This Article Free Full Text (Free PDF) Free References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Zavala, L. Articles by Israel, A. Search for Related Content PubMed PubMed Citation Articles by Zavala, L. Articles by Israel, A. Social Bookmarking                         What's this?

Neurohumoral mechanism in the natriuretic action of intracerebroventricular administration of renin

School of Medicine, Universidad Experimental Francisco de Miranda, Coro, Estado Falcón

Yarisma Barbella

Laboratory of Neuropeptides, School of Pharmacy, Universidad Central de Venezuela

Anita Israel

Laboratory of Neuropeptides, School of Pharmacy, Universidad Central de Venezuela, astern88{at}hotmail.com

Introduction Intracerebroventricular (IVT) administration of renin (R) decreases urinary volume and increases urinary sodium excretion. We investigated whether IVT-R-induced natriuresis could be associated with the release of atrial natriuretic peptide (ANP), its interaction with renal ANP-A receptors (ANPR-A) and the subsequent increase of urinary cyclic 3'-5' guanosine monophosphate (cGMP).

Methods In IVT cannulated rats, the left carotid artery was catheterised with PE-50 tubing for blood collection, renin was injected IVT and arterial blood samples were collected at 0, 2, 5, 10 and 15 minutes of injection, and urinary sodium and cGMP excretion at 1-, 3- and 6-hour periods of urine collection. Plasma ANP levels and urinary cGMP were determined by radioimmunoassay, and each urine sample was analysed for sodium concentration using a flame photometer.

Results Our results demonstrate that IVT-R administration increases plasma ANP levels after two minutes of injection and urinary cGMP concentration at 1-, 3-and 6 hour period of urine collection. The natriuretic action induced by IVT-R was blunted by peripheral administration of anantin, an ANPR-A antagonist. We assessed the role of brain angiotensin II (Ang II) AT₁-receptors on the IVT-induced antidiuresis, natriuresis and cGMP urinary excretion, the last as an indirect index of ANP secretion. Blockade of brain Ang II AT ₁-receptors with losartan (LOS; 120 µg/3 µl, IVT), inhibited the antidiuretic action and blocked the increased urinary sodium and cGMP excretion induced by IVT-R (7.14 mGU/5 µl). The increase in urinary cGMP was independent of nitric oxide synthase stimulation, since L-NAME pre-treatment did not alter the renal actions induced by IVT-R.

Conclusions Our results suggest that there is a link between the brain and the kidney. The activation of brain angiotensinergic neurons and stimulation of AT₁ receptors may stimulate the release of ANP to the circulation. The released ANP circulates to the kidneys where it acts through renal ANPR-As and the consequent increase in cGMP to produce natriuresis.

Key Words: renin • natriuresis • atrial natriuretic peptide • losartan • GMPc

Journal of Renin-Angiotensin-Aldosterone System, Vol. 5, No. 1, 39-44 (2004)
DOI: 10.3317/jraas.2004.007


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?