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Articles by Stephanie W. Watts
Total Records ( 2 ) for Stephanie W. Watts
  Bridget Mahon Seitz and Stephanie W. Watts
  Background: Long-term serotonin (5-hydroxytryptamine, 5-HT) infusion produces a sustained reduction in mean arterial pressure (MAP) and a decrease in total peripheral resistance (TPR) through a mechanism dependent on Nitric Oxide Synthase (NOS) in rats. This study sought to determine if the reduction in resistance induced by 5-HT is caused by NOS-dependent relaxation of vessels to all major organs of the body or in a specific vascular bed. Materials and Methods: Alzet mini-pumps containing vehicle (saline) or 5-HT (25 μg kg-1 min-1) were implanted in male Sprague Dawley rats. A separate group of rats was treated with the NOS inhibitor Nω-nitro-L-arginine (LNNA; 0.5 g L-1) prior to 5-HT administration. Results: 5-HT reduced MAP after 24 h (veh = 87±3, 5-HT = 75±2 mm Hg; p<0.05), a fall prevented by LNNA (LNNA/5-HT= 115±10 mm Hg). Yellow-green fluorescent microspheres, used to measure blood flow (300, 000 spheres; size 15 μm), were introduced into the left ventricle of the heart. Microspheres were recovered in arterial reference blood sample and organs using sedimentation through centrifugation. The intensity of dye extracted from the microspheres was measured spectrophotometrically. The 5-HT significantly decreased resistance to the spleen (48%) and small intestine (35%) compared to vehicle-treated animals; this decrease was abolished by LNNA. By contrast, resistance to the ear (175%) was increased by 5-HT. Resistance in brain, liver, lungs, kidneys and muscle did not show a statistically significant reduction by 5-HT. Conclusion: These findings underscore the importance of the splanchnic (particularly intestinal) circulation and NOS in 5-HT-induced reduction in blood pressure.
  Abigail Moore , Brian A. Zabel , Robert Burnett and Stephanie W. Watts
  Background: Chemerin is an adipokine typically known for its role in inflammation. Recent studies suggest that it plays a part in the development of obesity and hypertension. Because of the importance of the sympathetic nervous system in blood pressure control and because the adrenal is an important effector of this system, we hypothesized that chemerin would be present in the adrenal glands and would release catecholamines through activation of its main receptor, chemokine like receptor 1 (CMKLR1, ChemR23). Methodology: Immunohistochemistry was used to assess the presence of chemerin and two of its receptors, CMKLR1 and G protein coupled receptor 1 (GPR1), in isolated whole adrenal glands from normal male, Sprague Dawley rats. There was a moderate level of chemerin expression in the medulla and the cortex. The CMKLR1 expression was moderate in the cortex and absent in the medullae. By contrast, a robust level of GPR1 in the cortex and medulla was observed. High-pressure liquid chromatography (HPLC) was used to measure the amount of norepinephrine and epinephrine released by the adrenal medullae when incubated in vitro with a stimulus. Results: Chemerin-9 (100 nM, a shorter and stable chemerin analog) caused a significant 90.0±24.0% increase of norepinephrine and a 69.0±3.4% increase of epinephrine vs vehicle paired adrenal medullae. However, the CMKLR1 antagonist CCX832 did not block chemerin-9 induced release of catecholamines from the medulla. Conclusion: These data are the first to suggest that chemerin may have a function within the adrenal, causing active release of catecholamines, an action that would support an elevation in blood pressure.
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