Effects of intracarotid injection of 17beta-estradiol on electrical activity of rostral ventrolateral medullary neurons in male rats.
- Author:
Sheng WANG
1
;
Rui-Rong HE
Author Information
1. Department of Physiology, Hebei Medical University, Shijiazhuang 050017, syho@hebmu.edu.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Carotid Arteries;
Electrophysiology;
Estradiol;
pharmacology;
Injections, Intra-Arterial;
Male;
Medulla Oblongata;
cytology;
drug effects;
physiology;
Neurons;
drug effects;
physiology;
Nitric Oxide;
metabolism;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2002;54(1):47-54
- CountryChina
- Language:English
-
Abstract:
The purpose of this study was to determine the effects of 17beta-estradiol (E(2)) on electrical activity of the rostral ventrolateral medulla (RVLM) neurons in rats. Male Sprague-Dawley rats were anesthetized with urethane (1.0 g/kg) and subjected to sino-aortic denervation. Blood pressure, heart rate and spontaneous discharge of RVLM neurons were recorded simultaneously. Intracarotid injection of E(2) (10 ng/kg) decreased the discharge rate from 14.46+/-0.47 to 9.73+/-0.33 spikes/s (P<0.001) in 25 out of 30 RVLM neurons, while blood pressure and heart rate showed no significant change. The inhibitory effect of E(2) on RVLM neuronal activity was rapid at the onset (within 1 min) and long-lasting (>5 min). Prior administration of antiestrogen tamoxifen (TAM) did not affect the effect of E(2). However, pretreatment with N( )-nitro-L-arginine-methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthase, significantly attenuated the inhibitory effect of E(2). In addition, NO donor 3-morpholinosydnonimine (SIN-1) potentiated the effect of E(2). These results suggest that E(2) may inhibit spontaneous electrical activity of RVLM neurons, an effect which is mediated by the activation of NOS with the resultant of NO release via nongenomic actions.
