Brain vasopressin and sodium appetite

Abstract

ventricular injections of vasopressin (VP) and antagonists with varying degrees of specificity for the VP receptors were used to identify the action of endogenous brain VP on 0.3 M NaCl intake by sodium-deficient rats. Lateral ventricular injections of 100 ng and 1 g VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. 8 ]VP (MeT-AVP) significantly suppressed NaCl intake by sodium-deficient rats without causing motor disturbances. MeT-AVP had no effect on sucrose intake (0.1 M). In contrast, the selective V2 receptor antagonist had no significant effect on NaCl intake. Last, injections of 100 ng MeT-AVP decreased mean arterial blood pressure (MAP), whereas 100 ng VP elevated MAP and pretreatment with MeT-AVP blocked the pressor effect of VP. These results indicate that the effects produced by 100 ng MeT-AVP represent receptor antagonistic activity. These findings suggest that the effect of exogenous VP on salt intake is secondary to motor disruptions and that endogenous brain VP neurotransmission acting at V1 receptors plays a role in the arousal of salt appetite. neurohypophysial peptides; taste; blood pressure; V 1 receptor; V2 receptor VASOPRESSIN (VP) has diverse biological actions and target systems. In addition to the well-known neuroendocrine effects, VP meets the criteria for a brain neurotransmitter. For example, it is synthesized in several brain nuclei, including the paraventricular nucleus of the hypothalamus, medial amygdala, and bed nucleus of the stria terminalis (1, 5). Also, physiological stimuli trigger the release of VP in specific brain regions where it exerts its effects on pre-and postsynaptic membranes (11, 31).VP exerts its effects through receptors that have been divided into two broad classes, the V 1 and V 2 receptors. The V 1 class can be further divided into the V 1a and V 1b receptors (16,17,42). The receptors differ in their distribution and associated second messenger system (17). Neurons that synthesize VP have extensive vasopressinergic projections to sites along the neuraxis, including the septum, hippocampus, amygdala, subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT), nucleus of the solitary tract, dorsal motor nucleus of the vagus, and spinal cord (1,29,40). Radioligand receptor autoradiography and in situ hybridization results indicate that VP binding sites are distributed in the brain and that the distribution of these sites often overlaps with the terminal distributions of vasopressinergic neurons (22,32,46).Brain release and pituitary release of VP often parallel one another. For example, systemic osmotic and hypovolemic stimuli that increase circulating VP levels also stimulate the release of VP in the lateral septum and lateral ventricle (4). Manipulations that facilitate salt intake can also stimulate the systemic release of VP. The simultaneous administration of furosemide and a low dose of the angiotensin-converting enzyme captopril arouses a sodium appetite and increases ...

SGK1 as a determinant of kidney function and salt intake in response to mineralocorticoid excess

“…Mineralocorticoids have further been shown to upregulate Fos (41,42), angiotensin receptors (51), oxytocin receptors (51), vasopressin (20), and the vasopressin V 1a receptor (41,42). Vasopressin (11) and angiotensin II (9,29,45,50,51) in turn stimulate, whereas oxytocin (53) inhibits, salt intake. Interestingly, the effect of mineralocorticoids or salt depletion on salt appetite may be modified by glucocorticoids (18,34,50) and amphetamine (5).…”

Ventral Pallidum Firing Codes Hedonic Reward: When a Bad Taste Turns Good

“…Sodium depletion was induced by injections of furosemide (7.5 mg/kg, administered subcutaneously [sc]) and deoxycorticosterone acetate (DOCA, 5 mg/kg, sc) (Flynn et al 2005), followed 2 h later by an additional injection of 7.5 mg/kg furosemide (Tamura and Norgren 1997). Pilot studies indicated that this combination induced a more robust behavioral salt appetite than either single hormone alone in our lab and therefore the combination was selected for this electrophysiological and taste reactivity study (personal observations).…”

Centrally administered vasopressin cross-sensitizes rats to amphetamine and drinking hypertonic NaCl

“…Rats were removed from the home cage, administered an intraventricular injection of angiotensin II (50 g/3 l; Sigma, St. Louis, MO), and returned to the cage. Water intake was measured for 20 min, and rats were determined to have correct placement of a patent cannula if they drank Ͼ5.0 ml of water following the angiotensin II injection (13,14). The experiments began 1-2 wk later.…”

“…In addition, the neurohypophyseal hormones, oxytocin and VP, are associated with the control of sodium balance (14). More specifically, many treatments that arouse the ingestion of sodium solutions also stimulate the release of VP into the blood (15,18,22,47,55).…”