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The European Respiratory Journal Jan 2016
Topics: Humans; Hypoxia; Lung; Pulmonary Artery; Pulmonary Circulation; Vasoconstriction
PubMed: 26721961
DOI: 10.1183/13993003.01753-2015 -
Prague Medical Report 2020Reversible cerebral vasoconstriction syndrome (RCVS) is characterised by severe thunderclap headaches (with or without the presence of acute neurological symptoms) and... (Review)
Review
Reversible cerebral vasoconstriction syndrome (RCVS) is characterised by severe thunderclap headaches (with or without the presence of acute neurological symptoms) and segmental vasoconstriction of cerebral arteries that resolves spontaneously in a period of three months. Cases have been described in the literature with producing and non-producing masses of metanephrines. Within these reports, associations with cavernous haemangioma, medulloblastoma, colon cancer, paraganglioma, pheochromocytoma, uterine fibroids, among others were found. However, no association with adrenal masses which do not produce metanephrines was found. In this context, we reported the case of a woman with this type of tumour associated with RCVS which provided a treatment challenge, as well as we reviewed the literature on cases of RCVS associated with masses.
Topics: Female; Headache Disorders, Primary; Humans; Paraganglioma; Vasoconstriction; Vasospasm, Intracranial
PubMed: 32553094
DOI: 10.14712/23362936.2020.9 -
American Journal of Physiology. Heart... Oct 2023Exercising muscle blood flow is reduced in patients with heart failure with a preserved ejection fraction (HFpEF), which may be related to disease-related changes in the...
Exercising muscle blood flow is reduced in patients with heart failure with a preserved ejection fraction (HFpEF), which may be related to disease-related changes in the ability to overcome sympathetic nervous system (SNS)-mediated vasoconstriction during exercise, (i.e., "functional sympatholysis"). Thus, in 12 patients with HFpEF (69 ± 7 yr) and 11 healthy controls (Con, 69 ± 4 yr), we examined forearm blood flow (FBF), mean arterial pressure (MAP), and forearm vascular conductance (FVC) during rhythmic handgrip exercise (HG) at 30% of maximum voluntary contraction with or without lower-body negative pressure (LBNP, -20 mmHg) to increase SNS activity and elicit peripheral vasoconstriction. SNS-mediated vasoconstrictor responses were determined as LBNP-induced changes (%Δ) in FVC, and the "magnitude of sympatholysis" was calculated as the difference between responses at rest and during exercise. At rest, the LBNP-induced change in FVC was significantly lesser in HFpEF compared with Con (HFpEF: -9.5 ± 5.5 vs. Con: -21.0 ± 8.0%; < 0.01). During exercise, LBNP-induced %ΔFVC was significantly attenuated in Con compared with rest (HG: -5.8 ± 6.0%; < 0.05) but not in HFpEF (HG: -9.9 ± 2.5%; = 0.88). Thus, the magnitude of sympatholysis was lesser in HFpEF compared with Con (HFpEF: 0.4 ± 4.7 vs. Con: -15.2 ± 11.8%; < 0.01). These data demonstrate a diminished ability to attenuate SNS-mediated vasoconstriction in HFpEF and provide new evidence suggesting impaired functional sympatholysis in this patient group. Data from the current study suggest that functional sympatholysis, or the ability to adequately attenuate sympathetic nervous system (SNS)-mediated vasoconstriction during exercise, is impaired in patients with heart failure with preserved ejection fraction (HFpEF). These observations extend the current understanding of HFpEF pathophysiology by implicating inadequate functional sympatholysis as an important contributor to reduced exercising muscle blood flow in this patient group.
Topics: Humans; Sympatholytics; Hand Strength; Heart Failure; Stroke Volume; Muscle Contraction; Muscle, Skeletal; Vasoconstriction; Sympathetic Nervous System; Forearm; Regional Blood Flow
PubMed: 37566111
DOI: 10.1152/ajpheart.00450.2023 -
Journal of Integrative Neuroscience Sep 2021Peripheral vasoconstriction is a centrally mediated physiological effect known to play an important role in regulating body temperature by adjusting heat exchange with... (Review)
Review
Peripheral vasoconstriction is a centrally mediated physiological effect known to play an important role in regulating body temperature by adjusting heat exchange with the external environment. However, peripheral vasoconstriction as a component of sympathetic activation also occurs following exposure to various salient stimuli and during motivated behavior at stable environmental temperatures. This review aims to consider available evidence suggesting a significant contribution of this peripheral effect to physiological increases in both brain temperature and entry of oxygen and glucose into the brain's extracellular space. While these effects are triggered by neuronal activation, constriction of blood vessels in the skin and most internal organs results in redistribution of blood from the peripheral to central domains, thus dilating cerebral vessels, increasing global cerebral blood flow, and enhancing the intra-brain entry of oxygen and glucose from arterial blood. This powerful influence appears to determine the long duration of physiological increases in both brain temperature and brain levels of glucose and oxygen and their basic similarity across different brain structures. This work underscores the tight interrelationship between the brain and periphery and a significant contribution of cardiovascular effects in providing the enhanced inflow of oxygen and glucose into brain tissue to prevent metabolic deficit during functional neural activation.
