Brain Atrial Natriuretic Peptide Family Abolishes Cardiovascular Haemodynamic Alterations Caused By Hypertonic Saline In Rats

Abstract

1. Regional haemodynamic alterations caused by hypertonic NaCl solution (Hi-Salt; 10%, 10 microL) injected intracerebroventricularly (i.c.v.) were investigated by using radioactive microspheres in anaesthetized rats. 2. Intracerebroventricular injections of Hi-Salt increased regional vascular resistance of visceral organs, including the kidney, and elevated plasma levels of vasopressin. 3. Intracerebroventricular pretreatment with TCV-11974 (50 micrograms/10 microL/nat), an angiotensin AT1 receptor antagonist, attenuated the pressor response and vasopressin release to subsequently injected Hi-Salt, but did not affect regional haemodynamic effects of i.c.v. Hi-Salt on vascular resistance. 4. In contrast, i.c.v. pretreatment with atrial natriuretic polypeptide (ANP) or type-C natriuretic polypeptide (CNP) almost completely abolished the haemodynamic changes and vasopressin release caused by i.c.v. Hi-Salt. 5. The present findings indicate that a natriuretic family in the brain may be involved to a great degree in the central regulation of salt-induced hypertension in rats, while brain angiotensin II is likely to participate only in vasopressin release.

The central mechanism underlying hypertension: a review of the roles of sodium ions, epithelial sodium channels, the renin–angiotensin–aldosterone system, oxidative stress and endogenous digitalis in the brain

“…183, 184 In particular, renal nerve activity markedly increases with ICV injection of hypertonic saline, 185 and renal arterial blood flow, as measured with radioactive microspheres, decreases. 186 As this response is reversed by ICV pretreatment with atrial natriuretic peptide or C-type natriuretic peptide, it appears that these peptides compete with the RAAS in the brain. There are natriuretic peptides in the brain, 187, 188 and brain natriuretic peptide and C-type natriuretic peptide were originally isolated from the brain.…”

Upregulation of the Renin-Angiotensin-Aldosterone-Ouabain System in the Brain Is the Core Mechanism in the Genesis of All Types of Hypertension

“…Therefore, increased brain RAAS by sodium has been suggested to be involved in hypertensive actions of sodium. Thereby, abdominal SNSA, an upstream event of renal nerve stimulation, is markedly increased, as confirmed by the decreased renal blood flow observed using radioactive microspheres that indicate activated renal SNSA [58]. Increased renal SNSA decreases renal excretion of sodium by decreasing renal blood flow and increasing renal tubular sodium reabsorption [59].…”