Neural tube defects (NTDs) are a group of birth defects in which an opening in the spine or cranium remains from early in human development. In the third week of pregnancy called gastrulation, specialized cells on the dorsal side of the embryo begin to change shape and form the neural tube. When the neural tube does not close completely, an NTD develops. Specific types include: spina bifida which affects the spine, anencephaly which results in little to no brain, encephalocele which affects the skull, and iniencephaly which results in severe neck problems.NTDs are one of the most common birth defects, affecting over 300,000 births each year worldwide. For example, spina bifida affects approximately 1,500 births annually in the United States, or about 3.5 in every 10,000 (0.035% of US births), which has decreased from around 5 per 10,000 (0.05% of US births) since folate fortification of grain products was started. The number of deaths in the US each year due to neural tube defects also declined from 1,200 before folate fortification was started to 840. Types
There are two classes of NTDs: open, which are more common, and closed. Open NTDs occur when the brain and/or spinal cord are exposed at birth through a defect in the skull or vertebrae (spinal column). Open NTDs include anencephaly, encephaloceles, hydranencephaly, iniencephaly, schizencephaly, and the most common form, spina bifida. Closed NTDs occur when the spinal defect is covered by skin. Types of closed NTDs include lipomeningocele, lipomyelomeningocele, and tethered cord.
Interactions
It may potentiate the antihypertensive effects of:

Drugs subject to a strong first-pass effect such as beta blockers may increase the bioavailability of hydralazine. Epinephrine (adrenaline), by its heart rate-accelerating effects as increased by hydralazine,  may lead to toxicity. Mechanism of action
Hydralazine is a drug that conducts the blood pressure lowering effects by vasoconstrictive repression. It is a direct-acting smooth muscle relaxant and acts as a vasodilator primarily in resistance arterioles, also known as the smooth muscle of the arterial bed. The molecular mechanism involves inhibition of inositol trisphosphate-induced Ca2+ release from the sarcoplasmic reticulum in arterial smooth muscle cells. By relaxing vascular smooth muscle, vasodilators act to decrease peripheral resistance, thereby lowering blood pressure and decreasing afterload. Chemistry
Hydralazine belongs to the hydrazinophthalazine class of drugs. History
The antihypertensive activity of hydralazine was discovered by scientists at Ciba, who were trying to discover drugs to treat malaria; it was initially called C-5968 and 1-hydrazinophthalazine; Cibas patent application was filed in 1945 and issued in 1949, and the first scientific publications of its blood pressure-lowering activities appeared in 1950. It was approved by the FDA in 1953.It was one of the first antihypertensive medications that could be taken by mouth. Research
Hydralazine has also been studied as a treatment for myelodysplastic syndrome in its capacity as a DNA methyltransferase inhibitor. See also
Arteriolar vasodilator
Cadralazine
Dihydralazine
Endralazine
Sodium nitroprusside

References
External links
"Hydralazine". Drug Information Portal. U.S. National Library of Medicine.