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Items: 4

1.
Figure 1

Figure 1. From: Perivascular adipose tissue from human systemic and coronary vessels: the emergence of a new pharmacotherapeutic target.

PVAT is the source of a number of vasoactive and metabolically significant adipokines.

Reza Aghamohammadzadeh, et al. Br J Pharmacol. 2012 Feb;165(3):670-682.
2.
Figure 4

Figure 4. From: Perivascular adipose tissue from human systemic and coronary vessels: the emergence of a new pharmacotherapeutic target.

The presence of macrophages is the key modulator of increased vascular contractility in vessels with hypoxic PVAT (). (A) When PVAT from mouse vessels is rendered hypoxic, there is increased sensitivity of the vessel to cumulative doses of noradrenaline. (B) In CD11b–diphtheria toxin (DT) receptor (DTR) transgenic mice (DT administration selectively kills monocytes/macrophages), hypoxia has no effect on vascular contractility. KPSS, high potassium physiological saline solution; NE, norepinephrine.

Reza Aghamohammadzadeh, et al. Br J Pharmacol. 2012 Feb;165(3):670-682.
3.
Figure 3

Figure 3. From: Perivascular adipose tissue from human systemic and coronary vessels: the emergence of a new pharmacotherapeutic target.

Effect of obesity and the metabolic syndrome on anticontractile capacity of PVAT on small arteries from subcutaneous gluteal fat, *P < 0.01 (). (A) In healthy control participants PVAT exerts a significant anticontractile effect (P = 0.009, multiple anova) when compared with contractility of arteries without PVAT (n = 10). (B) In patients with obesity and metabolic syndrome, presence of PVAT has no effect on contractility (n = 10). KPSS, high potassium physiological saline solution; NA, noradrenaline.

Reza Aghamohammadzadeh, et al. Br J Pharmacol. 2012 Feb;165(3):670-682.
4.
Figure 2

Figure 2. From: Perivascular adipose tissue from human systemic and coronary vessels: the emergence of a new pharmacotherapeutic target.

Potential mechanisms via which perivascular adipocytes, vascular smooth muscle cells and endothelial cells interact. Dotted lines represent unproven pathways. ADRF, adventitium-derived relaxing factor; AMPK, AMP-activated protein kinase; Ang II, angiotensin II; BKca, large conductance calcium-activated potassium channel; H2O2, hydrogen peroxide; ERK, extracellular signal-regulated kinases; 5-HT, 5-hydroxytryptamine (serotonin); GTP, guanosine triphosphate; cGMP, cyclic guanosine monophosphate; IP3, inositol triphosphate; IRAG, IP3 receptor-associated cGMP kinase substrate; IKca, intermediate conductance calcium-activated potassium channel; Kv, voltage-gated potassium channel; KATP, ATP-sensitive potassium channel; L-Arg, L-Argine; NA, noradrenaline; NO, nitric oxide; NOS, nitric oxide synthase; O2.-, superoxide anion; ONOO, peroxynitrite; PCS, prostacyclin pathway; PHE, phenylephrine; PGH2,prostaglandin H2; PGI2, prostaglandin I2 (prostacyclin); PKG, protein kinase G; R, receptor; sGC, soluble guanylate cyclise; SKca, small conductance calcium-activated potassium channel; SOD, superoxide dismutase; SR, sarcoplasmic reticulum; TNF, tumour necrosis factor; VSMC, vascular smooth muscle cell.

Reza Aghamohammadzadeh, et al. Br J Pharmacol. 2012 Feb;165(3):670-682.

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