Intracerebroventricular angiotensin II‐induced thirst and sodium appetite in rat are blocked by the AT1 receptor antagonist, Losartan (DuP 753), but not by the AT2 antagonist, CGP 42112B

Beresford, M; Jt, Fitzsimons

doi:10.1113/expphysiol.1992.sp003643

Cited by 82 publications

(36 citation statements)

References 5 publications

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“…In specific areas of the hypothalamus (thirst centre), ANGII has been shown to stimulate water intake via AT 1 (Beresford & Fitzsimons, 1992) and AT 2 receptor activation (Hogarty et al 1992;Li et al 2003). In our present study, we found that AT 1 expression in the rat hypothalamus increased significantly during pregnancy.…”

Section: Changes In Angii Receptor Expression In the Hypothalamussupporting

confidence: 70%

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

Bédard

Sicotte

St‐Louis

et al. 2005

The Journal of Physiology

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We previously reported that sodium restriction during pregnancy reduces plasma volume expansion and promotes intra-uterine growth restriction (IUGR) in rats while it activates the renin-angiotensin-aldosterone system (RAAS). In the present study, we proceeded to determine whether expression of the two angiotensin II (ANGII) receptor subtypes (AT 1 and AT 2 ) change in relation to maternal water-electrolyte homeostasis and fetal growth. To this end, pregnant (gestation day 15) and non-pregnant Sprague-Dawley rats were randomly assigned to two groups fed either normal, or Na + -restricted diets for 7 days. At the end of the treatment period, plasma aldosterone and renin activity as well as plasma and urine electrolytes were measured. Determinations for AT 1 and AT 2 mRNA and protein were made by RNase protection assay and photoaffinity labelling, respectively, using a number of tissues implicated in volume regulation and fetal growth. In non-pregnant rats, Na + restriction decreases Na + excretion without altering plasma volume, plasma Na + concentration or the expression of AT 1 and AT 2 mRNA or protein in the tissues examined. In normally fed pregnant rats when compared to non-pregnant controls, AT 1 mRNA increases in the hypothalamus as well as pituitary and declines in uterine arteries, while AT 1 protein decreases in the kidney and AT 2 mRNA declines in the adrenal cortex. In pregnant rats, Na + restriction induces a decrease in plasma Na + , an increase in plasma urea, as well as a decline in renal urea and creatinine clearance rates. Protein levels for both AT 1 and AT 2 in the pituitary and AT 2 mRNA in the adrenal cortex are lower in the Na + -restricted pregnant group when compared to normally fed pregnant animals. Na + restriction also induces a decrease in AT 1 protein in the placenta. In conclusion, these results suggest that pregnancy may increase sensitivity to Na

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Section: Changes In Angii Receptor Expression In the Hypothalamussupporting

confidence: 70%

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

Bédard

Sicotte

St‐Louis

et al. 2005

The Journal of Physiology

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“…The largest pressor response after ANG II injection into the MSA was reached within 3 min, with 10-30 min needed for the values to return to baseline. take action of centrally administered ANG II can be abolished by AT 1 receptor antagonists (11). More importantly, the data showed that the AT 2 receptor antagonist, PD 123319, also caused a marked reduction of the effects of ANG II on water and sodium intake.…”

Section: Mean Arterial Pressurementioning

confidence: 61%

Interaction between paraventricular nucleus and septal area in the control of physiological responses induced by angiotensin II

