Article
Tyrosine hydroxylase and b2-adrenergic receptor expression in leukocytes of spontaneously hypertensive rats: putative peripheral markers of central sympathetic activity
Registro en:
NISIMURA, L. M. et al. Tyrosine hydroxylase and b2-adrenergic receptor expression in leukocytes of spontaneously hypertensive rats: putative peripheral markers of central sympathetic activity. Brazilian Journal of Medical and Biological Research, Ribeirão Preto, v. 53, n. 12, e9615, 2020.
1414-431X
10.1590/1414-431X20209615
Autor
Nisimura, L. M.
Bousquet, P.
Muccillo, F.
Tibiricá, E.
Garzoni, L. R.
Resumen
The sympathetic nervous system (SNS) plays a fundamental role in the pathophysiology of cardiovascular diseases, including
primary arterial hypertension. In this study, we aimed to investigate whether the expression of the rate-limiting enzyme in
catecholamine synthesis, tyrosine hydroxylase (TH), and the b2-adrenergic receptor (b2-AR) in immune cells from peripheral
blood, reflect central SNS activity in spontaneously hypertensive rats (SHR). TH expression in the lower brainstem and adrenal
glands and b2-AR expression in the lower brainstem were analyzed by western blot analyses. In the leukocytes, TH and b2-AR
expression was evaluated by flow cytometry before and after chronic treatment with the centrally-acting sympathoinhibitory drug
clonidine. Western blot analyses showed increased TH and b2-AR expression in the lower brainstem and increased TH in
adrenal glands from SHR compared to normotensive Wistar Kyoto rats (WKY). Lower brainstem from SHR treated with
clonidine presented reduced TH and b2-AR levels, and adrenal glands had decreased TH expression compared to SHR treated
with vehicle. Flow cytometry showed that the percentage of leukocytes that express b2-AR is higher in SHR than in WKY.
However, the percentage of leukocytes that expressed TH was higher in WKY than in SHR. Moreover, chronic treatment with
clonidine normalized the levels of TH and b2-AR in leukocytes from SHR to similar levels of those of WKY. Our study
demonstrated that the percentage of leukocytes expressing TH and b2-AR was altered in arterial hypertension and can be
modulated by central sympathetic inhibition with clonidine treatment.