Recent studies have shown that adipose tissue is an active endocrine and paracrine organ secreting several mediators called adipokines. Adipokines include hormones, inflammatory cytokines and other proteins. In obesity, adipose tissue becomes dysfunctional, resulting in an overproduction of proinflammatory adipokines and a lower production of anti-inflammatory adipokines. The pathological accumulation of dysfunctional adipose tissue that characterizes obesity is a major risk factor for many other diseases, including type 2 diabetes, cardiovascular disease and hypertension. Multiple physiological roles have been assigned to adipokines, including the regulation of vascular tone. For example, the unidentified adipocyte-derived relaxing factor (ADRF) released from adipose tissue has been shown to relax arteries. Besides ADRF, other adipokines such as adiponectin, omentin and visfatin are vasorelaxants. On the other hand, angiotensin II and resistin are vasoconstrictors released by adipocytes. Reactive oxygen species, leptin, tumour necrosis factor α, interleukin-6 and apelin share both vasorelaxing and constricting properties. Dysregulated synthesis of the vasoactive and proinflammatory adipokines may underlie the compromised vascular reactivity in obesity and obesity-related disorders.

Adipokines secreted by visceral, subcutaneous, and perivascular adipocytes are involved in the regulation of vascular tone by acting as circulatory hormones (leptin, adiponectin, omentin, visfatin, angiotensin II, resistin, tumor necrosis factor-α, interleukin-6, apelin) and/or via local paracrine factors (perivascular adipocyte-derived relaxing and contractile factors). Vascular tone regulation by adipokines is compromised in obesitas and obesity-related disorders. Hypoxia created in growing adipose tissue dysregulates synthesis of vasoactive adipokines in favor of harmful proinflammatory adipokines, while the levels of the cardioprotective adipokines adiponectin and omentin decrease. Considering the potential of the role of adipokines in obesity-related vascular diseases, strategies to counter these diseases by targeting the adipokines are discussed.

No abstract

Retinal blood flow is regulated by local factors. In vitro bioassay experiments give evidence that retinal tissue from different species (dogs, pigs, sheep, cows, rats, and mice) continuously releases a factor lowering tone of isolated retinal arteries. This factor is a general relaxant as it was effective in relaxing different types of vascular as well as nonvascular smooth muscle preparations. This factor is called the retinal relaxing factor (RRF) and its characteristics do not correspond with those of the many well-known vasorelaxants found in retina (i.e., NO, prostanoids, adenosine, ADP, ATP, lactate, glutamate, GABA, taurine, adrenomedullin, CGRP, ANP, BNP, and CNP). This unknown RRF is transferable, hydrophilic, and heat-stable. Its relaxing effect is independent of the presence of the vascular endothelium and of NO-synthase, adenylyl cyclase, guanylyl cyclase, and cyclooxygenase activity. RRF might have a role in hypoxic vasodilation in retinal arteries since hypoxia induces relaxation only when retinal tissue is present. Thus, the RRF pathway is sensitive to changes in oxygen tension and might be a sensitive mechanism for adjusting vascular diameter to retinal oxygen levels. Diminished RRF release might explain the decreased retinal circulation observed in disease with atrophic retina.

No abstract