The salusins are bioactive peptides with hemodynamic effects. They play a role in
hypertension, atherogenesis and cardiovascular diseases. In this review we focus on new actions,
which are related to the regulation of blood pressure.
Decrease in salusin-α and the increase in salusin-β concentrations are known to contribute to the
development of the metabolic syndrome and atherosclerosis.
Microinjections of salusin-β in the paraventricular nucleus (PVN) increases the plasma argininevasopressin
(AVP) and norepinephrine levels, which contribute to hypertension. It also increases
the AVP release from the rostral ventrolateral medulla (RVLM) via the projection from PVN to
RVLM. Increased activity of the RVLM neurons is transmitted to the intermediolateral nucleus
(IML) cell column of the spinal cord, where peripheral sympathetic nerves to the heart, arterioles
and kidneys are activated, thus increasing blood pressure. Microinjection of salusin-β into the
RVLM increased renal sympathetic nerve activity, median arterial pressure (MAP) and heart rate (HR). There was no
significant effect on the AVP level in the RVLM and plasma.
Microinjection of salusin-β in the nucleus tractus solitarii (NTS) produces a dose dependent hypotension and bradycardia.
Intravenous injection of salusin-β significant increased MAP, but did not have a meaningful outcome on HR. Nevertheless,
intravenous injection of a very high dose of salusin-β caused instantaneous decrease in both MAP and HR.
Salusin-β overexpression provoked severe and prolonged hypertension accompanied by tachycardia in rats.
It is clear that more research needs to be done to evaluate the function of salusin-β in the mechanism of essential hypertension,
atherosclerosis, and the metabolic syndrome.