scholarly journals The Vascular Reactivity to Vasoactive Substances and the Electrolyte Contents in Arterial Walls

1965 ◽  
Vol 86 (4) ◽  
pp. 366-379 ◽  
Author(s):  
Hiroshi Demura ◽  
Soitsu Fukuchi ◽  
Hidenori Takahashi ◽  
Koji Goto
Keyword(s):  
Vascular Reactivity ◽  
Arterial Walls ◽  
Vasoactive Substances

Consomic strategies to localize genomic regions related to vascular reactivity in the Dahl salt-sensitive rat

2006 ◽  
Vol 26 (3) ◽  
pp. 218-225 ◽  
Author(s):  
Mary Pat Kunert ◽  
Ines Drenjancevic-Peric ◽  
Melinda R. Dwinell ◽  
Julian H. Lombard ◽  
Allen W. Cowley ◽  
...  
Keyword(s):  
Vascular Reactivity ◽  
Aortic Ring ◽  
Gene Interaction ◽  
Brown Norway ◽  
Single Chromosome ◽  
Salt Diet ◽  
Vasoactive Substances ◽  
Consomic Strain ◽  
Genomic Regions ◽  
Or Genes

Chromosomal substitution strains afford the opportunity to discover regions of the rat genome that contain genes related to cardiovascular traits with the long-range goal of linking these genes to physiological function. PhysGen (Programs for Genomic Applications) created a consomic panel of rats derived from the introgression of a single chromosome (≥95% of the BN chromosome, one at a time) of the Brown Norway (BN/NHsdMcwi) rat onto the homogeneous genetic background of the Dahl salt-sensitive rat (SS/JrHsdMcwi). For 3 wk before the experiment, the rats were maintained on a low-salt diet (0.4% NaCl). The dose response of aortic rings from each strain of rat to phenylephrine, acetylcholine, sodium nitroprusside, and three different levels of tissue bath hypoxia (10, 5, and 0% O2) was measured and compared with the parental SS rat. To maximize the possibility that differences among the strains would become apparent, each strain of rat including the parental SS and BN was also studied after being maintained on a high-salt diet (4.0% NaCl) for 3 wk. If the response of the aortic ring from a consomic strain to these vasoactive substances was different from that of the SS parental strain, it was concluded that the introgressed chromosome contained a gene or genes that contributed to that difference. Because the BN chromosome is removed from its native background and the SS rat loses a native chromosome, it is also necessary to consider the contribution of changes in gene-to-gene interaction.

Nitric oxide and vascular reactivity in developing zebrafish,Danio rerio

2000 ◽  
Vol 279 (6) ◽  
pp. R2200-R2207 ◽  
Author(s):  
Regina Fritsche ◽  
Thorsten Schwerte ◽  
Bernd Pelster
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Methyl Ester ◽  
Vascular Reactivity ◽  
Vascular System ◽  
Vascular Endothelial Cells ◽  
Vessel Diameter ◽  
No Donor ◽  
Dorsal Vein ◽  
Vasoactive Substances

We used a newly developed digital motion analysis video technique to study the effects of nitric oxide (NO) and epinephrine on the early larval arterial and venous vasculature of zebrafish. Application of the NO donor sodium nitroprusside resulted in a significant increase in both the venous and arterial vessel diameters, whereas N G-nitro-l-arginine methyl ester caused a significant decrease in the same diameters. Thus our results show that both the venous and arterial vasculature of the 5- and 6-day-old zebrafish larvae are influenced by endogenously produced NO. By use of immunohistochemistry, NO synthase immunoreactivity was demonstrated in endothelial cells of the dorsal vein. Local application of epinephrine onto the dorsal artery had no effect on vessel diameter. However, if the embryos were preincubated with N ω-nitro-l-arginine methyl ester, addition of epinephrine resulted in a significant reduction in both arterial and venous vessel diameters. Thus this study provides increasing evidence that before a functional autonomic innervation of the peripheral vascular system, vascular tone in larval tissue is regulated by a complex interaction of vasoactive substances that are produced locally by vascular endothelial cells.

scholarly journals Hemodynamic Consequences of Common Carotid Artery Thrombosis and Thrombogenically Activated Blood in Rats

1991 ◽  
Vol 11 (6) ◽  
pp. 957-965 ◽  
Author(s):  
W. Dalton Dietrich ◽  
Ricardo Prado ◽  
Brant D. Watson ◽  
Raul Busto ◽  
Myron D. Ginsberg
Keyword(s):  
Carotid Artery ◽  
Common Carotid Artery ◽  
Vascular Reactivity ◽  
Systemic Circulation ◽  
Border Zone ◽  
Humoral Factors ◽  
Carotid Artery Thrombosis ◽  
Cerebrovascular Injury ◽  
Vasoactive Substances ◽  
Artery Thrombosis

We documented the hemodynamic consequences of nonocclusive common carotid artery thrombosis (CCAT) and tested the hypothesis that vasoactive substances capable of altering local CBF (LCBF) are released into the systemic circulation following cerebrovascular injury. Ten minutes after photochemically induced CCAT, an autoradiographic determination of LCBF was conducted with [14C]iodoantipyrine. In blood transfusion studies using donor and recipient rats, a 1-ml sample of thrombogenically activated blood (TAB) collected downstream from the forming thrombus was reinjected into a recipient rat 15 or 60 min before CBF study. A heterogeneous pattern of abnormal LCBF was documented in the ipsilateral hemisphere of CCAT rats and recipient rats receiving TAB 15 min before CBF study. Acute hemodynamic abnormalities included ischemic (< 35% of control) and hyperemic (> 125% of control) foci and more global reductions (50–80% of control) in cortical and subcortical LCBF. Border zone hyperemia exceeding 2.0 ml/g/min was associated with focal sites of severe LCBF reductions. Although recipient rats that received TAB 15 min before CBF study displayed similar hemodynamic abnormalities, LCBF values in 60-min recipient rats were not significantly different from control despite ischemic foci. Humoral factors generated during CCAT appear to be responsible for the acute LCBF consequences of cerebrovascular thrombosis. Vasoactive substances released from a thrombotic site, capable of regionally affecting vascular reactivity in a time-dependent fashion, might be expected to participate in the pathogenesis of transient ischemic attacks and acute stroke.

