			Home About us Contact

Vascular Segments (vascular + segment)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

2,2,-Nitrophenylisatogen potentiates P2X1 receptor mediated vascular contraction and blood pressure elevation

DRUG DEVELOPMENT RESEARCH, Issue 1 2003
Anna-Karin Wihlborg
Abstract The objective of this research was to examine the effects of chemical compounds with possible P2 receptor modulating effects and to characterize the potentiating effects of 2,2,-nitrophenylisatogen (NPI) on P2X1 receptors in vitro and in vivo. Chemical compounds were tested in an in vitro pharmacological assay using vascular segments from the rat mesenteric artery stimulated by P2 receptor-specific agonists. Contractions were expressed as a percentage of 60 mM K+ -induced contractions. Blood pressure was evaluated in pithed rats. NPI (30 ,M) added 15 min before addition of the P2X1 receptor-specific agonist ,,-MeATP increased the maximum vasoconstriction from 23% to 49% (an increase of 113%). Furthermore, NPI prevented the desensitization of repeated ,,-MeATP contractions. Related compounds were examined, and 2-(3-methoxy-phenyl)-1-oxy-indol-3-one (MPI) had similar effects as NPI, but several others lacked effect. NPI had no effect on ADP,S (P2Y1) or acetylcholine-mediated vasodilatation, nor on UTP (P2Y2/4), UDP (P2Y6), or noradrenaline-mediated contractions. In pithed rats, the blood pressure response to 50 nmol/kg-infusion of ,,-MeATP was increased from 50±6 to 63±5 mmHg (P<0.05), but had no effect on basal blood pressure or on the cardiovascular response to preganglionic nerve stimulation. In conclusion, NPI and MPI potentiates P2X1 receptor vascular contractions in vitro and (NPI) blood pressure effects in vivo. It is possible that the effect is mediated by an inhibition of P2X1 receptor desensitization. Drug Dev. Res. 59:82,87, 2003. © 2003 Wiley-Liss, Inc. [source]

Roles of Endothelial Cell Migration and Apoptosis in Vascular Remodeling during Development of the Central Nervous System

MICROCIRCULATION, Issue 5 2000
SUZANNE HUGHES
ABSTRACT Objective: To examine the roles of apoptosis, macrophages, and endothelial cell migration in vascular remodeling during development of the central nervous system. Methods: The terminal deoxynucleotide transferase-mediated dUTP nick end labeling (TUNEL) technique was combined with Griffonia simplicifolia isolectin B4 histochemistry to detect apoptotic endothelial cells in retinal whole-mount preparations derived from rats at various stages of postnatal development as well as from rat pups exposed to hyperoxia. Macrophages were detected by immunohistochemistry with the monoclonal antibody ED1, and proliferating endothelial cells were identified by incorporation of bromodeoxyuridine. Results: Only small numbers of TUNEL-positive endothelial cells were detected during normal development of the retinal vasculature, with the apoptotic cell density in the inner plexus peaking during the first postnatal week and decreasing markedly during the second week, at a time when vessel retraction was widespread. Neither apoptotic endothelial cells nor macrophages were apparent at sites of initiation of vessel retraction. TUNEL-positive endothelial cells were observed in vessels destined to remain. Hyperoxia induced excessive vessel withdrawal, resulting in the generation of isolated vascular segments containing apoptotic endothelial cells. A topographical analysis showed low numbers of proliferating endothelial cells at sites of angiogenesis whereas vascular proliferation was increased in the adjacent inner plexus. Conclusions: Endothelial cell apoptosis and macrophages do not initiate vessel retraction, but rather contribute to the removal of redundant cells throughout the vasculature. We suggest that vessel retraction is mediated by endothelial cell migration and that endothelial cells derived from retracting vascular segments are redeployed in the formation of new vessels. Only when retraction results in compromised circulation and redeployment is not possible, does endothelial cell apoptosis occur. [source]

Reversal Blood Flow Component as Determinant of the Arterial Functional Capability: Theoretical Implications in Physiological and Therapeutic Conditions

ARTIFICIAL ORGANS, Issue 3 2009
Daniel Bia
Abstract In several physiological, pathological, and therapeutic circumstances, the arterial blood flow is acutely modified, increasing, in some vascular segments the reversal (SSR) and oscillatory (SSO) components of the shear stress. Recently, in an in vivo model we found a relationship between acute changes in SSR and SSO, and variations in the arterial viscoelasticity. As the arterial viscoelasticity and diameter are the main determinants of the arterial buffering (BF) and conduit (CF) functions, changes in those functions could be expected associated with variations in SSR and SSO. The aim was to analyze the association between acute increases in SSR and SSO, and changes in the aortic CF and BF. Aortic flow, pressure, and diameter were measured in 16 sheep under basal and high reversal and oscillatory flow conditions (high SSR and SSO). Aortic BF and CF were quantified, and their potential association with the SSR and SSO components were analyzed. During high reversal flow rate conditions, a smooth muscle contraction-pattern was evidenced, with an increase in BF and a decrease in CF. Changes in BF and CF were associated with the changes in SSR and SSO. The acute effects on the arterial wall biomechanics of variations in SSR and SSO could contribute to comprehend their chronic effects, and the meaning of the acute vascular effects of changes in SSR and SSO would depend on the situation. Increases in SSR and SSO could be associated with smooth muscle tone increase-dependent changes in arterial BF and CF. [source]

Adrenergic mechanisms in canine nasal venous systems

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2003
Min Wang
We investigated the adrenergic mechanisms of the two venous systems that drain the nasal mucosa, thereby their exact role in eliciting nasal decongestion. The action of endogenously released noradrenaline and exogenous adrenergic agonists on different segments of the nasal venous systems, i.e. collecting (LCV, SCV) and outflow (SPV) veins of posterior venous system, collecting (ACV) and outflow (DNV) veins of anterior venous system and venous sinusoids of the septal mucosa (SM), were studied. In vitro isometric tension of the vascular segments was measured. Transmural nerve stimulation (TNS) produced constriction in ACV, DNV and SM, primary constriction followed by secondary dilatation in LCV and SCV and dilatation in SPV. Tetrodotoxin (10,6M) abolished all responses. Phentolamine (10,6M), prazosin (10,6M) and rauwolscine (10,7M) inhibited the constriction in all venous vessels. Propranolol (10,6M), atenolol (10,6M) and ICI 118,551 (10,6M) inhibited the relaxation in SPV but not in LCV and SCV. Phenylephrine and clonidine constricted whereas dobutamine and terbutaline relaxed all venous vessels dose-dependently. These results indicate ,1 -, ,2 -, ,1 - and ,2 -adrenoceptors are present in both venous systems. TNS causes constriction of anterior venous system, venous sinusoids and posterior collecting veins primarily via postjunctional ,2 -adrenoceptors but relaxation of posterior outflow vein equally via postjunctional ,1 - and ,2 -adrenoceptors. The combined action of the two adrenergic mechanisms can reduce nasal airway resistance in vivo by decreasing vascular capacitance and enhancing venous drainage via the posterior venous system. British Journal of Pharmacology (2003) 138, 145,155. doi:10.1038/sj.bjp.0705020 [source]