39 research outputs found

    Poor sleep quality is associated with cardiac autonomic dysfunction in treated hypertensive men

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    Hypertensives present cardiac autonomic dysfunction. Reduction in sleep quality increases blood pressure (BP) and favors hypertension development. Previous studies suggested a relationship between cardiovascular autonomic dysfunction and sleep quality, but it is unclear whether this association is present in hypertensives. Thus, this study evaluated the relationship between sleep quality and cardiac autonomic modulation in hypertensives. Forty-seven middle-aged hypertensive men under consistent anti-hypertensive treatment were assessed for sleep quality by the Pittsburgh Sleep Quality Index (PSQI—higher score means worse sleep quality). Additionally, their beat-by-beat BP and heart rate (HR) were recorded, and cardiac autonomic modulation was assessed by their variabilities. Mann-Whitney and t tests were used to compare different sleep quality groups: poor (PSQI > 5, n = 24) vs good (PSQI ≤ 5, n = 23), and Spearman’s correlations to investigate associations between sleep quality and autonomic markers. Patients with poor sleep quality presented lower cardiac parasympathetic modulation (HR high-frequency band = 26 ± 13 vs 36 ± 15 nu, P =.03; HR total variance = 951 ± 1373 vs 1608 ± 2272 ms2, P =.05) and cardiac baroreflex sensitivity (4.5 ± 2.3 vs 7.1 ± 3.7 ms/mm Hg, P =.01). Additionally, sleep quality score presented significant positive correlation with HR (r = +0.34, P =.02) and negative correlations with HR high-frequency band (r = −0.34, P =.03), HR total variance (r = −0.35, P =.02), and cardiac baroreflex sensitivity (r = −0.42, P =.01), showing that poor sleep quality is associated with higher HR and lower cardiac parasympathetic modulation and baroreflex sensitivity. In conclusion, in treated hypertensive men, poor sleep quality is associated with cardiac autonomic dysfunction

    Effect of priming on germinability and salt tolerance in seeds and seedlings of Physalis peruviana L

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    In some species, pre-germination treatments such as priming can increase germinability and the speed of the process, besides conferring tolerance to abiotic stress. The central effect of priming is the slow and controlled absorption of water in seed tissues, allowing the membranes to reorganize and synthesize protective substances against stress. This study was performed to assess the effects of priming on the invigoration of seeds and seedlings of Physalis peruviana subjected to salt stress. Seeds of P. peruviana were primed in polyethylene glycol 6000 to -0.8 MPa and were germinated in solutions with different salt concentrations (0, 4, 8 and 12 dS m-1). In addition to the rate of radical emergence, post-seminal development was also evaluated until the emergence of the cotyledons. Germinability decreased with increasing salt solution concentrations in both types of seeds. Priming appeared to alleviate the effects of salt stress in the early stages of development of P. peruviana. Total dry mass of seedlings increased under saline conditions, suggesting possible physiological adjustments induced by priming.Keywords: Germination, priming, salt stress, SolanaceaeAfrican Journal of Biotechnology, Vol 13(19), 1955-196

    Schistosomiasis differentially affects vasoconstrictor responses: up-regulation of 5-HT receptor-mediated aorta contraction

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    Schistosomiasis, classified by the World Health Organization as a neglected tropical disease, is an intravascular parasitic disease associated to a chronic inflammatory state. Evidence implicating inflammation in vascular dysfunction continues to mount, which, broadly defined, reflects a failure in the control of intracellular Ca2+ and consequently, vascular contraction. Therefore, we measured aorta contraction induced by 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1), two important regulators of vascular contraction. Isometric aortic contractions were determined in control and Schistosoma mansoni-infected mice. In the infected animals, 5-HT induced a 50% higher contraction in relation to controls and we also observed an increased contraction in response to Ca2+ mobilisation from sarcoplasmic reticulum. Nevertheless, Rho kinase inhibition reduced the contraction in response to 5-HT equally in both groups, discarding an increase of the contractile machinery sensitivity to Ca2+. Furthermore, no alteration was observed for contractions induced by ET-1 in both groups. Our data suggest that an immune-vascular interaction occurs in schistosomiasis, altering vascular contraction outside the mesenteric portal system. More importantly, it affects distinct intracellular signalling involved in aorta contraction, in this case increasing 5-HT receptor signalling
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