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La Revue Du Praticien Oct 2022
Topics: Humans; Vasoconstriction; Syndrome
PubMed: 36511992
DOI: No ID Found -
Current Topics in Membranes 2022The delicate balance between constrictor and dilator mechanisms is a vital determinant of blood pressure and blood flow. The maintenance of this balance requires...
The delicate balance between constrictor and dilator mechanisms is a vital determinant of blood pressure and blood flow. The maintenance of this balance requires constant communication between different cell-types in the vascular wall. In this regard, the transient receptor potential vanilloid type 4 (TRPV4) ion channel, a Ca-permeable non-selective cation channel, has emerged as a crucial regulator of Ca-mediated changes in vascular reactivity. Recent studies suggest that TRPV4 channels regulate vasoconstriction and arterial pressure in the systemic and pulmonary vasculature. New emerging data support a dilatory role of endothelial TRPV4 channels, and both constrictor and dilator roles of smooth muscle TRPV4 channels. Moreover, TRPV4 channel activity has been implicated in physiological functions of vascular support cells, such as fibroblasts and pericytes, to assist the sustenance of vascular reactivity in response to changes in intravascular pressure or external stimulation. Importantly, a growing body of evidence connects abnormal TRPV4 channel activity to multiple vascular disorders. This chapter will review the current literature on the cell-type specific roles of vascular TRPV4 channels in regulating physiological function. Additionally, we summarize our understanding of the contribution of abnormal TRPV4 channel activity to various vascular disorders.
Topics: Blood Pressure; TRPV Cation Channels; Vasoconstriction
PubMed: 36210146
DOI: 10.1016/bs.ctm.2022.07.003 -
Stroke Apr 2024Reversible cerebral vasoconstriction syndrome (RCVS) refers to segmental, multifocal constriction of intracranial arteries along with acute headache and resolves within... (Review)
Review
Reversible cerebral vasoconstriction syndrome (RCVS) refers to segmental, multifocal constriction of intracranial arteries along with acute headache and resolves within weeks. It occurs more commonly in women, and 1 well-known manifestation of RCVS is postpartum angiopathy. Furthermore, the female sex is included in scoring systems designed to assist with diagnosing RCVS. Nonetheless, the literature is mixed regarding the true role of female and pregnancy-related factors in the pathophysiology of RCVS, and it is similarly unclear whether management of this disorder differs by sex. Given the association of RCVS with female sex and the importance of highlighting, recognizing, and managing stroke etiologies in women, herein, the author reviews what is currently known and unknown about the topic of RCVS in women.
Topics: Pregnancy; Humans; Female; Vasoconstriction; Vasospasm, Intracranial; Stroke; Headache; Headache Disorders, Primary
PubMed: 38362763
DOI: 10.1161/STROKEAHA.123.046312 -
Trends in Molecular Medicine Sep 2017Sphingosine kinase 1 (SphK1) knockout mice are protected against pulmonary hypertension and expression levels of the enzyme are increased in the lungs of pulmonary... (Review)
Review
Sphingosine kinase 1 (SphK1) knockout mice are protected against pulmonary hypertension and expression levels of the enzyme are increased in the lungs of pulmonary arterial hypertensive (PAH) patients. Moreover, sphingosine 1-phosphate can promote vascular remodeling/vasoconstriction in rodent and human pulmonary arterial smooth muscle cell models. Therefore, SphK1 might be a novel target for treatment of PAH. However, in our opinion, more refined strategies to target SphK1 are needed because this enzyme is protective against endothelial dysfunction and can become resistant to SphK1 inhibitors in vascular smooth muscle, thereby potentially limiting their effectiveness in PAH. In addition, SphK1 is involved in maladaptive hypertrophy and we propose that heart failure might be an additional direct target for therapeutic intervention with SphK1 inhibitors.
Topics: Animals; Endothelium, Vascular; Enzyme Inhibitors; Humans; Hypertension, Pulmonary; Mice; Mice, Knockout; Phosphotransferases (Alcohol Group Acceptor); Vascular Remodeling; Vasoconstriction
PubMed: 28789830
DOI: 10.1016/j.molmed.2017.07.001 -
Radiologic Clinics of North America Nov 2019The clinical and radiologic manifestations of posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome are reviewed. The... (Review)
Review
The clinical and radiologic manifestations of posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome are reviewed. The relationship between these entities is discussed. A hypothesis of a common underlying pathophysiology is proposed and substantiated based on the current medical literature.
Topics: Brain; Brain Diseases; Humans; Magnetic Resonance Imaging; Posterior Leukoencephalopathy Syndrome; Syndrome; Tomography, X-Ray Computed; Vasoconstriction
PubMed: 31582040
DOI: 10.1016/j.rcl.2019.07.001 -
Cephalalgia : An International Journal... Jun 2020The pathophysiology of reversible cerebral vasoconstriction syndrome is unclear. An unbiased systems-based approach might help to illustrate the metabolite profiling and...
BACKGROUND
The pathophysiology of reversible cerebral vasoconstriction syndrome is unclear. An unbiased systems-based approach might help to illustrate the metabolite profiling and underlying pathophysiology.
