Effects of Endogenous Nitric Oxide Synthesis Inhibition on the Depressor Response to Intracerebroventricular Calcium.
10.4070/kcj.2000.30.3.326
- Author:
Cheol Ho YEUM
;
In Keun MOON
;
Jae Yeoul JUN
;
Jeong Hoe LIEE
;
Kyu Bae CHEON
;
Pyung Jin YOON
- Publication Type:Original Article
- Keywords:
Calcium;
Intracerebroventricular;
Depressor response;
Nitric oxide
- MeSH:
Animals;
Arterial Pressure;
Blood Pressure;
Calcium Channels;
Calcium*;
Cerebral Ventricles;
Diltiazem;
Drinking Water;
Eating;
Femoral Artery;
Heart Rate;
NG-Nitroarginine Methyl Ester;
Nitric Oxide*;
Rats
- From:Korean Circulation Journal
2000;30(3):326-333
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Aside from its well known peripheral antihypertensive effects, calcium also lowers blood pressure, when administered into the cerebral ventricle. The present study was aimed to determine whether the central depressor response to calcium is mediated by a stimulation of endogenous L-arginine-nitric oxide (NO) pathway. METHODA: Mean arterial pressure (MAP) and heart rate (HR) were continuously recorded from the femoral artery in anesthetized rats. Administration of calcium was performed into the right lateral cerebral ventricle. The effects of N G-nitro-L-arginine methyl ester (L-NAME) on the cardiovascular response to calcium were examined. RESULTS: Intracerebroventricular (ICV) injection of calcium consistently produced a decrease in MAP and HR. The depressor and bradycardiac responses to calcium showed a dose-dependent fashion. Pretreatment with a calcium channel blocker, diltiazem (1 micromol, ICV), attenuated cardiovascular responses to calcium. ICV infusion (1 microl/min) of L-NAME (200 microgram/kg and 20 microgram/kg/min for 60 min) increased MAP without significant changes in HR. Chronic ingestion of L-NAME (5 mg/100 ml in drinking water, 4 weeks) also increased the systolic blood pressure as compared with control. The depressor effect of ICV calcium was significantly diminished in acute or chronic L-NAME treated rats. CONCLUSION: These findings suggest that the central depressor response to calcium, at least in part, is NO-dependent.
