Cortical Vasculature (cortical + vasculature)

Distribution by Scientific Domains


Selected Abstracts


Role of adrenocorticotropic hormone in the development and maintenance of the adrenal cortical vasculature

MICROSCOPY RESEARCH AND TECHNIQUE, Issue 3 2003
Michaël Thomas
Abstract The adrenal cortex is a highly vascularized endocrine tissue. A dense network of blood capillaries centripetally irrigates the adrenal gland, allowing every endocrine cell to be in contact with an endothelial cell. The pituitary hormone ACTH controls the coordinated development of the vasculature and the endocrine tissue mass. This suggests that paracrine secretions between steroidogenic adrenocytes and capillary endothelial cells participate in the control of adrenocortical homeostasis. Besides its effect on the vascular tone of arteries, ACTH induces the expression of the angiogenic cytokine VEGF-A (vascular endothelial growth factor-A) in primary cultures of adrenocortical cells. This growth factor is a specific mitogen for endothelial cells and is likely to mediate the hormonal control of adrenocortical vascularization through a paracrine mechanism. The newly discovered angiogenic factor EG-VEGF (endocrine-gland-derived vascular endothelial growth factor), the expression of which is restricted to endocrine glands and which is preferentially mitogenic for endocrine tissue-derived endothelial cells, is another candidate mediator of great potential interest. Microsc. Res. Tech. 61:247,251, 2003. © 2003 Wiley-Liss, Inc. [source]


Using forward calculations of the magnetic field perturbation due to a realistic vascular model to explore the BOLD effect

NMR IN BIOMEDICINE, Issue 6 2008
José P. Marques
Abstract This paper assesses the reliability of the infinite cylinder model used previously in the literature to simulate blood oxygenation level dependent (BOLD) signal changes. A three-dimensional finite element method was applied to a realistic model of the cortical vasculature, and the results compared with those generated from a simple model of the vasculature as a set of independent, randomly oriented, infinite cylinders. The realistic model is based on scanning electron microscopy measurements of the terminal vascular bed in the superficial cortex of the rat. Good agreement is found between the two models with regard to the extravascular R2* and R2 dependence on the cerebral blood volume and blood oxygenation fraction. Using the realistic model, it is also possible to gain further understanding of the relative importance of intravascular and extravascular BOLD contrast. A simple parameterisation of the dependence of the relaxation rates on relative cerebral blood volume and blood,tissue susceptibility difference was carried out, allowing discussion of the variation in the form of the haemodynamic response with field strength. Copyright © 2007 John Wiley & Sons, Ltd. [source]


Influence of high dietary sodium intake on the functional subtypes of ,1 -adrenoceptors in the renal cortical vasculature of Wistar,Kyoto rats

AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 1-2 2009
R. N. Kazi
Summary 1,Increased renal vascular resistance is one renal functional abnormality that contributes to hypertension, and ,1 -adrenoceptors play a pivotal role in modulating this renal vascular resistance. This study investigates the functional contribution of ,1 -adrenoceptor subtypes in the renal cortical vasculature of Wistar,Kyoto rats on a normal sodium diet (WKYNNa) compared with those given saline to drink for 6 weeks (WKYHNa). 2,The renal cortical vascular responses to the adrenergic agonists noradrenaline (NA), methoxamine (ME) and phenylephrine (PE) were measured in WKYHNa and WKYNNa rats either in the absence (the control phase) or presence of chloroethylclonidine (CEC), an ,1B -adrenoceptor antagonist, 5-methylurapidil (5-MeU), an ,1A antagonist, or BMY7378, an ,1D antagonist. 3,Results showed a greater renal cortical vascular sensitivity to NA, PE and ME in the WKYHNa compared with WKYNNa rats (P < 0.05). Moreover, 5-MeU and BMY7378 attenuated adrenergically induced renal cortical vasoconstriction in WKYHNa and WKYNNa rats; this response was largely blunted in CEC-treated WKYHNa rats (all P < 0.05) but not in CEC-treated WKYNNa rats. 4,The data suggest that irrespective of dietary sodium content, in Wistar,Kyoto rats ,1A - and ,1D -subtypes are the major ,1 -adrenoceptors in renal cortical vasculature; however, there appears to be a functional involvement of ,1B -adrenoceptors in the WKYHNa rats. [source]