METHODS
Urine samples were collected from reversible cerebral vasoconstriction syndrome patients and matched controls recruited in Taipei Veterans General Hospital. H-Nuclear magnetic resonance was used to initially explore the metabolic profile, and liquid chromatography tandem mass spectrometry was then used to identify metabolic alterations in reversible cerebral vasoconstriction syndrome. Untargeted metabolite screening was randomly performed on 10 reversible cerebral vasoconstriction syndrome patients and 10 control subjects in the discovery phase. The selected untargeted metabolites were further validated on 47 reversible cerebral vasoconstriction syndrome patients during their ictal stage (with 40 of them having remission samples) and 47 controls in the replication phase.
RESULTS AND CONCLUSION
Six metabolites-hippurate, citrate, 1,3,7-trimethyluric acid, ascorbic acid, D-glucurono-6,3-lactone, and D--isocitric acid-with t-test derived -value < 0.05 and VIP score >1, were identified as potential urine signatures that can well distinguish reversible cerebral vasoconstriction syndrome subjects at ictal stage from controls. Among them, citrate, hippurate, ascorbic acid, and D-glucurono-6,3-lactone were significantly lower, and 1,3,7-trimethyluric acid and D--isocitric acid were higher in reversible cerebral vasoconstriction syndrome patients. Of these, four selected metabolites, citrate, D-glucurono-6,3-lactone, ascorbic acid, and 1,3,7-trimethyluric acid, returned to normal levels in remission. These metabolites are related to pathways associated with free radical scavenging, with the hub molecules being associated with endothelial dysfunction or sympathetic overactivity. Whether these metabolites and their implicated networks play a role in the pathogenesis of reversible cerebral vasoconstriction syndrome remains to be confirmed.
Topics: Adult; Aged; Brain; Cerebrovascular Disorders; Female; Headache Disorders, Primary; Humans; Male; Metabolomics; Middle Aged; Syndrome; Vasoconstriction
PubMed: 31910660
DOI: 10.1177/0333102419897621 -
Life Sciences Dec 2018The pathophysiology of pulmonary arterial hypertension (PAH) is underlined by cell proliferation and vasoconstriction of pulmonary arterioles this involves multiple... (Review)
Review
The pathophysiology of pulmonary arterial hypertension (PAH) is underlined by cell proliferation and vasoconstriction of pulmonary arterioles this involves multiple molecular factors or proteins, but it is not clear what the exact roles of these factors/proteins are. In addition, there may be other factors/proteins that have not been identified that contribute to PAH pathophysiology. Therefore, research has focused on investigating novel role players, in order to facilitate a better understanding of how PAH develop. Evidence suggest that mitochondrial regulators are key role players in PAH pathophysiology, but regulators that have not received sufficient attention in PAH are metallothioneins (MTs). In PAH patients, MT expression is elevated compared to healthy individuals, suggesting that MTs may be possible biomarkers. In other disease-models, MTs have been shown to regulate cell proliferation and vasoconstriction, processes that are instrumental in PAH pathophysiology. Due to the involvement of these processes in PAH pathophysiology and the ability of MTs to modulate them, this paper propose that cellular MTs may also play a role in PAH development. This paper suggests that PAH-research should perhaps begin to investigate the involvement of cellular MTs in the development of PAH.
Topics: Animals; Cell Proliferation; Gene Expression Regulation; Humans; Hypertension, Pulmonary; Metallothionein; Oxidative Stress; Vasoconstriction
PubMed: 30355531
DOI: 10.1016/j.lfs.2018.10.039 -
Basic & Clinical Pharmacology &... Aug 2020Almost fifty years ago, experiments on isolated veins showed that acute hypoxia augments venoconstrictor responses in vitro and that such facilitation relied on... (Review)
Review
Almost fifty years ago, experiments on isolated veins showed that acute hypoxia augments venoconstrictor responses in vitro and that such facilitation relied on anaerobic glycolysis. Over the years, this phenomenon was extended to a number of arterial preparations of different species and revisited, from a mechanistic point of view, with the successive demonstration that it depends on calcium handling in the vascular smooth muscle cells, is endothelium-dependent and requires the production of nitric oxide (NO) by endothelial nitric oxide synthase (eNOS) and the activation of soluble guanylyl cyclase (sGC). However, rather than the vasodilator cyclic nucleotide 3',5'-cyclic guanosine monophosphate (cGMP), its canonical product, the latter enzyme produces 3',5'-cyclic inosine monophosphate (cIMP) instead during acute hypoxia; this non-canonical cyclic nucleotide facilitates the contractile process in the vascular smooth muscle cells. This 'biased' activity of soluble guanylyl cyclase appears to involve stimulation of NAD(P)H:quinone oxidoreductase 1 (NQO-1). The exact interactions between hypoxia, anaerobic metabolism and NQO-1 leading to biased activity of soluble guanylyl cyclase remain to be established.
