Although the precise causes of abnormal NGF status in primary hypertension cannot be fully clarified in the present study, several mechanisms could be proposed as follows: First, catecholamines, neurotransmitters released from sympathetic nerve endings, have been demonstrated to modulate NGF synthesis in vascular smooth muscle and cardiomyocytes in both in vitro and in vivo experiments [21–23]. This evidence concerns the gene NGF and essential hypertension.