Endothelium-Derived Vasoactive Substances

2015 ◽  
pp. 3-42
Keyword(s):  
Vasoactive Substances

Effect of Ridogrel on Vascular Contractions Gaused by Vasoactive Substances Released during Platelet Activation

1990 ◽  
Vol 64 (01) ◽  
pp. 091-096 ◽  
Author(s):  
W J Janssens ◽  
F J S Cools ◽  
L A M Hoskens ◽  
J M Van Nueten
Keyword(s):  
Smooth Muscle ◽  
Blood Vessel ◽  
Platelet Activation ◽  
Prostaglandin F2α ◽  
Thromboxane A2 ◽  
Femoral Arteries ◽  
Vasoactive Substances ◽  
Caudal Artery ◽  
Isolated Rat ◽  
Rat Platelets

SummaryRidogrel (6.3 × 10−6 to 10−4 M) inhibited contractions of isolated rat caudal arteries and rabbit femoral arteries caused by U-46619. The slope of an Arunlakshana-Schild plot (pA2-value: 3.4 × 10−6 M) on the caudal artery was slightly higher than one (1.14). This effect was maximal within}D min of incubation of the blood vessel with the compound and easily reversible. Ridogrel antagonised contractions of isolated rabbit femoral arteries caused by prostaglandin Fzo2α in the same concentration range. Ridogrel also inhibited contractions induced by aggregating rat platelets on isolated rat caudal arteries (itt the presence of ketanserin 4 × 10−7 M) and on isolated rabbit pulmonary and femoral arteries (in the absence of ketanserin). Ridogrel had no effect on Ca2+-induced contractions in depolarised isolated rabbit femoral arteries, and at 10−4 M antagonised serotonin-induced contractions in this blood vessel. Its effect on serotonin-induced contractions was statistically significant but very small on isolated rat caudal arteries. These observations indicate that ridogrel is an antagonist of prostaglandin endoperoxide/thromboxane A2 and prostaglandin F2α raCeptors on vascular smooth muscle.

Time course of serum levels of leukemia inhibitory factor (LIF) and soluble LIF receptor (sLIF-R) in development of stage II essential hypertension

2017 ◽  
pp. 63-69
Author(s):  
О.А. Радаева ◽  
А.С. Симбирцев
Keyword(s):  
Antihypertensive Therapy ◽  
Time Course ◽  
Pulse Wave ◽  
Antihypertensive Drugs ◽  
Peripheral Resistance ◽  
Serum Levels ◽  
Stage Ii ◽  
Healthy Individuals ◽  
Vasoactive Substances ◽  
Essential Arterial Hypertension

Цель - изучение сывороточных уровней LIF, sLIr и их соотношение с гемодинамическими параметрами (ЧСС, САД, ДАД, ПАД, ЦАД, срАД, УО, МОК, ОПСС, СПВ) и содержанием вазоактивных веществ (AT II, ET-1, NO, ADMA, SDMA, eNOS, iNOS, NT-proСNP, NT-proBNP) у пациентов с эссенциальной артериальной гипертензией (ЭАГ) II стадии. Методы: количество LIF, sLIF-R/gp190 и вазоактивные вещества в сыворотке определяли иммуноферментным методом. Результаты: у пациентов с ЭАГ II стадии вне зависимости от проведения гипотензивной терапии была более высокая концентрация LIF (7,54 (2,8) пг/мл, 7,5 (2,1) пг/мл), по сравнению с условно здоровыми - 1,25 (0,5) пг/мл, р<0,001. При этом у пациентов, не получавших гипотензивные препараты, увеличивался уровень sLIr - (5800 (1470 pg/ml)) по сравнению с больными на фоне гипотензивной терапии (4100 (1380) пг/мл, р<0,001) и условно здоровыми (3800 (1100) пг/мл, р<0,001). При уровне sLIF-R выше 4800 пг/мл обнаруживали связь с увеличением содержания в сыворотке iNOS, NT-proBNP, ADMA, SDMA, (r = 0,5-0,8, р<0,05-0,001) и уменьшением уровня eNOS (r = -0,56-0,86, р<0,05-0,001), что соответствует прогрессированию заболевания. Корреляции между LIF и указанными вазоактивными веществами выявлено не было, что дает основание предполагать, что sLIFr вызывает собственные патогенетические эффекты помимо антагонистической активности по отношению к LIF. Aim. To study levels of serum LIF and sLIF-R and their correlations with hemodynamic parameters (heart rate, systolic BP, diastolic BP, pulse pressure, central BP, mean BP, stroke volume, total peripheral resistance, and pulse wave velocity) and vasoactive substances (AT II, ET-1, NO, ADMA, SDMA, eNOS, iNOS, NT-proСNP, and NT-proBNP) in patients with stage II essential arterial hypertension (EAH). Methods. Serum levels of LIF and sLIF-R/gp190 were measured using ELISA in 180 patients with stage II ЕAН. Results: Patients with EAH II (with or without antihypertensive therapy) had higher serum levels of LIF (7.54 (2.8) pg/ml and 7.5 (2.1) pg/ml, respectively) compared to healthy individuals (1.25 (0.5) pg/ml), р<0.001. Patients not receiving a therapy had higher serum levels of sLIF-R (5800 (1470 pg/ml) than patients receiving antihypertensive drugs (4100 (1380) pg/ml, р<0.001) and healthy individual (3800 (1100) pg/ml, р<0.001). In patients with EAH, sLIF-R levels higher than 4800 pg/ml correlated with increases in iNOS, NT-proBNP, ADMA, and SDMA (r = 0.5-0.8, р<0.05-0.001) and decreases in eNOS (r = -0.56-0.86, р<0.05-0.001), which corresponded to disease progression. LIF did not show any significant correlations with these vasoactive substances, which suggested that sLIF-R exerted its own pathogenetic effects besides antagonizing LIF. Generally, this trend was typical for patients with EAH (II stage) without antihypertensive therapy.

