Vasodilator Effects of Leptin on Canine Isolated Mesenteric Arteries and Veins

Abstract

1. Although leptin increases sympathetic nerve activity and blood pressure, its direct action on large arterial rings is to cause relaxation. However, it is the small resistance arteries and veins that are important in blood pressure control. The effects of leptin on these small vessels has not been reported previously in the canine and the effect of leptin on the capacitance vessels is not known. 2. In the present study, third- or fourth-order canine mesenteric arteries and veins were isolated and placed in a perfusion myograph and preconstricted with noradrenaline. The responses to graded concentrations of leptin were determined and the role of nitric oxide was assessed by administration of N(G)-nitro-l-arginine methyl ester (l-NAME), a blocker of nitric oxide synthase. 3. Leptin induced dose-related dilatations in both arterial and venous segments. The mean (+/-SEM) maximum increases in the diameter of the arteries and veins were 25.0 +/- 4.8 and 29.9 +/- 2.0% of the initial preconstriction, respectively. Relaxations of both arteries and veins were abolished by l-NAME or by endothelium denudation, although dilatations were still obtained to sodium nitroprusside, a nitric oxide donor. 4. These results indicate that leptin dilates canine small mesenteric arteries and veins by a mechanism involving endothelial release of nitric oxide. This observation may result in a decrease of peripheral resistance and venous return and, hence, counteract the leptin-induced neurally mediated vasoconstriction that has been reported previously.

Vascular dysfunction in young, mid-aged and aged mice with latent cytomegalovirus infections

“…As aged mice are no longer reproductively active (24), increased uterine artery blood flow is less important than in young and mid-aged mice. In contrast, it is essential to compensate for vascular dysfunction in systemic (mesenteric) vascular beds that regulate blood pressure and cardiovascular function (36). The increase in ME-dependent vasodilation in mesenteric arteries from aged latently infected mice does not appear to be dependent on NOS or prostaglandin activity or an increase in smooth muscle sensitivity to NO, similar to findings in cremaster arteries from young persistently CMV-infected mice (31).…”

The Relationship between Changes in Body Mass Index and Retinal Vascular Caliber in Children

“…39 Leptin, expressed in excess by adipose cells, could increase nitric oxide synthesis leading to venular dilatation. 40 Second, an increase in body mass may exert an effect on the microvasculature independent of inflammation, 24 as part of a wider metabolic derangement similar to the alteration in microvascular perfusion seen in diabetes. 41 Third, the venous system is a major reservoir for blood volume, which may increase in persons with greater body mass because of growth.…”

The influence of perivascular adipose tissue on vascular homeostasis

“…Similarly to adiponectin, leptin plays other important roles systemically, such as modulating the endocrine hypothalamic-pituitary signals to the gonads, thyroid, and the adrenal gland, as well as modulating insulin sensitivity, bone metabolism, and immune system function. In the cardiovascular system, where the six leptin receptors are also expressed, the effects of leptin are generally those of vasodilation, producing hypotension upon acute in vivo infusion and exerting direct vasodilatory effects on various vascular beds 24–26. Leptin-induced vasorelaxation may be mediated by endothelial NO-dependent or independent mechanisms 26–28.…”