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Nihon Arukoru Yakubutsu Igakkai Zasshi... Jun 2015Vascular function is regulated by a balance of vasoconstriction and vasorelaxation. Disorder in this balance due to alcohol consumption causes various clinical... (Review)
Review
Vascular function is regulated by a balance of vasoconstriction and vasorelaxation. Disorder in this balance due to alcohol consumption causes various clinical conditions. In this review, we discuss the effects of acute and chronic ethanol consumption on vascular responses, including vasoconstriction, endothelium-dependent vasorelaxation, and nerve-mediated vasorelaxation. Acute ethanol administration induces vasoconstriction in ethanol-naive animals in vitro. Furthermore, ethanol can both potentiate and suppress agonist-induced Ca(2+)-dependent vasoconstriction. Moreover, ethanol augments Ca(2+)-independent vasoconstriction by increasing Ca2+ sensitivity. Endothelium-dependent relaxation is mediated by the nitric oxide (NO) pathway and the endothelium-derived hyperpolarizing factor (EDHF) pathway. Acute ethanol treatment inhibits both NO- and EDHF-mediated relaxation. Furthermore, acute ethanol ingestion can also potentiate and suppress calcitonin gene-related peptide (CGRP)-induced nerve-mediated relaxation. These opposing effects may be due to differences in species or vascular beds. Thus, acute ethanol treatment decreases vasorelaxation, thereby shifting the contraction-relaxation balance towards contraction. Combined, these effects are one mechanism by which acute heavy alcohol consumption causes circulatory disturbances such as vasospasms or ischemic heart disease. In contrast, chronic low-dose ethanol has no effect on vasoconstriction, whereas chronic high-dose ethanol increases vasoconstriction. Additionally, chronic ethanol intake has diminished, unchanged, and even increased effects on nerve-mediated relaxation; therefore, conclusions on these effects are not possible at present. Interestingly, chronic low-dose ethanol administration enhanced endothelium-dependent relaxation; however, higher doses inhibited these responses. Therefore, regular or light-to-moderate alcohol intake increases vasorelaxation and may suppress elevated blood pressure, whereas chronic heavy alcohol consumption may raise blood pressure, causing various clinical conditions.
Topics: Animals; Blood Pressure; Ethanol; Humans; Time Factors; Vasoconstriction; Vasodilation
PubMed: 26502571
DOI: No ID Found -
Science Signaling Feb 2015Sympathetic vasoconstriction plays an important role in the control of blood pressure and the distribution of blood flow. In this issue of Science Signaling, Billaud et... (Review)
Review
Sympathetic vasoconstriction plays an important role in the control of blood pressure and the distribution of blood flow. In this issue of Science Signaling, Billaud et al. show that sympathetic vasoconstriction occurs through a complex scheme involving the activation of large-pore pannexin 1 channels and the subsequent release of adenosine triphosphate that promotes contraction in an autocrine and paracrine manner. This elaborate mechanism may function as a point of intercept for other signaling pathways—for example, in relation to the phenomenon "functional sympatholysis," in which exercise abrogates sympathetic vasoconstriction in skeletal muscle. Because pannexin 1 channels are inhibited by nitric oxide, they may function as a switch to turn off adrenergic signaling in skeletal muscle during exercise.
Topics: Animals; Blood Pressure; Connexins; Humans; Muscle, Smooth, Vascular; Nerve Tissue Proteins; Receptors, Adrenergic, alpha-1; Signal Transduction; Vasoconstriction
PubMed: 25690011
DOI: 10.1126/scisignal.aaa7312 -
Journal of the American Heart... Feb 2022
Topics: Muscle, Smooth, Vascular; Receptor, Angiotensin, Type 1; Vasoconstriction
PubMed: 35156384
DOI: 10.1161/JAHA.121.024740 -
Molecular Aspects of Medicine Jun 2017Adenosine is a nucleoside that is particularly interesting to many scientific and clinical communities as it has important physiological and pathophysiological roles in... (Review)
Review
Adenosine is a nucleoside that is particularly interesting to many scientific and clinical communities as it has important physiological and pathophysiological roles in the kidney. The distribution of adenosine receptors has only recently been elucidated; therefore it is likely that more biological roles of this nucleoside will be unveiled in the near future. Since the discovery of the involvement of adenosine in renal vasoconstriction and regulation of local renin production, further evidence has shown that adenosine signaling is also involved in the tubuloglomerular feedback mechanism, sodium reabsorption and the adaptive response to acute insults, such as ischemia. However, the most interesting finding was the increased adenosine levels in chronic kidney diseases such as diabetic nephropathy and also in non-diabetic animal models of renal fibrosis. When adenosine is chronically increased its signaling via the adenosine receptors may change, switching to a state that induces renal damage and produces phenotypic changes in resident cells. This review discusses the physiological and pathophysiological roles of adenosine and pays special attention to the mechanisms associated with switching homeostatic nucleoside levels to increased adenosine production in kidneys affected by CKD.
