Search
Close
Search
Advanced Search
Search Menu
AI Discovery Assistant

Abstract

Previous studies have demonstrated that Parathyroid Hypertensive Factor (PHF) influences blood pressure through effects on both peripheral vascular resistance and cardiac output. In terms of cardiac effects, PHF has been shown to affect cardiac contractility through a variety of mechansisms including sympthetic stimulation, endocardial NO generation and direct myocardial effects. As TNFα can stimulate endocardial NO generation, the purpose of this study was to determine whether the effects of PHF on cardiac controactility might also be partially mediated through THFα.

Sprague-Dawley rats weighing 300-325 g were anesthetized with pentobarbital, pre-treated with guanethidine and a left ventricular cannula inserted via the left carotid artery. One group of rats was then treated with L-NMMA, another group with anti-TNFα antibody and a control group with vehicle. A minimum of 6 rats was used for each group. Effects of i.v. PHF (1 absorbance unit per rat) on cardiac contractility and blood pressure were then recorded over 90 minutes using a cardiac performance monitor. Results were assessed using repeated measures ANOVA.

PHF alone resulted in a decrease in dP/dT by 17% (p<.0001) as has been previously described. When rats were pre-treated with L-NMMA, PHF increased dP/dT by 18% (p<.0001). In the presence of anti-TNFα antibody, PHF increased dP/dT by 79% (p<.0001). Anti-TNFα antibody alone had no effect on dP/dT.

These results suggest that part of the cardiodepressant effect of PHF may be mediated through TNFα - induced stimulation of NO release or production. However, non - NO mediated effects of TNFα also likely play a significant role in the cardiac effects of PHF.

contractility, parathyroid hypertensive factor, TNF
This content is only available as a PDF.
© American Journal of Hypertension, Ltd. 2001
Topic:
Issue Section:
Abstracts
You do not currently have access to this article.
Download all slides