogenic pressor activity and thereby cause hypertension. Sprague Dawley rats on high-salt diet received either vehicle or Ang II (angiotensin II) infusion. On day 4, the developmental stage of hypertension, brains from different sets of control and Ang II–treated rats were collected for measuring L-PGDS expression, PGD2 levels, and DP1R (type 1 PGD2 receptor) expression. In a different set of 14-day Ang II-salt–treated rats, mini-osmotic pumps were used to infuse either a nonselective COX (cyclooxygenase) inhibitor ketorolac, L-PGDS inhibitor AT56, or DP1R inhibitor BWA868C to test the role of brain COX-PGD2-DP1R signaling in Ang II-salt hypertension. The acute depressor response to ganglion blockade with hexamethonium was used to quantify neurogenic pressor activity. During the developmental stage of Ang II-salt hypertension, L-PGDS expression was higher in cerebrospinal fluid, and PGD2 levels were increased in the choroid plexus, cerebrospinal fluid, and the cardioregulatory brain region rostral ventrolateral medulla. DP1R expression was decreased in rostral ventrolateral medulla. Both brain COX inhibition with ketorolac and L-PGDS inhibition with AT56 lowered mean arterial pressure by altering neurogenic pressor activity compared with vehicle controls. Blockade of DP1R with BWA868C, however, increased the magnitude of Ang II-salt hypertension and significantly increased neurogenic pressor activity. In summary, we establish that the development of Ang II-salt hypertension requires increased COX- and L-PGDS–derived PGD2 production in the brain, making L-PGDS a possible target for treating neurogenic hypertension.

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