Are μ-opioid receptors involved in the control of endothelin-1 release from the pituitary gland in normal and dehydrated rats?

The role of endothelins in the regulation of pituitary function

“…Taken together, these findings suggest a possible role for ETs in the central control of fluid and electrolyte homeostasis. This idea is further supported by the observation, that in dehydrated rats ET-1, as well as vasopressin plasma levels, are increased (Plonowski et al, 1997), indicating that elevated circulating ET-1 might participate in the stimulation of vasopressin in the posterior pituitary. In addition, the content of ET-1 in the cells of the posterior lobe is significantly decreased in dehydrated rats (Yoshizawa et al, 1990;Ritz et al, 1992).…”

“…It is not clear whether endothelin-stimulated intracellular calcium plays a role in ET-1-and ET-3-induced vasopressin release since contrasting findings have been published (Ritz et al, 1992;Rossi, 1995;Nakai et al, 1999). As in the anterior and intermediate lobe, naltrexone also inhibits ET-1 expression in the posterior pituitary, indicating that ET-1 production is under the control of the m-opioid system (Plonowski et al, 1997).…”

“…All of the endothelins have been detected in the rat and ovine intermediate lobe, however ET-3 was predominant (Samson et al, 1991a;Mansour et al, 1997;Plonowski et al, 1997). In ovine pars intermedia, ET-1 was shown to colocalise with MSH-immunopositive cells (Mansour et al, 1997) ( Table 1).…”

“…Singh et al (1994) found an increased ET-1 content in the anterior lobe tissue of thyroxine-induced hypertensive rats in vivo, in comparison to euthyroid normotensive rats Plonowski et al (1997). demonstrated that not only were the plasma ET-1 levels, but also the ET-1 content in the anterior lobe, was markedly increased in dehydrated animals in comparison with euhydrated control animals, suggesting that both extra-and intrapituitary endothelins act together to normalise disturbances Review 107…”

Hydration Status and Cardiovascular Function

“…Results from one rodent study suggest that increased plasma [AVP] during hypohydration contributes to the production of ROS, elicits cerebrovascular dysfunction (via reduced vasodilator function as assessed by increasing doses of acetylcholine (Ach)), and cognitive dysfunction as AVP receptor antagonist SR49059 prevents these changes following 48 hours of water deprivation in rodents [20]. Hypohydration has also been demonstrated to increase plasma [endothelin-1] in both rodents [155] and humans [156]. This could be problematic as greater plasma [endothelin-1] has been associated with reduced peripheral vasodilatory function [157,158].…”