Introduction

The cardiovascular system is the first systemic organ to function in ontogenesis, and the stability of the system is essential for normal organogenesis of the embryo. In the mature individual, the autonomic nervous system and the endocrine system are vital for maintenance of the homeostasis of circulation, but both systems mature and begin to function at late stages of organogenesis or after birth. It has been thought that before these systems participate in cardiovascular control, the embryonic cardiovascular system is controlled exclusively by intrinsic characteristics of the heart, such as the Frank-Starling mechanism (Wagman, Hu, & Clark, 1990), and by changes of heart rate and vascular resistance to environmental temperature (Nakazawa etal., 1985; Nakazawa etal., 1986).

In addition to intrinsic mechanisms, atrial natriuretic peptide is present in the embryonic myocardium as early as day 11 of gestation in the rat (Toshimori et al., 1987; Scott & Jennes, 1988). The gene for atrial natriuretic peptide is first expressed at day 8 in mouse embryonic myocardial cells (Zeller et al., 1987), although the amount of the peptide is much less than that in late gestation or in the mature heart (Dolan & Dobrozsi, 1987). Atrial natriuretic factor is present in the human embryo heart at 8–9 gestational weeks, when ventricular septation is almost completed (Larsen, 1990). Atrial natriuretic factor is a potent vasodilator and reduces venous return in the early chick embryonic circulation (Nakazawa et al., 1990a; Hu et al., 1994); therefore, this peptide could have a hemodynamic role via an endocrine or paracrine pathway in the prenephric system.