Open AccessNeurohumoral mechanism in the natriuretic action of intracerebroventricular administration of renin
Author(s) -
L Zavala,
Yarisma Barbella,
A Israel
Publication year - 2004
Publication title -
jraas. journal of the renin-angiotensin-aldosterone system/journal of the renin-angiotensin-aldosterone system
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.457
H-Index - 46
eISSN - 1752-8976
pISSN - 1470-3203
DOI - 10.3317/jraas.2004.007
Subject(s) - endocrinology , natriuresis , medicine , atrial natriuretic peptide , plasma renin activity , renin–angiotensin system , urinary system , cyclic guanosine monophosphate , excretion , angiotensin ii , chemistry , receptor , blood pressure , nitric oxide
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) AT 1 -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 AT 1 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.