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Brain Atrial Natriuretic Peptide Family Abolishes Cardiovascular Haemodynamic Alterations Caused By Hypertonic Saline In Rats
Author(s) -
Sakamoto Masatoshi,
Nishimura Masato,
Takahashi Hakuo
Publication year - 1999
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.1999.03112.x
Subject(s) - atrial natriuretic peptide , hypertonic saline , medicine , hemodynamics , tonicity , brain natriuretic peptide , saline , npr1 , npr2 , endocrinology , cardiology , natriuretic peptide , heart failure
SUMMARY 1. Regional haemodynamic alterations caused by hypertonic NaCl solution (Hi‐Salt; 10%, 10 μL) 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 μg/10 μL/nat), an angiotensin AT 1 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.