Topics: Animals; Body Temperature; Body Temperature Regulation; Brain; Cerebrovascular Circulation; Glucose; Humans; Oxygen; Vasoconstriction
PubMed: 34645109
DOI: 10.31083/j.jin2003080 -
Journal of Physiology and Pharmacology... Feb 2016The genomic action of aldosterone has already been known to the scientific community and is well-documented to a satisfactory degree. However, the existence of rapid,... (Review)
Review
The genomic action of aldosterone has already been known to the scientific community and is well-documented to a satisfactory degree. However, the existence of rapid, non-genomic aldosterone actions has repeatedly been proven. These actions are apparent to a lot of tissues, among which the cardiac tissue, with the cardiac cells being responsible for the secretion of endogenous aldosterone. In the genomic pathway, the connection between the hormone and its receptor results increased reabsorption of sodium and water and excretion of potassium. Thus, the genomic procedure reacts indirectly on cardiovascular system by altering the blood pressure. New studies have shed light on unknown aspects of the non-genomic mechanism, which is sometimes performed by means of mineralocorticoid receptor (MR), while others through an MR-independent pathway. It is believed that aldosterone exerts its non-genomic action with the help of a different receptor, probably a G protein coupled receptor. A possible target is protein kinase C (PKC), and PKCε is postulated increase the permeability of the membrane of the cardiac cells to sodium, resulting in delayed repolarization and prolongation of action potential. These findings totally agree with and account for the serendipitous finding of our laboratory, that there is a positive correlation between plasma aldosterone levels and left ventricle (LV) contraction duration. Also, aldosterone has been proven to exacerbate the oxidative stress and induce vasoconstriction by acting on the vascular resistance and the cardiac output. Finally, this article deals with the role of aldosterone in cardiac fibrosis and the latest aspects of aldosterone actions on the heart muscle as well as providing a historical overview of the landmarks pertaining aldosterone's research.
Topics: Aldosterone; Animals; Heart Ventricles; Humans; Myocardium; Receptors, Mineralocorticoid; Vascular Resistance; Vasoconstriction
PubMed: 27010892
DOI: No ID Found -
Physiological Reports Feb 2016Exercise training (ET) increases sympathetic vasoconstrictor responsiveness and enhances contraction-mediated inhibition of sympathetic vasoconstriction (i.e.,...
Exercise training (ET) increases sympathetic vasoconstrictor responsiveness and enhances contraction-mediated inhibition of sympathetic vasoconstriction (i.e., sympatholysis) through a nitric oxide (NO)-dependent mechanism. Changes in α2-adrenoreceptor vasoconstriction mediate a portion of these training adaptations, however the contribution of other postsynaptic receptors remains to be determined. Therefore, the purpose of this study was to investigate the effect of ET on α1-adrenoreceptor-mediated vasoconstriction in resting and contracting muscle. It was hypothesized that α1-adrenoreceptor-mediated sympatholysis would be enhanced following ET. Male Sprague Dawley rats were randomized to sedentary (S; n = 12) or heavy-intensity treadmill ET (n = 11) groups. Subsequently, rats were anesthetized and instrumented for lumbar sympathetic chain stimulation and measurement of femoral vascular conductance (FVC) at rest and during muscle contraction. The percentage change in FVC in response to sympathetic stimulation was measured in control, α1-adrenoreceptor blockade (Prazosin; 20 μg, IV), and combined α1 and NO synthase (NOS) blockade (l-NAME; 5 mg·kg(-1) IV) conditions. Sympathetic vasoconstrictor responsiveness was increased (P < 0.05) in ET compared to S rats at low, but not high (P > 0.05) stimulation frequencies at rest (S: 2 Hz: -25 ± 4%; 5 Hz: -45 ± 5 %; ET: 2 Hz: -35 ± 7%, 5 Hz: -52 ± 7%), whereas sympathetic vasoconstrictor responsiveness was not different (P > 0.05) between groups during contraction (S: 2 Hz: -11 ± 8%; 5 Hz: -26 ± 11%; ET: 2 Hz: -10 ± 7%, 5 Hz: -27 ± 12%). Prazosin blunted (P < 0.05) vasoconstrictor responsiveness in S and ET rats at rest and during contraction, and abolished group differences in vasoconstrictor responsiveness. Subsequent NOS blockade increased vasoconstrictor responses (P < 0.05) in S at rest and during contraction, whereas in ET vasoconstriction was increased (P < 0.05) in response to sympathetic stimulation at 2 Hz at rest and unchanged (P > 0.05) during contraction. ET enhanced (P < 0.05) sympatholysis, however the training-mediated improvements in sympatholysis were abolished by α1-adrenoreceptor blockade. Subsequent NOS inhibition did not alter (P > 0.05) sympatholysis in S or ET rats. In conclusion, ET augmented α1-adrenoreceptor-mediated vasoconstriction in resting skeletal muscle and enhanced α1-adrenoreceptor-mediated sympatholysis. Furthermore, these data suggest that NO is not required to inhibit α2-adrenoreceptor- and nonadrenoreceptor-mediated vasoconstriction during exercise.