Modification of vascular reactivity by alteration of intimal permeability: effect of TNF-alpha

1993 ◽  
Vol 264 (6) ◽  
pp. H1847-H1853 ◽  
Author(s):  
T. Matsuki ◽  
J. M. Beach ◽  
R. L. Klindt ◽  
B. R. Duling
Keyword(s):  
Vascular Reactivity ◽  
Water Soluble ◽  
Tnf Alpha ◽  
Necrosis Factor Alpha ◽  
Small Water ◽  
Vasoactive Substances ◽  
Before And After ◽  
Arteriolar Wall ◽  
Factor Alpha ◽  
Cheek Pouches

We investigated the effects of alterations in intimal permeability on microvascular reactivity to small hydrophilic agents in isolated, cannulated, perfused arterioles (65 +/- 6 microns ID) from hamster cheek pouches. Arterioles are 300-fold less responsive to the hydrophilic alpha 1-agonist, phenylephrine, applied to the lumen than when applied to the adventitia. Luminal treatment with tumor necrosis factor-alpha (TNF-alpha, 0.625 micrograms/ml, 1–2 h) potentiated reactivity to luminally applied phenylephrine, but the treatment did not change reactivity to adventitially applied phenylephrine. Similar results were obtained with a brief treatment with the detergent, 3-[(3-cholamidopropyl)dimethylammonio]-1- propanesulfonate (CHAPS; 0.3%, < 30 s). To confirm that a change in permeability had occurred, we measured the movement across the arteriolar wall of a low-molecular-weight hydrophilic fluorescent molecule, fluorescein, before and after luminal treatment with TNF-alpha or CHAPS. Either TNF-alpha or CHAPS significantly increased the rate of movement of fluorescein across the arteriolar wall. These data suggest that one element in the pathophysiology of TNF-alpha is an increase in arteriolar permeability to small, water-soluble agents, which may modify reactivity to circulating vasoactive substances.

Effect of High Ethanol Intake on Vascular Reactivity to Serotonin, Vasopressin and Acetylcholine in Normotensive Rats

1993 ◽  
Vol 21 (3) ◽  
pp. 133-137 ◽  
Author(s):  
J G P Pires ◽  
A M Cabral ◽  
E C Vasquez ◽  
N S Bissoli
Keyword(s):  
Blood Pressure ◽  
Vascular Reactivity ◽  
Ethanol Intake ◽  
Chronic Ethanol ◽  
Mesenteric Arteries ◽  
Ethanol Administration ◽  
Response Curves ◽  
Relaxant Effect ◽  
Vasoactive Substances ◽  
Chronic Ethanol Administration

Chronic ethanol administration causes hypertension and alterations of vascular reactivity in rats. In several models of hypertension, alterations of vascular reactivity are believed to be secondary to the sustained increase in blood pressure. The present study investigated the effects of serotonin (5-hydroxytryptamine [5-HT]), vasopressin and acetylcholine (ACh) in the isolated perfused mesenteric arteries from Wistar rats submitted to an 8-week course of chronic ethanol intake (8 g/kg day). No significant differences were observed in the dose – response curves with regard to: pressor effect of 0.04 — 10.0 nmole 5-HT; relaxant effect of 0.05 — 50.0 nmole ACh; or the pressor effects of two 1.5-nmole doses of vasopressin between control rats and ethanol-fed rats. These results suggest that modifications in arterial reactivity to endogenous vasoactive substances (observed in other studies involving more prolonged ethanol treatment in rats) may be, in part, secondary to the increase in blood pressure.

Cutaneous vascular reactivity in atopic children

1965 ◽  
Vol 92 (6) ◽  
pp. 621-624 ◽  
Author(s):  
L. A. Johnson
Keyword(s):  
Vascular Reactivity

History of vascular reactivity models and their involvement in hypertension pathogenesis

VASA ◽  
2017 ◽  
Vol 46 (6) ◽  
pp. 431-439 ◽  
Author(s):  
Ana Gabriela Conceição-Vertamatti ◽  
Filipy Borghi ◽  
Fernando Canova ◽  
Dora Maria Grassi-Kassisse
Keyword(s):  
Blood Pressure ◽  
Adrenergic Receptors ◽  
Vascular Reactivity ◽  
Multifactorial Disease ◽  
Pharmacological Treatments ◽  
Beta Adrenergic Receptors ◽  
Vascular Area ◽  
History Of ◽  
Record Blood Pressure ◽  
Advance Knowledge

Abstract. Hypertension is a silent and multifactorial disease. Over two centuries ago, the first device to record blood pressure was developed, making it possible to determine normotension and to establish criteria for hypertension. Since then, several studies have contributed to advance knowledge in this area, promoting significant advances in pharmacological treatments and, as a result, increasing survival of hypertensive people. The main models developed for the study of hypertension and the main findings in the vascular area are included in this review. We considered aspects related to vascular reactivity, changes in the population, and action of beta adrenergic receptors in the pathogenesis of hypertension.

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.

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