Perivascular adipose tissue: An immune cell metropolis.

NEW FINDINGS: What is the topic of this review? The review discusses how eosinophils can contribute to the function of perivascular adipose tissue and explores the mechanisms involved. What advances does it highlight? Understanding the communication between the cell populations that constitute perivascular adipose tissue function is important for exploring therapeutic options in the treatment of obesity-related cardiovascular complications. This article highlights that eosinophils are able to contribute directly to healthy perivascular adipose tissue function. These immune cells contribute to adrenergic signalling and nitric oxide- and adiponectin-dependent mechanisms in perivascular adipose tissue. ABSTRACT: Perivascular adipose tissue is a heterogeneous tissue that surrounds most blood vessels in the body. This review focuses on the contribution of eosinophils located within the adipose tissue to vascular contractility. A high-fat diet reduces the number of these immune cells within perivascular adipose tissue, and this loss is linked to an increase in vascular contractility and hypertension. We explored the mechanisms by which eosinophils contribute to this function using genetically modified mice, ex vivo assessment of contractility and pharmacological tools. We found that eosinophils contribute to adrenergic signalling and nitric oxide- and adiponectin-dependent mechanisms in perivascular adipose tissue. It is now important to explore whether manipulation of these pathways in obesity can alleviate cardiovascular complications, in order to determine whether eosinophils are a valid target for obesity-related disease.

Responses of isolated pressurised rat uterine arteries to changes in pressure: effects of pre-constriction, endothelium and pregnancy.

Pregnancy-induced changes in uterine artery function play a critical role in ensuring adequate placental perfusion. Responses of these vessels to pressure (myogenic responsiveness) may contribute to this. The overall myogenic properties of uterine arteries may depend upon the integration of a number of different factors, including effects of pre-constrictor stimuli, and should be considered in terms of both initial and stable diameters both of which may be modulated by pregnancy. This study thus investigated the effects of pre-constriction, the endothelium and pregnancy on responses of isolated rat uterine arteries to changes in intravascular pressure (IvP). The effects on both the immediate transient diameter changes and stable diameters (myogenic tone) were studied. Isolated 3rd order uterine arteries from non-pregnant and days 19-21 pregnant Sprague-Dawley rats were mounted on a pressure myograph and responses to changes in IvP (20-120 mm Hg) examined. Arteries did not exhibit active responses to pressure in the absence of stimulation, however, all showed active myogenic constriction when pre-constricted by depolarization (30 or 60mM KCl) or arginine vasopressin (AVP). Pregnancy enhanced stable levels of myogenic tone with AVP, but not depolarization. This difference was not dependent upon the endothelium. Initial peak diameters were enhanced in arteries from pregnant rats due to endothelium-dependent mechanisms. Thus, both the peak and stable response of isolated rat uterine arteries to pressure can be differentially regulated and thus must both be considered when considering the influence of pressure on uterine artery reactivity during pregnancy.