CRITICAL ISSUES IN THE USE OF VASOACTIVE SUBSTANCES TO ASSESS LUNG MICROVASCULAR INJURY

1982 ◽  
Vol 384 (1 Mechanisms of) ◽  
pp. 435-457 ◽  
Author(s):  
S. Alex Stalcup ◽  
G. M. Turino ◽  
Robert B. Mellins
Keyword(s):  
Microvascular Injury ◽  
Vasoactive Substances ◽  
Critical Issues

scholarly journals The mechanism of ions in pulmonary hypertension

2021 ◽  
Vol 11 (1) ◽  
pp. 204589402098794
Author(s):  
Guogu Liu ◽  
Daiyan Fu ◽  
Heshen Tian ◽  
Aiguo Dai
Keyword(s):  
Pulmonary Hypertension ◽  
Calcium Ion ◽  
Pulmonary Arteries ◽  
Chloride Ion ◽  
Vasoactive Substances ◽  
Pulmonary Vasoconstriction ◽  
Concentration Of Ions ◽  
Inducing Factors ◽  
Effective Drugs ◽  
Pathological Manifestation

Pulmonary hypertension（PH）is a kind of hemodynamic and pathophysiological state, in which the pulmonary artery pressure (PAP) rises above a certain threshold. The main pathological manifestation is pulmonary vasoconstriction and remodelling progressively. More and more studies have found that ions play a major role in the pathogenesis of PH. Many vasoactive substances, inflammatory mediators, transcription-inducing factors, apoptosis mediators, redox substances and translation modifiers can control the concentration of ions inside and outside the cell by regulating the activity of ion channels, which can regulate vascular contraction, cell proliferation, migration, apoptosis, inflammation and other functions. We all know that there are no effective drugs to treat PH. Ions are involved in the occurrence and development of PH, so it is necessary to clarify the mechanism of ions in PH as a therapeutic target for PH. The main ions involved in PH are calcium ion (Ca2+), potassium ion (K+), sodium ion (Na+) and chloride ion (Cl–). Here, we mainly discuss the distribution of these ions and their channels in pulmonary arteries and their role in the pathogenesis of PH.

scholarly journals Effects of vasoactive substances on isolated canine posterior vena cava

1975 ◽  
Vol 25 ◽  
pp. 185-186
Author(s):  
Naohisa Ishikawa ◽  
Hiromichi Tsuru ◽  
Tatsuro Shigei
Keyword(s):  
Vena Cava ◽  
Vasoactive Substances

Pulmonary Endothelial Cells / Metabolism of Vasoactive Substances

1975 ◽  
Author(s):  
J. W. Ryan ◽  
Una S. Ryan
Keyword(s):  
Endothelial Cells ◽  
Angiotensin Ii ◽  
Angiotensin I ◽  
Clotting System ◽  
Arterial Circulation ◽  
Pulmonary Endothelial Cells ◽  
Vasoactive Substances ◽  
Metabolic Products ◽  
Relationship Of ◽  
The Relationship

The lungs metabolize a variety of vasoactive substances, including bradykinin (BK), angiotensin I (AT I), PGE2 and F2α, norepinephrine, 5-HT, 5’-ATP and 5’-AMP. In contrast, the lungs od not metabolize angiotensin II (AT II), PGA2, histamine and epinephrine. Of the substances metabolized, all (with the possible exceptions of the prostaglandins) are processed primarily by the pulmonary endothelial cells. Furthermore, the means by which the substances are processed suggest that endothelial cells determine the vasoactive substances allowed to enter the systemic arterial circulation. BK is inactivated while AT I is converted to its potent homolog, AT II. AT II enters the arterial circulation. The metabolism of BK and AT I may be effected by the same enzyme. Pulmonary endothelial cells are a rich source of thromboplastin, an enzyme capable of degrading BK and AT I. However, the relationship of thromboplastin to the fates of these hormones is not clear : The metabolic products produced are not those produced by intact lungs nor by endothelial cells in culture. In addition, thromboplastin degrades substances (e.g. AT II), which are not degraded by intact lungs. Possibly the extrinsic clotting system plays a role when activated but not under physiologic conditions.

Elevations of local intravascular pressures release vasoactive substances in humans

2012 ◽  
Vol 33 (1) ◽  
pp. 38-44 ◽  
Author(s):  
T. Gustafsson ◽  
R. Kölegård ◽  
P. Sundblad ◽  
B. Norman ◽  
O. Eiken
Keyword(s):  
Vasoactive Substances
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