Topics: Animals; Calcium; Cyclic IMP; Endothelium, Vascular; Humans; Hypoxia; Muscle, Smooth, Vascular; NAD(P)H Dehydrogenase (Quinone); Nitric Oxide; Soluble Guanylyl Cyclase; Vasoconstriction; Vasodilator Agents
PubMed: 31310708
DOI: 10.1111/bcpt.13295 -
American Journal of Physiology.... Jul 2021Angiotensin II (ANG II) is a potent vasoconstrictor and may reduce renal blood flow (RBF), causing renal hypoxia. Hypotensive hemorrhage elevates plasma ANG II levels...
Angiotensin II (ANG II) is a potent vasoconstrictor and may reduce renal blood flow (RBF), causing renal hypoxia. Hypotensive hemorrhage elevates plasma ANG II levels and is associated with increased risk of acute kidney injury. We hypothesized that ANG II antagonism prevents renal vasoconstriction and hypoxia caused by hemorrhage. Pigs were anaesthetized, surgically prepared, and randomized to intravenous losartan (1.5 mg·kg·h, = 8) or an equal volume of intravenous Ringer acetate (vehicle-treated, = 8). Hemorrhage was induced by continuous aspiration of blood to reach and sustain mean arterial pressure of <50 mmHg for 30 min. Plasma ANG II levels, hemodynamics and oxygenation were assessed 60 min prehemorrhage, 30-min after the start of hemorrhage, and 60 min posthemorrhage. Erythropoietin mRNA was analyzed in cortical and medullary tissue sampled at the end of the experiment. Hypotensive hemorrhage increased plasma ANG II levels and decreased RBF and oxygen delivery in both groups. Losartan-treated animals recovered in RBF and oxygen delivery, whereas vehicle-treated animals had persistently reduced RBF and oxygen delivery. In accordance, renal vascular resistance increased over time post hemorrhage in vehicle-treated animals but was unchanged in losartan-treated animals. Renal oxygen extraction rate and cortical erythropoietin mRNA levels increased in the vehicle group but not in the losartan group. In conclusion, ANG II antagonism alleviates prolonged renal vasoconstriction and renal hypoxia in a large animal model of hypotensive hemorrhage.
Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Disease Models, Animal; Hemodynamics; Hemorrhage; Hypotension; Hypoxia; Kidney; Losartan; Male; Oxygen; Swine; Vasoconstriction
PubMed: 34009032
DOI: 10.1152/ajpregu.00073.2021 -
Experimental Physiology Aug 2021What is the central question of this study? Sympathetically mediated vasoconstriction is preserved during hypoxaemia in humans, but our understanding of vascular control...
NEW FINDINGS
What is the central question of this study? Sympathetically mediated vasoconstriction is preserved during hypoxaemia in humans, but our understanding of vascular control comes from predominantly male cohorts. We tested the hypothesis that young women attenuate sympathetically mediated vasoconstriction during steady-state hypoxaemia, whereas men do not? What is the main finding and its importance? Sympathetically mediated vasoconstriction is preserved or even enhanced during steady-state hypoxia in young men, and the peripheral vascular response to sympathetic activation during hypoxaemia is attenuated in young women. These data advance our understanding of sex-related differences in hypoxic vascular control.
ABSTRACT
Activation of the sympathetic nervous system causes vasoconstriction and a reduction in peripheral blood flow. Sympathetically mediated vasoconstriction may be attenuated during systemic hypoxia to maintain oxygen delivery; however, in predominantly male participants sympathetically mediated vasoconstriction is preserved or even enhanced during hypoxaemia. Given the potential for sex-specific differences in hypoxic vascular control, prior results are limited in application. We tested the hypothesis that young women attenuate sympathetically mediated vasoconstriction during steady-state hypoxaemia, whereas men do not. Healthy young men (n = 13, 25 ± 4 years) and women (n = 11, 24 ± 4 years) completed two trials consisting of a 2-min cold pressor test (CPT, a well-established sympathoexcitatory stimulus) during baseline normoxia and steady-state hypoxaemia. Beat-to-beat blood pressure (finger photoplethysmography) and forearm blood flow (venous occlusion plethysmography) were measured continuously. Total and forearm vascular conductance (TVC and FVC, respectfully) were calculated. A change (Δ) in TVC and FVC from steady-state during the last 1 min of CPT was calculated and differences between normoxia and systemic hypoxia were assessed. In men, the reduction in TVC during CPT was greater during hypoxia compared to normoxia (ΔTVC, P = 0.02), whereas ΔTVC did not differ between conditions in women (P = 0.49). In men, ΔFVC did not differ between normoxia and hypoxia (P = 0.92). In women, the reduction in FVC during CPT was attenuated during hypoxia (ΔFVC, P < 0.01). We confirm sympathetically mediated vasoconstriction is preserved or enhanced during hypoxaemia in young men, whereas peripheral vascular responsiveness to sympathetic activation during hypoxaemia is attenuated in young women. The results advance our understanding of sex-related differences in hypoxic vascular control.
Topics: Blood Pressure; Female; Forearm; Humans; Hypoxia; Male; Regional Blood Flow; Sex Characteristics; Sympathetic Nervous System; Vasoconstriction
PubMed: 34187092
DOI: 10.1113/EP089461