Central inhibition of nitric oxide synthase preferentially augments release of oxytocin during dehydration

Summy-Long, Joan Y.; Bui, Vuong; Mantz, S L; Koehler, Ellen; Weisz, Judith; Kadekaro, Massako

doi:10.1016/0304-3940(93)90515-m

Cited by 118 publications

(58 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…NO was first recognized as a neuronal messenger molecule by Garthwaite et al (46), who showed that glutamate, acting on the N-methyl-Daspartate receptor in cultures of cerebellar granule cells, releases a factor with properties resembling those of NO. It is now clear that NO has a physiological role in the regulation of water balance (47). NO synthase (NOS), an enzyme involved in the synthesis of NO and constitutively expressed in neurons and endothelial cells, utilizes the semiessential amino acid L-arginine, reducing equivalents from NADPH and molecular O 2 to catalyze the formation of NO and its coproduct citrulline via a Ca 2+ -calmodulin-dependent mechanism.…”

Section: Participation Of the Nitrergic System In Hydromineral Metabomentioning

confidence: 99%

See 1 more Smart Citation

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

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

View full text Add to dashboard Cite

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...

show abstract

Section: Participation Of the Nitrergic System In Hydromineral Metabomentioning

confidence: 99%

“…It has been demonstrated that during dehydration the central inhibition of NOS preferentially augments OT release (47,53). Interestingly, the increase in NO production in the PVN and SON of hypertensive rats was ineffective in inhibiting AVP secretion (54).…”

Section: Participation Of the Nitrergic System In Hydromineral Metabomentioning

confidence: 99%

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

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

View full text Add to dashboard Cite

show abstract

“…These studies indicated that NO participates in the regulation of endocrine function in AVP and OXT system in the adult rat [15,25,26,34,35]. However, there is some disagreement as to the extent of this coexistence, mainly due to technical problems [27].…”

Section: Posterior Pituitarymentioning

confidence: 99%

“…Stimulatory action was augmented by inhibitors of NO formation, suggesting that endogenous NO has an inhibitory effect on the release of these peptides [30,34,35].…”

Section: Posterior Pituitarymentioning

confidence: 99%

Postnatal Development of NADPH-Diaphorase Activity in the Rat. The Role of Nitric Oxide in the Ontogeny of Arginine Vasopression and Oxytocin.

et al. 2000

View full text Add to dashboard Cite

Abstract.To clarify the role of nitric oxide (NO) in the ontogeny of arginine vasopressin (AVP) and oxytocin (OXT) neurons in the hypothalamo-neurohypophysial system (HNS), we observed the coexpression pattern of NADPHdiaphorase (NADPH-d) activity and AVP-or OXT-immunoreactivity (IR) in the rat hypothalamus and posterior pituitary during the postnatal period. The enzymatic activity of NADPH-d was observed in the supraoptic nucleus (SON), paraventricular nucleus (PVN), median eminence (ME) and posterior pituitary throughout the postnatal development. AVP-containing neurons were clearly observed from postnatal day 1 in both the SON and PVN, while OXT-containing neurons were recognized from postnatal day 14. The coexistence of NADPH-d and AVP or OXT was detected in the SON from postnatal day 14. At postnatal day 21, the coexpression pattern was approximately the same as that of the SON and PVN in adult rats. Our findings indicated that the expression of NADPH-d and OXT was observed from almost the same postnatal period in both the SON and PVN. In addition, the pattern of increased numbers of NADPH-d positive fibers was similar to that of OXT-immunoreactive fibers in both the inner layer of the ME and the posterior pituitary.A good correlation was thus obtained between OXT expression and NADPH-d activity in the HNS during postnatal development.The present study suggests that NO is more closely involved in the expression and regulation of secretion of OXT than AVP.

show abstract

“…Some studies have demonstrated that hypothalamic NO inhibits release of AVP [17,19,20] and central NO tonically inhibits basal release of AVP and oxytocin [21,22]. Thus, NO may play an important role in the modulation of secretion of AVP and oxytocin in the hypothalamo-neurohypophysial system [17,19,23].…”

Section: : 640±648]mentioning

confidence: 99%

Upregulation of hypothalamic nitric oxide synthase gene expression in streptozotocin-induced diabetic rats

et al. 1998

View full text Add to dashboard Cite

The peripheral administration of streptozotocin (STZ) causes marked hyperglycaemia, plasma hyperosmolality, hypoinsulinaemia, hyperphagia and polydipsia. In STZ-induced diabetic animals, insulin treatment reverses these symptoms. Several studies have demonstrated that insulin deficiency induced diabetes causes alteration of hypothalamic transmitters and the gene expressions of neuropeptides [1±7]. These studies suggest that the alteration of monoamine and neuropeptides in the hypothalamus may play a role in the multiple behavioural and hormonal abnormalities in STZ-induced diabetic rats.Recent studies have demonstrated that nitric oxide (NO) may be associated with various functions of the central nervous system, including feeding [8±12] and drinking behaviour [13,14]. It has been demonstrated that both systemic administration of a competitive antagonist of NO synthase (NOS) and Diabetologia (1998) Summary Plasma arginine vasopressin (AVP) is known to be elevated in patients with uncontrolled insulin-dependent diabetes mellitus who have plasma hyperosmolality with hyperglycaemia. Although osmotic stimuli cause an increase in nitric oxide synthase (NOS) activity as well as synthesis of AVP and oxytocin in the paraventricular (PVN) and supraoptic nuclei (SON), it is not known whether NOS activity in the hypothalamus changes in the diabetic patients who have plasma hyperosmolality with hyperglycaemia caused by insulin deficiency. Expression of the neuronal (n) NOS gene in the PVN and SON in streptozotocin (STZ)-induced diabetic rats was investigated by using in situ hybridization histochemistry and NADPH-diaphorase histochemical staining. Four weeks after intraperitoneal (i. p.) administration of STZ, male Wistar rats developed hyperglycaemia and plasma hyperosmolality. The expression of nNOS gene and NADPH-diaphorase staining in the PVN and SON remarkably increased in STZ-induced diabetic rats compared to control rats. Three weeks after administration of STZ, the diabetic rats were subcutaneously treated with insulin for 1 week, which resulted in significant suppression of the induction of nNOS, AVP and oxytocin gene expression in the PVN and SON. Furthermore, the induction of nNOS gene expression in the PVN and SON was suppressed in STZ-induced diabetic rats treated with phlorizin and diet to normalize hyperglycaemia without insulin treatment. These results suggest that upregulation of nNOS gene expression as well as AVP and oxytocin gene expression in the PVN and SON in STZ-induced diabetic rats may be associated with hyperglycaemia and plamsa hyperosmolality. [Diabetologia (1998) 41: 640±648]

show abstract

Central inhibition of nitric oxide synthase preferentially augments release of oxytocin during dehydration

Cited by 118 publications

References 20 publications

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

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

Postnatal Development of NADPH-Diaphorase Activity in the Rat. The Role of Nitric Oxide in the Ontogeny of Arginine Vasopression and Oxytocin.

Upregulation of hypothalamic nitric oxide synthase gene expression in streptozotocin-induced diabetic rats

Contact Info

Product

Resources

About