The purpose of this review is to provide an overview of the current state of knowledge regarding the experience of intimate partner violence (IPV) during pregnancy. Pregnancy IPV is a significant problem worldwide, with rates varying significantly by country and maternal risk factors. Pregnancy IPV is associated with adverse newborn outcomes, including low birth weight and preterm birth. Many mechanisms for how IPV may impact birth outcomes have been proposed and include direct health, mental health, and behavioral effects, which all may interact. Screening for IPV during pregnancy is essential, yet due to time constraints and few clear recommendations for assessment, many prenatal providers do not routinely inquire about IPV, or even believe they should. More training is needed to assist health care providers in identifying and managing pregnancy IPV, with additional research needed to inform effective interventions to reduce the rates of pregnancy IPV and resultant outcomes.

In this sample, pregnancy IPV and smoking occurred at rates well above national averages. Additionally, while physical IPV during pregnancy was associated with several negative pregnancy health behaviors, the experience of psychological IPV, even in the absence of physical IPV, also placed women at increased risk for negative health behaviors, all of which have been linked to poor pregnancy and newborn outcomes.

The three cloned ␣ 1 -adrenergic receptor (AR) subtypes, ␣ 1B , ␣ 1C , and ␣ 1D , can all couple to the same effector, phospholipase C, and the reason(s) for conservation of multiple subtypes remain uncertain. All three ␣ 1 -ARs are expressed natively in cultured neonatal rat cardiac myocytes, where chronic exposure to the agonist catecholamine norepinephrine (NE) induces hypertrophic growth and gene transcription. We show here, using RNase protection, that the ␣ 1 -AR subtype mRNAs respond in distinctly different ways during prolonged NE exposure (12-72 h). ␣ 1B and ␣ 1D mRNA levels were repressed by NE, whereas ␣ 1C mRNA was induced. Changes in mRNA levels were mediated by an ␣ 1 -AR, were not explained by altered mRNA stability, and were reflected in receptor proteins by [ 3 H]prazosin binding. ␣ 1 -AR-stimulated phosphoinositide hydrolysis and myocyte growth were not desensitized. Three other hypertrophic agonists in culture, endothelin-1, PGF2␣, and phorbol 12-myristate 13-acetate, also induced ␣ 1C mRNA and repressed ␣ 1B mRNA. In myocytes from hearts with pressure overload hypertrophy, ␣ 1 mRNA changes were identical to those produced by NE in culture. These results provide the first example of a difference in regulation among ␣ 1 -AR subtypes expressed natively in the same cell. Transcriptional induction of the ␣ 1C -AR could be a mechanism for sustained growth signaling through this receptor and is a common feature of a hypertrophic phenotype in cardiac myocytes. The natural catecholamines norepinephrine (NE)1 and epinephrine activate adrenergic receptors (ARs) in three families, ␣ 1 , ␣ 2 , and ␤. Multiple subtypes have been cloned within each family: three ␣ 1 -ARs (B, C, and D), 2 three ␣ 2 -ARs (A, B, and C; also called C10, C2, and C4, respectively), and three ␤-ARs (1, 2, and 3) (1). The reason(s) for conservation of multiple subtypes remain uncertain, since all subtypes in each family couple preferentially to the same effector when overexpressed, ␣ 1 -ARs to activation of phospholipase C (PLC), ␣ 2 -ARs to inhibition of adenylyl cyclase, and ␤-ARs to activation of adenylyl cyclase (1). An intriguing difference among ␤-AR and ␣ 2 -AR subtypes has been suggested recently, in the regulation of receptor levels during prolonged agonist exposure. Levels of the ␤ 3 -AR (2-4) and the ␣ 2C -AR (5, 6) are not down-regulated during long term agonist exposure, at least in some cells, in contrast with downregulation of ␤ 1 -and ␤ 2 -ARs, and ␣ 2A -and ␣ 2B -ARs. Downregulation of receptor expression is thought to be a major determinant of desensitization when catecholamine exposure is prolonged (7). Conversely, a receptor that is induced by agonist might be adapted to mediate catecholamine responses when sympathetic activity is increased chronically, a condition that occurs frequently in the intact organism.We have been studying a physiological response that develops over long periods of catecholamine exposure, ␣ 1 -adrenergic induction of hypertrophic growth and gene transcription in primary cultures of neon...

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