Brain Serotonergic Receptors and Control of Fluid Intake and Cardiovascular Function in Rats

Excerpt

Body fluid homeostasis is maintained by a steady-state interchange of water between extracellular fluid (ECF) and intracellular fluid compartments. The main source of body water in terrestrial vertebrates is from drinking and, once in the body, it is distributed between body fluid compartments. The mechanisms that keep the body fluid osmolarity within its narrow range (280–300 mOsm/L) depend on matching the water volume excreted by the kidneys and the fluid intake volume. Sodium is the main electrolyte in ECF and sodium loss or gain is usually accompanied by an increase or decrease in water in this compartment in order to maintain sodium concentration. Body sodium and fluid balance is achieved through mechanisms that control sodium intake and sodium urinary excretion. The relationship between water and sodium in ECF may change both the osmolarity and volume of this compartment. Whereas the osmolarity of ECF is regulated by water intake and renal water excretion, the volume is controlled by the sodium content in the ECF, which is determined by the amount of sodium intake and the amount of sodium excreted in the urine (Verbalis 2003).

Changes in the water and sodium content of ECF may result in severe consequences to the cardiovascular system. Furthermore, some pathological cardiovascular conditions may lead to changes in body fluid homeostasis. Increased sodium levels in ECF increase the effective circulating volume, leading to an enhancement in cardiac output and blood pressure (BP). On the other hand, heart failure may decrease water and sodium urinary excretion, promoting a fluid disorder in the body. Therefore, it is unsurprising to find overlapping mechanisms controlling cardiovascular function and body fluid homeostasis.

Multiple sensory signals that trigger thirst and sodium appetite in response to dehydration are basically produced by hyperosmolarity and/or hypovolemia of the ECF (Fitzsimons 1998; Johnson 2007; McKinley and Johnson 2004; Stricker and Sved 2000; Chapters 2, 3, 4, and 9 of this book). Such sensory information reaches the brain to facilitate or inhibit responses that correct changes in body fluid–mineral balance and control cardiovascular function, thus activating a neural network of noradrenergic, cholinergic, angiotensinergic, GABAergic, vasopressinergic, oxytocinergic, and serotonergic pathways (Johnson 2007).