Drinking induced by subcutaneous injection of angiotensin II in the rat is blocked by the selective AT1 receptor antagonist DuP 753 but not by the selective AT2 receptor antagonist WL 19

Dourish, C T; Duggan, Jane; Banks, R.J.A.

doi:10.1016/0014-2999(92)90271-5

Cited by 37 publications

(5 citation statements)

References 9 publications

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“…Subcutaneous Losartan resulted in a dose-dependent inhibition of water intake caused by subcutaneous angiotensin 1, II or III (Fregly & Rowland, 1991). Dourish, Duggan & Banks (1992) confirmed that Losartan inhibits peripheral angiotensin II-induced water intake, and found that the AT2 antagonist, WL 19, enhances drinking. Water intake induced by I.C.V.…”

Section: Introductionmentioning

confidence: 57%

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

Jt²

1992

Experimental Physiology

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Section: Introductionmentioning

confidence: 57%

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

Jt²

1992

Experimental Physiology

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“…Due to this reason, the inhibition of ACTH secretion is desirable for the study of steroid regulation by Ang II, especially under stressful conditions, such as capture and handling (Roesch et al, 2000). Ninety minutes after the administration of DEX, individuals were injected subcutaneously with Ang II (0.8 mg/Kg, n = 7; 3 males and 4 females) or saline solution (controls, n = 7; 6 males and 1 female), and 60 min later a second blood sample was obtained to determine hormone levels in response to the experimental treatments (Dourish et al, 1992). Given the uneven quantities of males and females in Ang II and saline-treated animals, we pooled the data from both sexes to allow a better statistical comparison between treatments.…”

Section: Responses Of Cortisol and Corticosterone To Ang IImentioning

confidence: 99%

Different regulation of cortisol and corticosterone in the subterranean rodent Ctenomys talarum: Responses to dexamethasone, angiotensin II, potassium, and diet

Vera

Antenucci

Zenuto

2019

General and Comparative Endocrinology

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When harmful environmental stimuli occur, glucocorticoids (GCs), cortisol and corticosterone are currently used to evaluate stress status in vertebrates, since their secretions are primarily associated to an increased activity of the hypothalamic-pituitaryadrenal (HPA) axis. To advance in our comprehension about GCs regulation, we evaluated the subterranean rodent Ctenomys talarum to assess cortisol and corticosterone response to (1) the negative feedback of the HPA axis using the dexamethasone (DEX) suppression test, (2) angiotensin II (Ang II), (3) potassium (K) intake, and (4) different diets (vegetables, grasses, acute fasting). Concomitantly, several indicators of individual condition (body mass, neutrophil to lymphocyte ratio, blood glucose, triglycerides and hematocrit) were measured for diet treatments. Results confirm the effect of DEX on cortisol and corticosterone in recently captured animals in the field but not on corticosterone in captive animals. Data suggest that Ang II is capable of stimulating corticosterone, but not cortisol, secretion. Neither cortisol nor corticosterone were responsive to K intake. Cortisol levels increased in animals fed with grasses in comparison to those fed with vegetables while corticosterone levels were unaffected by diet type. Moreover, only cortisol responded to fasting. Overall, these results confirm that cortisol and corticosterone are not interchangeable hormones in C. talarum.

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“…Saralasin does not discriminate between these receptor subtypes. Using the newer selective antagonists, it has been found that drinking induced by angiotensin II, but not that by non-renin-dependent challenges, is blocked by the AT1 receptor antagonist, losartan (Fregly & Rowland, 1991;Dourish, Duggan & Banks, 1992;Beresford & Fitzsimons, 1992;Kirby, Thunhorst & Johnson, 1992). Angiotensin-induced drinking was not inhibited by the AT2 antagonists, WL 19 (Dourish et al 1992) and CGP 42112B (Beresford & Fitzsimons, 1992).…”

Section: Introductionmentioning

confidence: 99%

The effect of the putative AT2 agonist, p‐aminophenylalanine6 angiotensin II, on thirst and sodium appetite in rats

Cooney

Jt²

1993

Experimental Physiology

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SUMMARYIntracerebroventricular injection of the putative AT2 agonist, p-aminophenylalanine6 angiotensin II (p-NH2Phe6-Ang II), caused dose-dependent increases in intakes of water and NaCl similar to those produced by angiotensin II but requiring more than one thousand times the dose. Very large doses of another AT2 agonist, angiotensin(1-7) heptapeptide (Ang(I-7)), had no effect on intakes of water and NaCl up to 24 h after injection, nor did Ang(1-7) affect angiotensin II-induced drinking when the two peptides were given together. The AT1 antagonist, losartan, but not the AT2 antagonist, CGP 42112B, inhibited p-NH2Phe6-Ang IIand angiotensin II-induced drinking, suggesting that p-NH2Phe6-Ang II, like angiotensin II, acts on AT1 but not AT2 receptors. However, large doses of the AT2 antagonist, PD 123319, inhibited drinking in response to both dipsogens. Since p-NH2Phe6-Ang II-and angiotensin IIinduced drinking were unaffected by CGP 42112B, this could mean that there are different AT2 receptor subtypes of which only the PD 123319-sensitive one is involved in drinking. But because of the very large doses of PD 123319 used it is also likely that there was loss of receptor specificity resulting in cross-reaction of PD 123319 with AT1 receptors. The results do not favour involvement of AT2 receptors in angiotensin-induced thirst and sodium appetite in the short term.

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Drinking induced by subcutaneous injection of angiotensin II in the rat is blocked by the selective AT1 receptor antagonist DuP 753 but not by the selective AT2 receptor antagonist WL 19

Cited by 37 publications

References 9 publications

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

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

Different regulation of cortisol and corticosterone in the subterranean rodent Ctenomys talarum: Responses to dexamethasone, angiotensin II, potassium, and diet

The effect of the putative AT2 agonist, p‐aminophenylalanine6 angiotensin II, on thirst and sodium appetite in rats

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