Symphony of Vascular Contraction

Maternal Vascular Physiology in Preeclampsia

“…79 Second messengers such as PKC, Rho kinase, and MAPKs increase sensitivity of contractile proteins to Ca 2+ , contributing to vascular smooth muscle contraction. 76 Increases in Ca 2+ sensitivity have been reported in subcutaneous resistance arteries from women with preeclampsia. 80 In summary, changes in the sGC/cGMP pathway, intracellular Ca 2+ concentrations, and sensitivity to Ca 2+ possibly underline dysfunction in the vascular smooth muscle cell layer in arteries from women with preeclampsia.…”

“…28,75 Release of Ca 2+ from intracellular stores and entry of Ca 2+ from the extracellular space cause an increase in intracellular Ca 2+ concentrations, which trigger the contraction of vascular smooth muscle. 76 Incubation of human umbilical smooth muscle cells cocultured with umbilical endothelial cells with serum from women with preeclampsia increased intracellular Ca 2+ concentrations and PKC-α (second messenger) activation. 77 In cultured rat aortic vascular smooth muscle cells, 4-hour incubation with serum from patients with preeclampsia had no effect on basal intracellular Ca 2+ concentrations but reduced hormonally mediated Ca 2+ transients.…”

Mechanisms Underlying Enhanced Noradrenaline-Induced Femoral Arterial Contractions of Spontaneously Hypertensive Rats: Involvement of Endothelium-Derived Factors and Cyclooxygenase-Derived Prostanoids

“…By contrast, contractions induced by beraprost (a stable PGI 2 analogue), PGE 2 , and U46619 (thromboxane/prostanoid receptor agonist) were similar between the SHR and WKY groups. Thus, NAdinduced femoral arterial contractions are augmented in SHR resulting from endothelial dysfunction and increased COX-derived vasoconstrictor prostanoid levels.Key words cyclooxygenase; endothelium; femoral artery; hypertension; contraction Hypertension is one of the most common chronic diseases in humans, 1) and hypertension-associated vascular complications such as stroke, heart failure, kidney diseases and peripheral arterial diseases are major sources of morbidity and mortality that exacerbate the quality of life.1-3) Because dysfunction and abnormal signaling in the main structural elements of the vasculature, such as endothelial cells and smooth muscle cells, are characteristic hypertension-associated vascular complications, [4][5][6][7][8][9] and functional impairments in these cells are observed in hypertensive patients and animal models of the disease, 10-19) a comprehensive understanding of the underlying mechanisms is indispensable for preventing and treating such complications.Among endothelium-derived factors, nitric oxide (NO) is of the greatest importance for modulating vascular function. 20,21) However, other factors including endothelium-derived hyperpolarizing factor (EDHF) and cyclooxygenase (COX)-derived prostanoids can also modulate vascular tone.…”

“…[1][2][3] Because dysfunction and abnormal signaling in the main structural elements of the vasculature, such as endothelial cells and smooth muscle cells, are characteristic hypertension-associated vascular complications, [4][5][6][7][8][9] and functional impairments in these cells are observed in hypertensive patients and animal models of the disease, [10][11][12][13][14][15][16][17][18][19] a comprehensive understanding of the underlying mechanisms is indispensable for preventing and treating such complications.…”

Mineralocorticoid regulation of cell function: the role of rapid signalling and gene transcription pathways

“…If MR is deleted, cGMP-and calcium-dependent signalling is impaired with reduction in baseline activation of the contractile regulators myosin light chain kinase (MLCK) and myosin light chain (MLC) 2 (Tarjus et al 2015a). The phosphorylation of MLC by MLCK is a necessary step in enabling actin-myosin coupling (Goulopoulou & Webb 2014) and occurs within 15 min of MR activation via PI3K signalling (Gros et al 2011a). The basal expression of genes coding for contractile elements, ion channels or signalling systems is unaffected by MR deletion in VSMC (Tarjus et al 2015a).…”