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

Abstract

The central nervous system plays an important role in the control of renal sodium excretion. We present here a brief review of physiologic regulation of hydromineral balance and discuss recent results from our laboratory that focus on the participation of nitrergic, vasopressinergic, and oxytocinergic systems in the regulation of water and sodium excretion under different salt intake and hypertonic blood volume expansion (BVE) conditions. High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. An increase in plasma concentrations in vasopressin (AVP), oxytocin (OT), atrial natriuretic peptide (ANP), and nitrate after hypertonic BVE was also demonstrated. The central inhibition of NOS by L-NAME caused a decrease in plasma AVP and no change in plasma OT or ANP levels after BVE. These data indicate that the increase in AVP release after hypertonic BVE depends on nitric oxide production. In contrast, the pattern of OT secretion was similar to that of ANP secretion, supporting the view that OT is a neuromodulator of ANP secretion during hypertonic BVE. Thus, neurohypophyseal hormones and ANP are secreted under hypertonic BVE in order to correct the changes induced in blood volume and osmolality, and the secretion of AVP in this particular situation depends on NOS activity. Central nervous system and hydromineral balancePrecise regulation of body fluid osmolality is essential. Osmolality is controlled by a finely tuned, intricate homeostatic mechanism that operates by adjusting both the rate of water intake and excretion. The central nervous system (CNS) plays an important role in the control of renal sodium excretion (1-7). Considerable evidence indicates that the median preoptic area (MnPO), anterior lateral hypothalamus, subfornical organ (SFO), anterior portion of the third ventricle (AV3V), supraoptic nucleus (SON), paraventricular nucleus (PVN), organum vasculosum laminae terminalis (OVLT), habenula, stria medullaris, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (1-3). Natriuresis accompanied by kaliuresis is induced by cholinergic or adrenergic stimulation of the medial septal area, MnPO, anterior lateral hypothalamus, SFO, and AV3V (1,4). Stimulation of AV3V with carbachol, a cholinergic drug, angiotensin II or hypertonic saline enhances natriuresis, which is blocked by the destruction of this brain area (1,4-7). Neurohypophyseal hormones and the control of sodium and water excretionAlthough the neuroendocrine control of sodium and water balance is not completely understood, alterations in volume and osmolality are responsible, at least in part, for changes in plasma vasopressin (AVP) concentration. Verney (8) originally demonstrated that AVP release into the blood is stimulated by the activation of os...

Carbon monoxide and nitric oxide modulate hyperosmolality-induced oxytocin secretion by the hypothalamus in vitro

“…Similar to our results, previous in vivo and in vitro studies have also shown that hyperosmotic stimulation causes an increase in OT release [30,31]. It is well known that OT inhibits salt intake, .…”

Central actions of glucocorticoids in the control of body fluid homeostasis: Review

“…Berghorn et al (37) reported that longterm hyperosmolality induced an increase in the number of receptors for glucocorticoids in magnocellular vasopressinergic cells. Furthermore, increased plasma corticosterone levels were also reported in response to salt loading (38)(39)(40). These investigators also suggested that the HPA responsiveness to either CRF or AVP seems to be impaired after long-term osmotic stimulation.…”

“…Ventura et al (40) demonstrated that the increase in plasma OT and AVP induced by salt loading was accompanied by an increased NO synthase activity in the SON and PVN, although the previous administration of NO synthase inhibitor produced different effects on the secretion of these peptides. These data indicate that NO differentially modulates the secretion of neurohypophyseal hormones in response to chronic salt loading.…”

Effects of nitric oxide on magnocellular neurons of the supraoptic nucleus involve multiple mechanisms

“…Such an effect was also reported after icv injection of angiotensin II (AngII), hypertonic solution treatment (60), and in hypovolemic rats (36). Besides this, NO seems to induce an increase in VP, but not in OT plasma levels induced by hypertonic blood volume expansion (61). Taken together, these findings indicate that, similar to what happens during hypovolemia, total and intracellular dehydration removes tonic inhibitory nitrergic modulation on VP neurons, but not on OT neurons.…”