Abstract
ObjectivesThis study was conducted to evaluate the effect of eplerenone on the RAAS and kidney function in rats with thyroid hormone disorders.MethodsThis study involved 30 male Wistar albino rats, divided into three groups. The first group (N = 6) served as a control. The second group involved 12 rats with experimentally induced hypothyroidism through receiving propylthiouracil (0.05% w/v) in drinking water for one month, which was divided into two subgroups of six rats each. The first subgroup served as a positive hypothyroid control, and the second subgroup received oral daily dose of eplerenone (100 mg/kg) for 14 days. The third group included 12 rats with induced hyperthyroidism with L‐thyroxin (0.0012% w/v) in drinking water, and rats in this group were also divided into two subgroups. The first subgroup served as a positive hyperthyroid control, and the second subgroup received oral eplerenone 100 mg/kg.ResultsEplerenone indicated a significant increase in renin and angiotensin I from 184.09 pg/ml and 178.66 pg/ml to 603.31 pg/ml and 250.88 pg/ml, respectively, meanwhile, aldosterone indicated no significant changes after inducing hypothyroidism and eplerenone administration.The induction of hyperthyroidism led to a significant increase in angiotensin I from 248.84 pg/ml to 292.22 pg/ml. Oral administration of eplerenone for 14 days caused a significant increase aldosterone from 364.23 pg/ml to 497.02 pg/ml.ConclusionEplerenone significantly increased the serum renin and angiotensin I in hypothyroid and aldosterone and angiotensin I in hyperthyroid rats. Aldosterone in hypothyroid rats was not changed by eplerenone.
Highlights
The renin-angiotensin-aldosterone system (RAAS) plays a major role in maintaining hemodynamic stability in response to the decreased blood volume, water and salts.[1,2] It mainly acts on the kidneys, but it on the brain, heart, blood vessels and adrenal glands.[3]Recent studies have suggested that AT2R-mediated signalling induces inhibition of cell growth or apoptosis by counteracting the AT1R signal.[4]
T3 and T4 were significantly reduced from 1.7383 nmol/l to 1.0268 nmol/l and from 78.88 nmol/l to 17.5217 nmol/l, respectively, while thyroid-stimulating hormone (TSH) was significantly increased from 6.08 ng/ml to 19.5483 ng/ml
Angiotensin I and Angiotensin II (II) were significantly reduced after the induction of hypothyroidism, while after using eplerenone for 14 days in hypothyroid rats angiotensin I significantly increased from 178.6618 pg/ml to 250.8897 pg/ml
Summary
The renin-angiotensin-aldosterone system (RAAS) plays a major role in maintaining hemodynamic stability in response to the decreased blood volume, water and salts.[1,2] It mainly acts on the kidneys, but it on the brain, heart, blood vessels and adrenal glands.[3]Recent studies have suggested that AT2R-mediated signalling induces inhibition of cell growth or apoptosis by counteracting the AT1R signal.[4]. The renin-angiotensin-aldosterone system (RAAS) plays a major role in maintaining hemodynamic stability in response to the decreased blood volume, water and salts.[1,2]. It mainly acts on the kidneys, but it on the brain, heart, blood vessels and adrenal glands.[3]. Recent studies have suggested that AT2R-mediated signalling induces inhibition of cell growth or apoptosis by counteracting the AT1R signal.[4]. The basal systolic blood pressure of AT2R-null mice is mildly elevated compared with wild-type (wild) mice.[5]. The AT2R is thought to be expressed in glomeruli in response to RAAS activation, such as during sodium depletion.[6]. The mechanism of AT2R signalling has not yet been fully elucidated
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