Blood pressure hyperreactivity: an early cardiovascular risk in normotensive men exposed to low-to-moderate inorganic arsenic in drinking water.

BACKGROUND: Essential hypertension is associated with chronic exposure to high levels of inorganic arsenic in drinking water. However, early signs of risk for developing hypertension remain unclear in people exposed to chronic low-to-moderate inorganic arsenic. OBJECTIVE: We evaluated cardiovascular stress reactivity and recovery in healthy, normotensive, middle-aged men living in an arsenic-endemic region of Romania. METHODS: Unexposed (n = 16) and exposed (n = 19) participants were sampled from communities based on WHO limits for inorganic arsenic in drinking water (<10 µg/l). Water sources and urine samples were collected and analyzed for inorganic arsenic and its metabolites. Functional evaluation of blood pressure included clinical, anticipatory, cold pressor test, and recovery measurements. Blood pressure hyperreactivity was defined as a combined stress-induced change in SBP (> 20 mmHg) and DBP (>15 mmHg). RESULTS: Drinking water inorganic arsenic averaged 40.2 ± 30.4 and 1.0 ± 0.2 µg/l for the exposed and unexposed groups, respectively (P < 0.001). Compared to the unexposed group, the exposed group expressed a greater probability of blood pressure hyperreactivity to both anticipatory stress (47.4 vs. 12.5%; P = 0.035) and cold stress (73.7 vs. 37.5%; P = 0.044). Moreover, the exposed group exhibited attenuated blood pressure recovery from stress and a greater probability of persistent hypertensive responses (47.4 vs. 12.5%; P = 0.035). CONCLUSIONS: Inorganic arsenic exposure increased stress-induced blood pressure hyperreactivity and poor blood pressure recovery, including persistent hypertensive responses in otherwise healthy, clinically normotensive men. Drinking water containing even low-to-moderate inorganic arsenic may act as a sympathetic nervous system trigger for hypertension risk.

Length-scale mediated adhesion and directed growth of neural cells by surface-patterned poly(ethylene glycol) hydrogels.

We engineered surfaces that permit the adhesion and directed growth of neuronal cell processes but that prevent the adhesion of astrocytes. This effect was achieved based on the spatial distribution of sub-micron-sized cell-repulsive poly(ethylene glycol) [PEG] hydrogels patterned on an otherwise cell-adhesive substrate. Patterns were identified that promoted cellular responses ranging from complete non-attachment, selective attachment, and directed growth at both cellular and subcellular length scales. At the highest patterning density where the individual hydrogels almost overlapped, there was no cellular adhesion. As the spacing between individual hydrogels was increased, patterns were identified where neurites could grow on the adhesive surface between hydrogels while astrocytes were unable to adhere. Patterns such as lines or arrays were identified that could direct the growth of these subcellular neuronal processes. At higher hydrogel spacings, both neurons and astrocytes adhered and grew in a manner approaching that of unpatterned control surfaces. Patterned lines could once again direct growth at cellular length scales. Significantly, we have demonstrated that the patterning of sub-micron/nano scale cell-repulsive features at microscale lengths on an otherwise cell-adhesive surface can differently control the adhesion and growth of cells and cell processes based on the difference in their characteristic sizes. This concept could potentially be applied to an implantable nerve-guidance device that would selectively enable regrowing axons to bridge a spinal-cord injury without interference from the glial scar.