Ultrastructure of the hypophyseal portal vessel in mature rats. SEM and TEM observations.

Satoh, Hiromi; Inokuchi, Tetsuo; Shimizu, Masahiko; Obayashi, Hiroaki; Nakashima, Yukihiro

doi:10.2739/kurumemedj.36.91

Cited by 10 publications

(9 citation statements)

References 10 publications

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“…If GHRH receptors are completely restricted to GH cells, then local alterations in flow are most likely a consequence of secretory activity from stimulated GH cells. The effectors of vascular flow change may be pericytes, which display long contractile cytoplasmic processes embracing the endothelial tube of portal capillary vessels (30). These express receptors for diffusible vascular signaling factors (31), such as nitric oxide (32), which is synthesized by GH cells (33,34).…”

Section: Discussionmentioning

confidence: 99%

Cellular in vivo imaging reveals coordinated regulation of pituitary microcirculation and GH cell network function

Lafont

Desarménien

Cassou

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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Growth hormone (GH) exerts its actions via coordinated pulsatile secretion from a GH cell network into the bloodstream. Practically nothing is known about how the network receives its inputs in vivo and releases hormones into pituitary capillaries to shape GH pulses. Here we have developed in vivo approaches to measure local blood flow, oxygen partial pressure, and cell activity at single-cell resolution in mouse pituitary glands in situ. When secretagogue (GHRH) distribution was modeled with fluorescent markers injected into either the bloodstream or the nearby intercapillary space, a restricted distribution gradient evolved within the pituitary parenchyma. Injection of GHRH led to stimulation of both GH cell network activities and GH secretion, which was temporally associated with increases in blood flow rates and oxygen supply by capillaries, as well as oxygen consumption. Moreover, we observed a time-limiting step for hormone output at the perivascular level; macromolecules injected into the extracellular parenchyma moved rapidly to the perivascular space, but were then cleared more slowly in a size-dependent manner into capillary blood. Our findings suggest that GH pulse generation is not simply a GH cell network response, but is shaped by a tissue microenvironment context involving a functional association between the GH cell network activity and fluid microcirculation.blood flow | hormone pulsatility | oxygen pressure | tissue microenvironment | extracellular space

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Section: Discussionmentioning

confidence: 99%

Cellular in vivo imaging reveals coordinated regulation of pituitary microcirculation and GH cell network function

Lafont

Desarménien

Cassou

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

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“…The portal vessels of the pituitary lack smooth muscle fibres, but are associated with many pericytes showing highly ramifying processes. Importantly, as in all endocrine organs, the endothelium has many fenestrations and channels, ensuring high permeability for molecules traveling from the interstitial fluid to the blood and vice versa ( 792 ). Thus, portal vessels are capillary sinusoids with pericytes rather than typical portal veins.…”

Section: Paracrine Control By Connective Tissue Cells Endothelial Cementioning

confidence: 99%

Paracrinicity: The Story of 30 Years of Cellular Pituitary Crosstalk

Denef

2007

J Neuroendocrinology

214

238

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Living organisms represent, in essence, dynamic interactions of high complexity between membrane‐separated compartments that cannot exist on their own, but reach behaviour in co‐ordination. In multicellular organisms, there must be communication and co‐ordination between individual cells and cell groups to achieve appropriate behaviour of the system. Depending on the mode of signal transportation and the target, intercellular communication is neuronal, hormonal, paracrine or juxtacrine. Cell signalling can also be self‐targeting or autocrine. Although the notion of paracrine and autocrine signalling was already suggested more than 100 years ago, it is only during the last 30 years that these mechanisms have been characterised. In the anterior pituitary, paracrine communication and autocrine loops that operate during fetal and postnatal development in mammals and lower vertebrates have been shown in all hormonal cell types and in folliculo‐stellate cells. More than 100 compounds have been identified that have, or may have, paracrine or autocrine actions. They include the neurotransmitters acetylcholine and γ‐aminobutyric acid, peptides such as vasoactive intestinal peptide, galanin, endothelins, calcitonin, neuromedin B and melanocortins, growth factors of the epidermal growth factor, fibroblast growth factor, nerve growth factor and transforming growth factor‐β families, cytokines, tissue factors such as annexin‐1 and follistatin, hormones, nitric oxide, purines, retinoids and fatty acid derivatives. In addition, connective tissue cells, endothelial cells and vascular pericytes may influence paracrinicity by delivering growth factors, cytokines, heparan sulphate proteoglycans and proteases. Basement membranes may influence paracrine signalling through the binding of signalling molecules to heparan sulphate proteoglycans. Paracrine/autocrine actions are highly context‐dependent. They are turned on/off when hormonal outputs need to be adapted to changing demands of the organism, such as during reproduction, stress, inflammation, starvation and circadian rhythms. Specificity and selectivity in autocrine/paracrine interactions may rely on microanatomical specialisations, functional compartmentalisation in receptor–ligand distribution and the non‐equilibrium dynamics of the receptor–ligand interactions in the loops.

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“…However, VSMC are absent from the pituitary, and are only found on large efferent arterioles in murine pancreatic islets (Lai et al 2007). Nevertheless, the microvasculature in these tissues possesses specific regulatory mechanisms to allow the control of blood flow (Satoh et al 1989). Pericytes, another type of mural cell related to VSMC, are putative candidates since they can induce vessel constriction and modify vascular diameter and blood flow (Rucker et al 2000, Peppiatt et al 2006).…”

Section: Regulation Of Blood Flowmentioning

confidence: 99%

Endocrine cells and blood vessels work in tandem to generate hormone pulses

Schaeffer¹,

Hodson²,

Lafont³

et al. 2011

Journal of Molecular Endocrinology

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Hormones are dynamically collected by fenestrated capillaries to generate pulses, which are then decoded by target tissues to mount a biological response. To generate hormone pulses, endocrine systems have evolved mechanisms to tightly regulate blood perfusion and oxygenation, coordinate endocrine cell responses to secretory stimuli, and regulate hormone uptake from the perivascular space into the bloodstream. Based on recent findings, we review here the mechanisms that exist in endocrine systems to regulate blood flow, and facilitate coordinated cell activity and output under both normal physiological and pathological conditions in the pituitary gland and pancreas.

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Ultrastructure of the hypophyseal portal vessel in mature rats. SEM and TEM observations.

Cited by 10 publications

References 10 publications

Cellular in vivo imaging reveals coordinated regulation of pituitary microcirculation and GH cell network function

Cellular in vivo imaging reveals coordinated regulation of pituitary microcirculation and GH cell network function

Paracrinicity: The Story of 30 Years of Cellular Pituitary Crosstalk

Endocrine cells and blood vessels work in tandem to generate hormone pulses

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