Camargo

Saad

Simões

et al. 2002

Braz J Med Biol Res

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We determined the effects of losartan (40 nmol) and PD 123319 (40 nmol) (both non-peptides and selective antagonists of the AT 1 and AT 2 angiotensin receptors, respectively), and [Sar 1 , Ala 8 ] angiotensin II (ANG II) (40 nmol) (a non-selective peptide antagonist of angiotensin receptors) injected into the paraventricular nucleus (PVN) on the water and salt appetite, diuresis and natriuresis and mean arterial pressure (MAP) induced by administration of 10 nmol of ANG II into the medial septal area (MSA) of male Holtzman rats weighing 250-300 g. The volume of drug solution injected was 0.5 µl over a period of 10-15 s. The responses were measured over a period of 120 min. ANG II alone injected into the MSA induced an increase in all the above parameters (8.1 ± 1.2, 1.8 ± 0.3, and 17.1 ± 1.0 ml, 217 ± 25 µEq/120 min, and 24 ± 4 mmHg, respectively, N = 10-12) compared with vehicle-treated rats (1.4 ± 0.2, 0.6 ± 0.1, and 9.3 ± 0.5 ml, 47 ± 5 µEq/120 min, and 4.1 ± 0.8 mmHg, respectively, N = 10-14). Pretreatment with losartan and [Sar 1 , Ala 8 ] ANG II completely abolished the water and sodium intake, and the pressor increase (0.5 ± 0.2, 1.1 ± 0.2, 0.5 ± 0.2, and 0.8 ± 0.2 ml, and 1.2 ± 3.9, 31 ± 4.6 mmHg, respectively, N = 9-12), whereas losartan blunted the urinary and sodium excretion induced by ANG II (13.9 ± 1.0 ml and 187 ± 10 µEq/120 min, respectively, N = 9). Pretreatment with PD 123319 and [Sar 1 , Ala 8 ] ANG II blocked the urinary and sodium excretion (10.7 ± 0.8, 9.8 ± 0.7 ml, and 67 ± 13 and 57 ± 17 µEq/120 min, respectively, N = 9), whereas pretreatment with PD 123319 partially blocked the water and sodium intake, and the MAP induced by ANG II administration (2.3 ± 0.3, 1.1 ± 0.1 ml, and 12 ± 3 mmHg, respectively, N = 9-10). These results suggest the angiotensinergic effect of the MSA on the AT 1 and AT 2 receptors of the PVN in terms of water and sodium homeostasis and MAP modulation.

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“…In this study the influence of hypothyroidism on the density of cerebral AT1 receptors was not investigated (7). Various studies have suggested the involvement of AT1 receptors in the expression of sodium appetite behavior using central administration of antagonists specific for these receptors (10)(11)(12). These alterations were revealed concomitantly with the observation of low genetic expression and reduced basal and stimulated release of atrial natriuretic peptide in hypothyroidism (9,13,14) together with the decreased capacity of proximal tubular sodium reabsorption (15).…”

Section: Introductionmentioning

confidence: 99%

Effect of chronic oral administration of a low dose of captopril on sodium appetite of hypothyroid rats: Influence of aldosterone treatment

Ventura

Olivares

Passos

et al. 2001

Braz J Med Biol Res

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Rats rendered hypothyroid by treatment with methimazole develop an exaggerated sodium appetite. We investigated here the capacity of hypothyroid rats (N = 12 for each group) to respond to a low dose of captopril added to the ration, a paradigm which induces an increase in angiotensin II synthesis in cerebral areas that regulate sodium appetite by increasing the availability of circulating angiotensin I. In addition, we determined the influence of aldosterone in hypothyroid rats during the expression of spontaneous sodium appetite and after captopril treatment. Captopril significantly increased (P<0.05) the daily intake of 1.8% NaCl (in ml/100 g body weight) in hypothyroid rats after 36 days of methimazole administration (day 36: 9.2 ± 0.7 vs day 32: 2.8 ± 0.6 ml, on the 4th day after captopril treatment). After the discontinuation of captopril treatment, daily 1.8% NaCl intake reached values ranging from 10.0 ± 0.9 to 13.9 ± 1.0 ml, 48 to 60 days after treatment with methimazole. Aldosterone treatment significantly reduced (P<0.05) saline intake before (7.3 ± 1.6 vs day 0, 14.4 ± 1.3 ml) and after captopril treatment. Our results demonstrate that, although hypothyroid rats develop a deficiency in the production of all components of the renin-angiotensin-aldosterone system, their capacity to synthesize angiotensin II at the cerebral level is preserved. The partial reversal of daily 1.8% NaCl intake during aldosterone treatment suggests that sodium retention reduces both spontaneous and captopril-induced salt appetite. Key wordsPrevious studies have shown a reduction in NaCl aversion in hypothyroid rats with urinary sodium loss and an increase in sodium appetite in different experimental models (1-4). However, controversies still exist regarding the physiological mechanism responsible for sodium appetite, since genetic expression, synthesis and release of the components of the renin-angiotensin-aldosterone system are reduced in hypothyroidism (3,(5)(6)(7)(8)(9). Moreover, angiotensin II receptor density is altered in hypothyroidism. An increase in

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Intracerebroventricular angiotensin II‐induced thirst and sodium appetite in rat are blocked by the AT1 receptor antagonist, Losartan (DuP 753), but not by the AT2 antagonist, CGP 42112B

Cited by 82 publications

References 5 publications

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

Modulation of body fluids and angiotensin II receptors in a rat model of intra‐uterine growth restriction

Interaction between paraventricular nucleus and septal area in the control of physiological responses induced by angiotensin II

Effect of chronic oral administration of a low dose of captopril on sodium appetite of hypothyroid rats: Influence of aldosterone treatment

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