Background: Increased vascular Ca1.2 channel function causes enhanced arterial tone during hypertension. This is mediated by elevations in angiotensin II/protein kinase C signaling.
View Article and Find Full Text PDFThe present study evaluated the effectiveness of breathing re-education with routine physical therapy. This mixed method study was conducted at the District Headquarter Hospital Faisalabad, Faisalabad from April 2020 to July 2020. Fourteen participants (6men and 8 women) with chronic neck pain were recruited over a 16-week period and were equally divided into breathing re-education and routine physical therapy groups.
View Article and Find Full Text PDFBackground: People with chronic neck pain show decreased endurance and strength of cervical muscles with compromised respiratory function. There is little evidence that improvement in breathing function of people with neck pain can help in enhancing cervical muscle strength and pulmonary function. The objective of this our clinical trial was to examine the effects of breathing re-education combined with physiotherapy on endurance and strength of deep neck flexors, and pulmonary function in patients with chronic neck pain.
View Article and Find Full Text PDFCigarette smoke, including secondhand smoke (SHS), has significant detrimental vascular effects, but its effects on myogenic tone of small resistance arteries and the underlying mechanisms are understudied. Although it is apparent that SHS contributes to endothelial dysfunction, much less is known about how this toxicant alters arterial myocyte contraction, leading to alterations in myogenic tone. The study's goal is to determine the effects of SHS on mesenteric arterial myocyte contractility and excitability.
View Article and Find Full Text PDFThe L-type Ca channel Ca1.2 is essential for arterial myocyte excitability, gene expression and contraction. Elevations in extracellular glucose (hyperglycemia) potentiate vascular L-type Ca channel via PKA, but the underlying mechanisms are unclear.
View Article and Find Full Text PDFElevated blood glucose (hyperglycemia) is a hallmark metabolic abnormality in diabetes. Hyperglycemia is associated with protein kinase A (PKA)-mediated stimulation of L-type Ca2+ channels in arterial myocytes resulting in increased vasoconstriction. However, the mechanisms by which glucose activates PKA remain unclear.
View Article and Find Full Text PDFElevated glucose increases vascular reactivity by promoting L-type Ca1.2 channel (LTCC) activity by protein kinase A (PKA). Yet, how glucose activates PKA is unknown.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
April 2019
Activation of ATP-sensitive potassium (K) channels in arterial smooth muscle (ASM) contributes to vasodilation evoked by a variety of endogenous and exogenous compounds. Although controversial, activation of K channels by neuropeptides such as calcitonin gene-related peptide (CGRP) and pituitary adenylate cyclase activating peptide (PACAP) in the trigeminovascular system, including the middle meningeal artery (MMA), has been linked to migraine headache. The objective of the current study was to determine if ongoing K channel activity also influences MMA diameter.
View Article and Find Full Text PDFLarge-conductance Ca-activated potassium (BK) channels are key determinants of vascular smooth muscle excitability. Impaired BK channel function through remodeling of BK β1 expression and function contributes to vascular complications in animal models of diabetes. Yet, whether similar alterations occur in native vascular smooth muscle from humans with type 2 diabetes is unclear.
View Article and Find Full Text PDFVoltage-gated potassium (K ) channels are key regulators of vascular smooth muscle contractility and vascular tone, and thus have major influence on the microcirculation. K channels are important determinants of vascular smooth muscle membrane potential (E ). A number of K subunits are expressed in the plasma membrane of smooth muscle cells.
View Article and Find Full Text PDFIntroduction: Moraxella catarrhalis previously considered as commensal of upper respiratory tract has gained importance as a pathogen responsible for respiratory tract infections. Its beta-lactamase-producing ability draws even more attention toward its varying patterns of resistance.
Methods: This was an observational study conducted to evaluate the prevalence and resistance pattern of M.
Pituitary adenylate cyclase activating polypeptide (PACAP) is a potent vasodilator of numerous vascular beds, including cerebral arteries. Although PACAP-induced cerebral artery dilation is suggested to be cyclic AMP (cAMP)-dependent, the downstream intracellular signaling pathways are still not fully understood. In this study, we examined the role of smooth muscle K(+) channels and hypothesized that PACAP-mediated increases in cAMP levels and protein kinase A (PKA) activity result in the coordinate activation of ATP-sensitive K(+) (KATP) and large-conductance Ca(2+)-activated K(+) (BK) channels for cerebral artery dilation.
View Article and Find Full Text PDFMigraine is a debilitating neurological disorder characterized by mild to severe headache that is often accompanied by aura and other neurological symptoms. Among proposed mechanisms, dilation of the dural vasculature especially the middle meningeal artery (MMA) has been implicated as one component underlying this disorder. Several regulatory peptides from trigeminal sensory and sphenopalatine postganglionic parasympathetic fibers innervating these vessels have been implicated in the process including pituitary adenylate cyclase-activating polypeptide (PACAP).
View Article and Find Full Text PDFIn the present study we report on the use of speed congenics to generate a C57BL/6J congenic line of HD-model R6/2 mice carrying 110 CAG repeats, which uniquely exhibits minimal intergenerational instability. We also report the first identification of the R6/2 transgene insertion site. The relatively stable line of 110 CAG R6/2 mice was characterized for the onset of behavioral impairments in motor, cognitive and psychiatric-related phenotypes as well as the progression of disease-related impairments from 4 to 10 weeks of age.
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