2013
DOI: 10.2478/folmed-2013-0029
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Effect of chronic treatment with angiotensin receptor ligands on water-salt balance in wistar and spontaneously hypertensive rats

Abstract: Chronic treatment with selective angiotensin receptor ligands modifies water-salt balance in rats through changes both in renal excretory function and ingestive behaviors.

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Cited by 5 publications
(3 citation statements)
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“…Our earlier data showed that blockade of brain AT2 receptors produced a pronociceptive effect in a visceral pain model [30]. Further, we have shown that the partial AT2 agonist was able to induce antinociception after acute treatment, whereas in a chronic regimen it can reverse this effect [31]. We can speculate that the stronger antinociceptive effect of NVK in female SHRs is a result of their increased non-classical RAS and reduced ratio of AT1/AT2 receptors, making females more susceptible to treatment with AT2 ligands [1,2,22,23].…”
Section: Resultsmentioning
confidence: 84%
“…Our earlier data showed that blockade of brain AT2 receptors produced a pronociceptive effect in a visceral pain model [30]. Further, we have shown that the partial AT2 agonist was able to induce antinociception after acute treatment, whereas in a chronic regimen it can reverse this effect [31]. We can speculate that the stronger antinociceptive effect of NVK in female SHRs is a result of their increased non-classical RAS and reduced ratio of AT1/AT2 receptors, making females more susceptible to treatment with AT2 ligands [1,2,22,23].…”
Section: Resultsmentioning
confidence: 84%
“…Pharmacological data showed that MAPK is specific for salt intake, as its inhibition suppresses sodium appetite without affecting thirst. Daniels et al [ 23 ] showed that ANG II stimulates thirst and salt intake via MAPK pathway, whereas the combined treatment with aldosterone and ANG II induces sodium appetite via IP3 signaling. In addition, aldosterone might increase the responsiveness of OVLT neurons to ANG II by reducing the activation of MAPK signaling in some neurons and increasing IP3 in others.…”
Section: Discussionmentioning
confidence: 99%
“…To better explain the role of angiotensin II in controlling water intake and sodium appetite, some experimental models have been discussed. For instance, the intracerebroventricular (ICV) infusion of ANG II increases water intake and sodium appetite, and this effect is abolished by the AT 1R antagonist losartan [ 23 , 24 ], but not AT 2R antagonism [ 25 ]. It has been reported that ANG II stimulates water intake and salt ingestion through two separate signaling pathways: (1) Protein Kinase C (PKC), a G protein-dependent pathway, and (2) Mitogen-Activated Protein Kinase (MAPK), a G protein-independent pathway.…”
Section: Introductionmentioning
confidence: 99%