Oxytocin mediates atrial natriuretic peptide release and natriuresis after volume expansion in the rat.

Abstract

Our previous studies have shown that stimulation of the anterior ventral third ventricular region increases atrial natriuretic peptide (ANP) release, whereas lesions of this structure, the median eminence, or removal of the neural lobe of the pituitary block ANP release induced by blood volume expansion (BVE). These results indicate that participation of the central nervous system is crucial in these responses, possibly through mediation by neurohypophysial hormones. In the present research we investigated the possible role of oxytocin, one of the two principal neurohypophysial hormones, in the mediation of ANP release. Oxytocin (1-10 nmol) injected i.p. caused significant, dose-dependent increases in urinary osmolality, natriuresis, and kaliuresis. A delayed antidiuretic effect was also observed. Plasma ANP concentrations increased nearly 4-fold (P < 0.01) 20 min after i.p. oxytocin (10 nmol), but there was no change in plasma ANP values in control rats. When oxytocin (1 or 10 nmol) was injected i.v., it also induced a dose-related increase in plasma ANP at 5 min (P < 0.001). BVE by intra-atrial injection of isotonic saline induced a rapid (5 min postinjection) increase in plasma oxytocin and ANP concentrations and a concomitant decrease in plasma arginine vasopressin concentration. Results were similar with hypertonic volume expansion, except that this induced a transient (5 min) increase in plasma arginine vasopressin. The findings are consistent with the hypothesis that baroreceptor activation of the central nervous system by BVE stimulates the release of oxytocin from the neurohypophysis. This oxytocin then circulates to the right atrium to induce release ofANP, which circulates to the kidney and induces natriuresis and diuresis, which restore body fluid volume to normal levels.Our previous studies have shown that the central nervous system controls atrial natriuretic peptide (ANP) release; osmotic, cholinergic, and noradrenergic stimulation of the anterior ventral third ventricular (AV3V) region induces ANP release (1). Conversely, lesions of the AV3V region decreased resting plasma ANP concentrations and largely blocked ANP release in response to blood volume expansion (BVE) (2). Neurons containing ANP, termed ANPergic neurons, have their perikarya in the AV3V region and axons that project to the median eminence and neural lobe of the pituitary gland (3-5). These appear critical to the volume expansion-induced release of ANP since antisera directed against ANP injected into the third ventricular region of rats (6) or sheep (7) can inhibit volume expansion-induced ANP release.Lesions of the median eminence or neural lobe of the pituitary gland, which interrupt neuronal pathways projecting from the AV3V region to the neurohypophysis, blocked volume expansion-induced ANP release (2). Therefore, we hypothesized that release of one or more neuropeptides from the neurohypophysis caused the increase in ANP release after volume expansion. As indicated above, the axons of ANP neurons terminate in the neuro...

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

“…Several lines of evidence indicate a possible physiologic function of OT in the mediation of ANP release since ip or iv injection of OT causes a dose-dependent increase in plasma ANP, urinary osmolality, natriuresis, kaliuresis, and a delayed antidiuretic effect (19). Isotonic BVE releases OT and ANP, but not AVP.…”

“…Oxytocin (OT) is also involved in hydromineral homeostasis and vascular and cardiac relaxation (17)(18)(19)(20)(21)(22)(23). It has long been recognized that OT increases renal electrolyte excretion in various species, and that the natriuretic and kaliuretic effects are AVP independent.…”

“…It has long been recognized that OT increases renal electrolyte excretion in various species, and that the natriuretic and kaliuretic effects are AVP independent. OT and AVP are secreted simultaneously in response to hyperosmolality and hypovolemia (19,24,25) and when systemically administered (iv or ip) induce natriuresis (26,27). OT is a more potent natriuretic hormone than AVP.…”

Oxytocin induces differentiation of P19 embryonic stem cells to cardiomyocytes

“…OT's indirect actions could be related to its cardiovascular functions observed in adult rats (7,(21)(22)(23). Indeed, we uncovered the entire OT͞OTR system in the rat heart, and showed that cardiac OTR activation is coupled to the release of atrial natriuretic peptide (ANP), a potent diuretic, natriuretic, and vasorelaxant hormone that is also involved in cell growth regulation (7,8).…”

Controle reflexo da pressão arterial: qual o papel da ocitocina como neurotransmissor autonômico?

“…Este peptídeo é classicamente estudado pela grande importância na função reprodutora, no entanto, a literatura científica relata que a OT liberada na circulação promove ajustes hidroeletrolíticos e cardiovasculares aumentando a natriurese, diminuindo a força de contração e frequência cardíaca (FC) (CHAN;SAWYER, 1962;COSTA-E-SOUSA et al, 2005;HAANWINCKEL et al, 1995). Na década de 1990 surgiram trabalhos sugerindo a relevância da OT não somente como hormônio, mas também como neurotransmissor.…”