**1. Introduction**

Edema is characterized as a swelling caused by an increase of fluids in the interstitial space. Interstitial liquid deregulation causes liquid accumulation in the body with harmful consequences to tissues and organs [1, 2]. The physiologist Ernest Starling defined the interaction between the fluids forces in blood vessels. The fluid movement (FM) in the blood vessel is correlated with blood vessel wall permeability (constant Kf) and the difference between hydrostatic pressure variations (ΔP) and colloid osmotic pressure (Δπ) forces [1, 3]. The following mathematical equation (Starling's equation) describes this interaction: FM = Kf. (ΔP- Δπ).

The liquid retention becomes harmful to tissues affecting the cellular balance and homeostasis. Several factors induce this phenomenon: hormones, plasma proteins, inflammation, infectious diseases, and disturbs in some organs [3–5]. After an injury, inflammatory mediators cause physiological reactions in the lesioned region. Some of these inflammatory molecules include interleukins (IL-1β, IL-6, and IL-18), tumor necrosis factor-alpha (TNF-α), vasodilators, arachidonic acid metabolites, nitric oxide (NO), among others [6–8]. The inflammatory agent overproduction mediates increase in vascular permeability and leukocyte recruitment, causing edema formation and hyperalgesia [2, 9].

Membrane receptors are a group of functional proteins located in the plasma and organelles membranes. These receptors are able to trigger intracellular chemical cascades [10]. Approaches in the pharmacological field investigated several plasma membrane receptors modulating inflammation [11], such as the purinergic system, TRP channels, and pattern recognition receptors (PRRs), are commonly associated with inflammatory pathways [12–16]. Therefore, this chapter will address the plasma membrane receptors modulation on inflammatory agents and subsequent edema formation.
