Role of brain angiotensin AT1 receptor in the carbachol-induced natriuresis and expression of nNOS in the locus coeruleus and proximal convoluted tubule

Title:

Role of brain angiotensin AT1 receptor in the carbachol-induced natriuresis and expression of nNOS in the locus coeruleus and proximal convoluted tubule

Creator:

Wang, M., Jiang, C. L., Wang, C. Y., and Yao, Q. Y.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:1e2b441c-1fd1-4f14-be60-529cafde9695
uuid:1e2b441c-1fd1-4f14-be60-529cafde9695
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie, biochemie, physiology, biochemistry, AT1 receptor, neuronová syntáza oxidu dusnatého, karbachol, locus coeruleus, neuronal nitrix oxide synthase, carbachol, proximal convoluted tubule, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

Central administration of losartan effectively blocked the increase of blood pressure and drinking response induced by angiotensin II (Ang II) or carbachol. However, the relationship between angiotensin AT1 receptors and the natriuresis induced by brain cholinergic stimuli is still not clear. The purpose of the study is to reveal the role of brain angiotensin AT1 receptor in the carbachol-induced natriuresis and expression of neuronal nitric oxide synthase (nNOS) in the locus coeruleus (LC) and proximal co nvoluted tubule (PCT). Our results indicated that 40 min after in tracerebroventricular (ICV) injection of carbachol (0.5 μg), urinary sodium excretion was significantly increased to 0.548±0.049 μmol·min-1·100 g-1. Immunohistochemistry showed that carbachol induced an increase of neuronal nitric oxide synthase immunoreactivity (nNOS-IR) in the LC and renal proximal tubular cells. After pretreatment with losartan (20 μg), carbachol-induced urinary sodium excretion was reduced to 0.249±0.067 μmol·min-1·100 g-1. The same was true for carbachol-induced increase of nNOS-IR in the LC and PCT. The present data suggest that ICV cholinergic stimulation could induce a natriuresis and upregulate the activity of nNOS in the LC and PCT. The blockade of AT1 receptors might downregulate the effects induced by carbachol in the LC and PCT. Consequently, we provide a new evidence that brain angiotensinergic pathway and NO-dependent neural pathway contribute to the natriuresis following brain cholinergic stimulation and thus play an important role in the regulation of fluid homeostasis. Furthermore, the final effect of nitric oxide on proximal tubular sodium reabsorption participated in the natriuresis induced by brain cholinergic stimulation., M. Wang, C. L. Jiang, C. Y. Wang, Q. Y. Yao., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2007 Volume:56 | Number:4

Harvested from:

CDK

Metadata only:

false