Topics: Adrenergic alpha-1 Receptor Antagonists; Animals; Enzyme Inhibitors; Male; Muscle Contraction; Muscle, Skeletal; NG-Nitroarginine Methyl Ester; Physical Conditioning, Animal; Prazosin; Rats; Rats, Sprague-Dawley; Receptors, Adrenergic, alpha-1; Rest; Sympathetic Nervous System; Vasoconstriction
PubMed: 26869686
DOI: 10.14814/phy2.12707 -
Pharmacology & Therapeutics Feb 2016In recent years, it has become apparent that the gaseous pollutant, hydrogen sulphide (H2S) can be synthesised in the body and has a multitude of biological actions.... (Review)
Review
In recent years, it has become apparent that the gaseous pollutant, hydrogen sulphide (H2S) can be synthesised in the body and has a multitude of biological actions. This review summarizes some of the actions of this 'gasotransmitter' in influencing the smooth muscle that is responsible for controlling muscular activity of hollow organs. In the vasculature, while H2S can cause vasoconstriction by complex interactions with other biologically important gases, such as nitric oxide, the prevailing response is vasorelaxation. While most vasorelaxation responses occur by a direct action of H2S on smooth muscle cells, it has recently been proposed to be an endothelium-derived hyperpolarizing factor. H2S also promotes relaxation in other smooth muscle preparations including bronchioles, the bladder, gastrointestinal tract and myometrium, opening up the opportunity of exploiting the pharmacology of H2S in the treatment of conditions where smooth muscle tone is excessive. The original concept, that H2S caused smooth muscle relaxation by activating ATP-sensitive K(+) channels, has been supplemented with observations that H2S can also modify the activity of other potassium channels, intracellular pH, phosphodiesterase activity and transient receptor potential channels on sensory nerves. While the enzymes responsible for generating endogenous H2S are widely expressed in smooth muscle preparations, it is much less clear what the physiological role of H2S is in determining smooth muscle contractility. Clarification of this requires the development of potent and selective inhibitors of H2S-generating enzymes.
Topics: Animals; Humans; Hydrogen Sulfide; Muscle Contraction; Muscle Relaxation; Muscle, Smooth; Myocytes, Smooth Muscle; Vasoconstriction; Vasodilation
PubMed: 26706238
DOI: 10.1016/j.pharmthera.2015.12.007 -
The Lancet. Respiratory Medicine Mar 2016Pulmonary hypertension is a well recognised complication of chronic hypoxic lung diseases, which are among the most common causes of death and disability worldwide.... (Review)
Review
Pulmonary hypertension is a well recognised complication of chronic hypoxic lung diseases, which are among the most common causes of death and disability worldwide. Development of pulmonary hypertension independently predicts reduced life expectancy. In chronic obstructive pulmonary disease, long-term oxygen therapy ameliorates pulmonary hypertension and greatly improves survival, although the correction of alveolar hypoxia and pulmonary hypertension is only partial. Advances in understanding of the regulation of vascular smooth muscle tone show that chronic vasoconstriction plays a more important part in the pathogenesis of hypoxic pulmonary hypertension than previously thought, and that structural vascular changes contribute less. Trials of existing vasodilators show that pulmonary hypertension can be ameliorated and systemic oxygen delivery improved in carefully selected patients, although systemic hypotensive effects limit the doses used. Vasoconstrictor pathways that are selective for the pulmonary circulation can be blocked to reduce hypoxic pulmonary hypertension without causing systemic hypotension, and thus provide potential targets for novel therapeutic strategies.
Topics: Chronic Disease; Hypertension, Pulmonary; Hypoxia; Lung Diseases; Muscle Contraction; Muscle, Smooth, Vascular; Nitric Oxide; Receptors, Epoprostenol; Signal Transduction; Vasoconstriction; Vasodilator Agents; rho-Associated Kinases
PubMed: 26895650
DOI: 10.1016/S2213-2600(15)00517-2 -
Hypertension (Dallas, Tex. : 1979) Aug 2020Increased arterial stiffness and vascular remodeling precede and are consequences of hypertension. They also contribute to the development and progression of...
