The Cardiovascular Functions And Mechanism Of Salusin αWithin The Nucleus Tractus Solitarii In Rats

In recent years, there is amount of evidence that hypertension, atherosclerosis and other cardiovascular diseases are highly related to cardiovascular active peptides. The discovery of a series of cardiovascular active peptides is abundant in the theory of atherosclerosis and other cardiovascular diseases, which spawn a number of new clinical drugs to improve the treating effects of atherosclerosis and other cardiovascular diseases and the quality of life of patients.Salusins was originally predicted from a human fulllength enriched cDNA library. Salusin a and salusin β are newly identified bioactive peptides of20and28amino acid, respectively, which are reported to widely distribute in hematopoietic system, endocrine system, and the central nervous system (CNS). They are responsible for causing hypotension, bradycardia and mitogenic activities. The cardiovascular functions of salusin a in the nucleus tractus solitarii (NTS) are not fully defined. The present study is to comparatively determine the cardiovascular functions of salusin a within the NTS in anesthetized rats.Male SD rats were employed in present study. The experiment was divided into four groups:1.The dose-dependant responses of blood pressure and heart rate were determined by bilateral microinjection salusin a into the NTS.2. The dose-dependant responses of blood pressure and heart rate were determined by unilateral microinjection salusin a into the NTS.3. The arterial baroreflex (ABR) function of rats of pre-post microinjection of salusin a into the NTS were defined in rats.4. KYN, bilateral vagotomy or aCSF/muscimol in RVLM were prior applied before salusins a (4pmol) was microinjected into the NTS. Artificial artificial cerebrospinal fluid (aCSF) was microinjected into corresponding part as the control.Bilateral or unilateral microinjection of salusin a into the NTS produced a dose-dependent hypotension and bradycardia. Bilateral microinjection of salusin a didn’t alter baroreflex sensitivity functions. Prior application of KYN (1nmol) or bilateral vagotomy into the NTS did not alter the hypotension and bradycardia induced by intra-NTS salusin α (P>0.05). But pretreatment with muscimol (10g-L-1) within RVLM almost completely abolished the hypotension and bradycardia evoked by intra-NTS salusin α (P<0.05)Microinjection of salusin a into the NTS produces significantly hypotension and bradycardia, which probably originates from the suppressing the activities of presympathetic neurons in the RVLM.