ole lowered fetal heart rates. The pertussis toxin treatment blocked A1 action displaying A1 was G-protein mediated. Drugs that alter cAMP levels and ion channel action displayed a1 action involves events mediated by cAMP, ATP-dependant K, L-type calcium, sodium and chloride channels, and the pacemaker current. Adenosine A1 potently regulate mammalian heart rates via multiple effector systems at very early stages of prenatal development. The findings also raise the possibility that activation of a1a during early embryonic development may result in fetal death, as factors that adversely affect cardiac output will result in fetal demise. Intrauterine hypoxia or stress triggers a cascade of a1ar mediated events resulting in bradycardia and assytole at embryonic development.(HOFMAN et al 1997)Two systems influence vascular tone and growth of smooth muscle cells. The effects of the pressor substances of these two systems, angiotensin II (ANG II) and noradrenaline (NA), are triggered by their interaction with specific receptors on the vascular wall. It has been demonstrated that the 1-adrenergic receptor mediates sympathetic vasoconstriction of the blood vessel, whereas most vascular ANG II receptors in all species studied to date are mainly of the type 1 ANG II receptor (AT1) that mediates contractile and growth effects of ANG II in vascular smooth muscle. "There are multiple interactions between the renin-angiotensin system and the sympathetic nervous system. For example, ANG II facilitates sympathetic neurotransmission at several sites, including the central nervous system, adrenal medulla, sympathetic ganglia, and presynaptic noradrenergic nerve terminals. Studies demonstrate that continuous infusion of NA without alteration of the blood pressure decreases AT1 mRNA levels in the aorta of the rats. Conversely, infusion of a nondepressor dose of prazosin increases aortic AT1 mRNA content. Studies also show that NA has a negative e...