Increased arterial stiffness and vascular remodeling precede and are consequences of hypertension. They also contribute to the development and progression of life-threatening cardiovascular diseases. Yet, there are currently no agents specifically aimed at preventing or treating arterial stiffening and remodeling. Previous research indicates that vascular smooth muscle actin polymerization participates in the initial stages of arterial stiffening and remodeling and that LIMK (LIM kinase) promotes F-actin formation and stabilization via cofilin phosphorylation and consequent inactivation. Herein, we hypothesize that LIMK inhibition is able to prevent vasoconstriction- and hypertension-associated arterial stiffening and inward remodeling. We found that small visceral arteries isolated from hypertensive subjects are stiffer and have greater cofilin phosphorylation than those from nonhypertensives. We also show that LIMK inhibition prevents arterial stiffening and inward remodeling in isolated human small visceral arteries exposed to prolonged vasoconstriction. Using cultured vascular smooth muscle cells, we determined that LIMK inhibition prevents vasoconstrictor agonists from increasing cofilin phosphorylation, F-actin volume, and cell cortex stiffness. We further show that localized LIMK inhibition prevents arteriolar inward remodeling in hypertensive mice. This indicates that hypertension is associated with increased vascular smooth muscle cofilin phosphorylation, cytoskeletal stress fiber formation, and heightened arterial stiffness. Our data further suggest that pharmacological inhibition of LIMK prevents vasoconstriction-induced arterial stiffening, in part, via reductions in vascular smooth muscle F-actin content and cellular stiffness. Accordingly, LIMK inhibition should represent a promising therapeutic means to stop the progression of arterial stiffening and remodeling in hypertension.
Topics: Adult; Animals; Arteries; Coronary Vessels; Female; Humans; Hypertension; Lim Kinases; Male; Mice; Mice, Transgenic; Middle Aged; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Protein Kinase Inhibitors; Signal Transduction; Vascular Remodeling; Vascular Stiffness; Vasoconstriction
PubMed: 32594801
DOI: 10.1161/HYPERTENSIONAHA.120.15203 -
Oxidative Medicine and Cellular... 2021We explored the role of ROS in cold-induced vasoconstriction and corresponding mechanism.
PURPOSE
We explored the role of ROS in cold-induced vasoconstriction and corresponding mechanism.
METHODS
Three experiments were performed. First, we measured blood flow in human hands before and after cold exposure. Second, 24 mice were randomly divided into 3 groups: 8 mice received saline injection, 8 received subcutaneous Tempol injection, and 8 received intrathecal Tempol injection. After 30 min, we determined blood flow in the skin before and after cold exposure. Finally, we used Tempol, CCG-1423, and Go 6983 to pretreat HAVSMCs and HUVECs for 24 h. Then, cells in the corresponding groups were exposed to cold (6 h, 4°C). After cold exposure, the cytoskeleton was stained. Intracellular Ca and ROS levels were measured by flow cytometry and fluorescence microscopy. We measured protein expression via Western blotting.
RESULTS
In the first experiment, after cold exposure, maximum skin blood flow decreased to 118.4 ± 50.97 flux units. Then, Tempol or normal saline pretreatment did not change skin blood flow. Unlike intrathecal Tempol injection, subcutaneous Tempol injection increased skin blood flow after cold exposure. Finally, cold exposure for 6 h shrank the cells, making them narrower, and increased intracellular Ca and ROS levels in HUVECs and HAVSMCs. Tempol reduced cell shrinkage and decreased intracellular Ca levels. In addition, Tempol decreased intracellular ROS levels. Cold exposure increased RhoA, Rock1, p-MLC-2, ET-1, iNOS, and p-PKC expression and decreased eNOS expression. Tempol or CCG-1423 pretreatment decreased RhoA, Rock1, and p-MLC-2 levels in HAVSMCs. Furthermore, Tempol or Go 6983 pretreatment decreased ET-1, iNOS, and p-PKC expression and increased eNOS expression in HUVECs.
CONCLUSION
ROS mediate the vasoconstrictor response within the cold-induced vascular response, and ROS in blood vessel tissues rather than nerve fibers are involved in vasoconstriction via the ROS/RhoA/ROCK1 and ROS/PKC/ET-1 pathways in VSMCs and endothelial cells.
Topics: Adult; Animals; Cold Temperature; Female; Humans; Male; Mice; Reactive Oxygen Species; Vasoconstriction
PubMed: 34868457
DOI: 10.1155/2021/8578452