Inhibition of Beta-1 Receptor but not Vagotomy Can Abolish the L-NAME Evoked Bradycardia in Anesthetized Rat

Title:

Inhibition of Beta-1 Receptor but not Vagotomy Can Abolish the L-NAME Evoked Bradycardia in Anesthetized Rat

Creator:

Vág, J., Hably, C., and Bartha, J.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:0a876220-f30c-4b7a-9a32-737e8d94e2a4
uuid:0a876220-f30c-4b7a-9a32-737e8d94e2a4
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, fyziologie člověka, human physiology, Nitric oxide, Vagotomy, Metoprolol, Heart rate, 14, and 612

Type:

article, studie, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

We reported previously that the nitric oxide synthesis inhibitor Nv-nitro-L-arginine methyl ester (L-NAME) decreases cardiac output. Several studies have shown that inhibition of nitric oxide synthesis decreases the heart rate. In the present study, we investigated the effect of a single bolus administration of L-NAME on blood pressure and heart rate monitored for one hour in anesthetized rats and the influence of vagotomy and b1-receptor blocker metoprolol on the L-NAME induced bradycardia. After L-NAME treatment, the blood pressure rose immediately after the injection of the drug (peak response in the third minute: +24 %, p<0.001) and fell to the control level in the 20th minute. The heart rate decreased immediately after L-NAME administration, the lowest value being reached in the 10th minute (-14 %, p<0.001). However, bradycardia was sustained even after the blood pressure had returned to the control level. Bilateral vagotomy failed to influence the negative chronotropic effect of L-NAME, but bradycardia was completely abolished by metoprolol pretreatment. We concluded that the bradycardia evoked by L-NAME is mainly due to the withdrawal of sympathetic tone upon the heart rate. However, the cause of sustained bradycardia after normalization of blood pressure cannot be elucidated., J. Vág, C. Hably, J. Bartha., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2002 Volume:51 | Number:3

Harvested from:

CDK

Metadata only:

false