Topics: Adenosine; Humans; Kidney; Kidney Tubules; Renal Insufficiency, Chronic; Signal Transduction; Vasoconstriction
PubMed: 28109856
DOI: 10.1016/j.mam.2017.01.004 -
Journal of Applied Physiology... Nov 2019Although respiratory sinus arrhythmia and blood pressure variability have been investigated extensively, there have been far fewer studies of the respiratory modulation... (Review)
Review
Although respiratory sinus arrhythmia and blood pressure variability have been investigated extensively, there have been far fewer studies of the respiratory modulation of peripheral blood flow in humans. Existing studies have been based primarily on noninvasive measurements using digit photoplethysmography and laser-Doppler flowmetry. The cumulative knowledge derived from these studies suggests that respiration can contribute to fluctuations in peripheral blood flow and volume through a combination of mechanical, hemodynamic, and neural mechanisms. However, the most convincing evidence suggests that the sympathetic nervous system plays the predominant role under normal, resting conditions. This mini-review provides a consolidation and interpretation of the key findings reported in this topical area. Given the need to extract dynamic information from noninvasive measurements under largely "closed-loop" conditions, we propose that the application of analytical tools based on systems theory and mathematical modeling can be of great utility in future studies. In particular, we present an example of how the transfer relation linking respiration to peripheral vascular conductance can be derived using measurements recorded during spontaneous breathing, spontaneous sighs, and ventilator-induced sighs.
Topics: Animals; Blood Flow Velocity; Blood Pressure; Humans; Models, Biological; Peripheral Nervous System; Photoplethysmography; Regional Blood Flow; Respiratory Mechanics; Vasoconstriction
PubMed: 31095465
DOI: 10.1152/japplphysiol.00111.2019 -
Stroke Aug 2023Subarachnoid hemorrhage (SAH) is characterized by an acute reduction of cerebral blood flow and subsequent cortical infarcts, but the underlying mechanisms are not well...
BACKGROUND
Subarachnoid hemorrhage (SAH) is characterized by an acute reduction of cerebral blood flow and subsequent cortical infarcts, but the underlying mechanisms are not well understood. Since pericytes regulate cerebral perfusion on the capillary level, we hypothesize that pericytes may reduce cerebral perfusion after SAH.
METHODS
Pericytes and vessel diameters of cerebral microvessels were imaged in vivo using NG2 (neuron-glial antigen 2) reporter mice and 2-photon microscopy before and 3 hours after sham surgery or induction of SAH by perforating the middle cerebral artery with an intraluminal filament. Twenty-four hours after, SAH pericyte density was assessed by immunohistochemistry.
RESULTS
SAH caused pearl-string-like constrictions of pial arterioles, slowed down blood flow velocity in pial arterioles by 50%, and reduced the volume of intraparenchymal arterioles and capillaries by up to 70% but did not affect pericyte density or induce capillary constriction by pericytes.
CONCLUSIONS
Our results suggest that perfusion deficits after SAH are not induced by pericyte-mediated capillary constrictions.
Topics: Mice; Animals; Pericytes; Capillaries; Subarachnoid Hemorrhage; Vasoconstriction; Perfusion
PubMed: 37381898
DOI: 10.1161/STROKEAHA.123.042936 -
Current Problems in Cardiology Jul 2018Decompensated or acute heart failure (AHF) is characterized by increased ventricular and atrial pressures which may lead to and be caused by circulatory congestion.... (Review)
Review
Decompensated or acute heart failure (AHF) is characterized by increased ventricular and atrial pressures which may lead to and be caused by circulatory congestion. Unless due to a primary decrease in cardiac function, congestion arises from volume expansion or vasoconstriction. In turn, volume expansion and vasoconstriction are due to neurohormonal imbalance since both result from activation of the sympathetic nervous system, the renin-angiotensin-aldosterone axis and excess secretion of arginine vasopressin. Outcomes in AHF remain dismal. Loop diuretics are the mainstay of therapy for AHF and may themselves aggravate neurohormonal imbalance. No adjunctive pharmacotherapy has yielded improvement in outcomes in AHF despite many attempts with various vasodilators and inotropes. We, therefore, propose that insufficient attention has been paid to neurohormonal imbalance in AHF. As in chronic HF, rectifying the effects of neurohormonal imbalance may lead to better outcomes. The use of alternative decongestive strategies or adjunctive pharmacotherapy directed at neurohormonal activation could yield benefit.
