Browsing by Subject "Vasoconstriction"
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Item The Effect of Extracellular Volume Status on Intradialytic Hypertension(2014-02-04) Molina, Christopher; Van Buren, Peter; Toto, RobertBACKGROUND: lntradialytic hypertension (HTN), defined as an increase in systolic blood pressure (BP) >10 mmHg from pre to post-hemodialysis (HD),occurs regularly in approximately 15o/o of HD patients. Previous studieshave shown patients with intradialytic HTN display higher overall ambulatory BP and have higher mortality rates when compared to HD controls. As extracellular volume overload contributes to HTN in HD patients, it has been proposed that intradialytic HTN patients have increased extracellular volume. Still, atypical ambulatory BP patterns seen in intradialytic HTN patients suggest extracellular volume may not be a primary determinant of BP in this population. Thus, we hypothesize extracellular fluid volume will be similar in patients with intradialytic HTN and HD controls when adjusting for total body water. METHODS: ln a case control study we recruited hypertensive HD patients with pre HD systolic BP >140 mmHg or post HD systolic BP >130 mmHg. Case subjects with intradialytic HTN were defined as having systolic BP increases >10 mmHg from pre to post-HD. Control subjects were defined as having systolic BP decreases >10 mmHg from pre to post- HD. We obtained measurements of total body water, extracellular water, and intracellular water before and after HD in all subjects using multifrequency bioimpedance spectroscopy. We compared the ratio of extracellular water to total body water between groups using t-tests for pre and post dialysis measurements. RESULTS: Case subjects (n=4) had an average ambulatory systolic BP of 140 mmHg (20) and controls (n=4) had an average of 1a0 (9.8). Before dialysis, case subjects had a ratio of 0.49 (.03) vs. 0.a6 (.02) in controls (p=0.2). After dialysis, the ratio was 0.45 (0.03) in cases and .44 (0.01) in controls (p=0.4). DISCUSSION: The ratio of extracellular water to total body water was similar in subjects with intradialytic HTN both before and after HD compared to HD controls. While a larger sample size will be required to establish whether extracellular volume status is different in this patient population, the results of this study suggest increased extracellular volume is not a distinguishing feature of intradialytic HTN. Further etiologies for increased BP including excessive vascular resistance should be explored to explain the phenomenon of intradialytic hypertension.Item Inhibition of L-Type and Cyclic Nucleotide-Gated Calcium Channels Demonstrates Synergistic Mechanisms for Prolonging Vascular Contractions Induced by a Mimetic of Thromboxane A2(2014-02-04) Kellum, Joseph; Monnet, Paige L.; Hinman, Maxwell R.; Orr, James A.Previous experiments have demonstrated that the rates of relaxation of blood vessels treated with the thromboxane-A2 mimetic, U-46619, are significantly lower when compared to vessels treated with other vasoactive agents (e.g. α-adrenergic agonists). As a means of investigating the molecular mechanisms responsible for this prolonged contraction, we examined the roles of two types of calcium channels. L-type Ca2+ channels have long been associated with the U-46619 contraction, while cyclic nucleotide-gated (CNG) Ca2+ channels have only recently been shown to be involved. We tested the hypothesis that functioning of both channels is necessary to prolong the U-46619 contraction. An isolated organ bath preparation was used to measure the rates of relaxation (g/min) in aortic vessel segments obtained from euthanized rabbits. Isolated vessels contracted with U-46619 were treated with either L-type channel inhibitor (nifedipine, 200 μM) or CNG channel inhibitor (L-cis-dilitiazem, 140 μM), or both inhibitors simultaneously. Mean rates of relaxation were obtained for the four treatment groups: nifedipine only (7.95 x 10-2 ± 0.562 x 10-2 g/min, n = 10), L-cis-diltiazem only (6.36 x 10-2 ± 0.603 x 10-2 g/min, n = 10), both inhibitors simultaneously (6.93 x 10-2 ± 0.875 x 10-2 g/min, n = 12), and a control with vehicle only (3.94 x 10-2 ± 0.494 x 10-2 g/min, n = 15). Statistical analysis of the data indicated that the mean relaxation rate for the vehicle-treated group differed significantly from the relaxation rates of the experimental groups (P < 0.001), which were deemed statistically synonymous (P = 0.324). These data indicate that inhibition of either calcium channel alone or both channels simultaneously leads to equivalent increases in the rate of relaxation. This demonstrates that optimal functioning of both channels is necessary for the prolonged contraction, characteristic of U-46619-treated vessels. These results may have implications for reversing the contractions in vessels during myocardial infarction or stroke.