Abstract

Salusin α and salusin β are newly found bioactive peptides of 20 and 28 amino acid respectively, distributed widely in hematopoietic system, endocrine system and the central nervous system. Our present study is to determine the cardiovascular functions of salusin β within the caudal ventrolateral medulla (CVLM) of rats. Unilateral microinjection of the artificial cerebrospinal fluid (aCSF) into the CVLM did not affect the blood pressure (BP) and heart rate (HR) in anesthetized rats. Topical application of salusin β into the CVLM produced a dose-dependently hypotension (0.04 pmol: -4 ± 2 mmHg; 0.4 pmol: -13 ± 4 mmHg; 4 pmol: -14 ± 2 mmHg) in anesthetized rats (P < 0.05, compared with aCSF: -2 ± 1 mmHg). Microinjection of higher dose salusin β (4 pmol) produced bradycardia (-15 ± 3 bpm vs. -4 ± 5 bpm with aCSF, P<0.05) significantly. Pretreatment with α2 receptor antagonist yohimbine (YOH, 12.8 nmol, n = 9), non-selective glutamate receptor antagonist kynurenic acid (KYN, 1 nmol, n = 7) or nicotinic receptor antagonist hexamethonium (HEX, 120 pmol, n = 7) into the CVLM of rats did not alter the hypotension and bradycardia induced by intra-CVLM salusin β (4 pmol). However, pretreatment with muscarinic receptor antagonist atropine (120 pmol, n = 9) or scopolamine (5 nmol, n = 7) within the CVLM effectively decreased the cardiovascular inhibition functions of intra-CVLM salusin β. Our present study shows that hypotension and bradycardia induced by microinjection of salusin β into the CVLM is mainly mediated by muscarinic receptors.

Key words: Salusin, rat, central, blood pressure, heart rate.