Topics: Acute Disease; Antidiuretic Hormone Receptor Antagonists; Heart Failure; Humans; Molecular Targeted Therapy; Renin-Angiotensin System; Sodium Potassium Chloride Symporter Inhibitors; Sympathetic Nervous System; Vasoconstriction
PubMed: 29310997
DOI: 10.1016/j.cpcardiol.2017.12.002 -
Evolving mechanisms of vascular smooth muscle contraction highlight key targets in vascular disease.Biochemical Pharmacology Jul 2018Vascular smooth muscle (VSM) plays an important role in the regulation of vascular function. Identifying the mechanisms of VSM contraction has been a major research goal... (Review)
Review
Vascular smooth muscle (VSM) plays an important role in the regulation of vascular function. Identifying the mechanisms of VSM contraction has been a major research goal in order to determine the causes of vascular dysfunction and exaggerated vasoconstriction in vascular disease. Major discoveries over several decades have helped to better understand the mechanisms of VSM contraction. Ca has been established as a major regulator of VSM contraction, and its sources, cytosolic levels, homeostatic mechanisms and subcellular distribution have been defined. Biochemical studies have also suggested that stimulation of Gq protein-coupled membrane receptors activates phospholipase C and promotes the hydrolysis of membrane phospholipids into inositol 1,4,5-trisphosphate (IP) and diacylglycerol (DAG). IP stimulates initial Ca release from the sarcoplasmic reticulum, and is buttressed by Ca influx through voltage-dependent, receptor-operated, transient receptor potential and store-operated channels. In order to prevent large increases in cytosolic Ca concentration ([Ca]), Ca removal mechanisms promote Ca extrusion via the plasmalemmal Ca pump and Na/Ca exchanger, and Ca uptake by the sarcoplasmic reticulum and mitochondria, and the coordinated activities of these Ca handling mechanisms help to create subplasmalemmal Ca domains. Threshold increases in [Ca] form a Ca-calmodulin complex, which activates myosin light chain (MLC) kinase, and causes MLC phosphorylation, actin-myosin interaction, and VSM contraction. Dissociations in the relationships between [Ca], MLC phosphorylation, and force have suggested additional Ca sensitization mechanisms. DAG activates protein kinase C (PKC) isoforms, which directly or indirectly via mitogen-activated protein kinase phosphorylate the actin-binding proteins calponin and caldesmon and thereby enhance the myofilaments force sensitivity to Ca. PKC-mediated phosphorylation of PKC-potentiated phosphatase inhibitor protein-17 (CPI-17), and RhoA-mediated activation of Rho-kinase (ROCK) inhibit MLC phosphatase and in turn increase MLC phosphorylation and VSM contraction. Abnormalities in the Ca handling mechanisms and PKC and ROCK activity have been associated with vascular dysfunction in multiple vascular disorders. Modulators of [Ca], PKC and ROCK activity could be useful in mitigating the increased vasoconstriction associated with vascular disease.
Topics: Animals; Calcium Signaling; Humans; Muscle Contraction; Muscle, Smooth, Vascular; Vascular Diseases; Vasoconstriction
PubMed: 29452094
DOI: 10.1016/j.bcp.2018.02.012 -
The Journal of Physiology Sep 2022
Topics: Muscle, Smooth, Vascular; Vasoconstriction
PubMed: 35848099
DOI: 10.1113/JP282890 -
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue May 2019In acute hypoxia, pulmonary vascular will contract and divert blood to better ventilated area to optimize ventilation/perfusion matching, which is known as hypoxic... (Review)
Review
In acute hypoxia, pulmonary vascular will contract and divert blood to better ventilated area to optimize ventilation/perfusion matching, which is known as hypoxic pulmonary vasoconstriction (HPV). In chronic hypoxia, irreversible pulmonary vascular remodeling can be induced, characterized by pulmonary artery middle smooth muscle cells and the outer fiber cell hyperplasia in luminal stenosis and pulmonary artery hypertension (PAH) eventually. Furthermore, PAH can cause increased ventricular afterload, and right heart failure in severe cases. Pulmonary artery smooth muscle cell (PASMC) elevated Ca concentration is one of the most important factors of its contractions, proliferation and migration. Recent studies on Ca promoting in HPV were summarized in order to provide evidence for clinical prevention of hypoxia and therapeutic PAH.
Topics: Calcium; Humans; Hypoxia; Myocytes, Smooth Muscle; Pulmonary Artery; Vasoconstriction
PubMed: 31198157
DOI: 10.3760/cma.j.issn.2095-4352.2019.05.025