Rat heart: A site of oxytocin production and action

Jankowski, Marek; Hajjar, Fadi; Kawas, Sausan Al; Mukaddam‐Daher, Suhayla; Hoffman, Gloria E.; McCann, Samuel M.; Gutkowska, Jolanta

doi:10.1073/pnas.95.24.14558

Cited by 171 publications

(143 citation statements)

References 25 publications

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“…Interestingly, most transcription factors identified so far in the heart are also present in other muscle cells, and myoblast transplantation to the injured heart improves regional systolic heart function (38). Assuming similarities in the differentiation mechanisms of skeletal and cardiac muscles and the expression (15) of both OT and OTR in these cells (8,37), we can speculate that OT plays a role in cardiac muscle regeneration.…”

Section: Discussionmentioning

confidence: 99%

“…The first-strand cDNA (5 l) was then used for PCR amplification with OT, OTR, or GAPDH exon-specific oligonucleotide primers in a Robocycler Gradient 40 thermocycler (Stratagene). Conditions for RT-PCR analysis of GAPDH, rat OT, and OTR transcripts (7,8) and mouse OTR (10) have already been described. OTR expression also was investigated in the human heart by using cDNA of Human Cardiovascular System MTC Panel (no.…”

Section: Methodsmentioning

confidence: 99%

“…7930 mesh 140, Corning). The RIA was developed in our laboratory by using specific antibodies generated against OT nonapeptide (8). Synthetic OT (Peninsula Laboratories) was labeled with Na 125 I by the lactoperoxidase method, and 200 l of sample or standards (0-200 pg) was incubated with 100 l of antibody (1:80,000) for 24 h at 4°C.…”

Section: Methodsmentioning

confidence: 99%

“…In addition, we have demonstrated that in isolated, perfused hearts, an OT antagonist (OTA) blocks basal ANP release (7), suggesting the presence of local OT in the heart. Further study revealed cardiac OT synthesis (8), with OT being detected in the medium of cultured neonatal rat cardiomyocytes (9).…”

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confidence: 99%

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Oxytocin in cardiac ontogeny

Jankowski

Danalache²,

Wang³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

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102

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Previous studies demonstrated the presence of oxytocin (OT) and oxytocin receptors (OTRs) in the heart. The present work provides results supporting a potential role of OT in cardiomyogenesis. Here, we show a maximal OT and OTR protein level in the developing rat heart at day 21 of gestation and postnatal days 1-4, when cardiac myocytes are at a stage of intense hyperplasia. Between postnatal days 1 and 66, OT decreased linearly in all heart chambers (4.1-to 6.6-fold). Correspondingly, immunocytochemistry demonstrated that OTRs, which were eminent in postnatal cardiomyocytes, declined with age to low levels in adults. Interestingly, in coronary vasculature, OTRs developed in endothelial cells at postnatal days 12 and 22 and achieved a plateau in adult rats. These findings suggest that OT can be involved in developmental formation of the coronary vessels. In vivo, the OT͞OTR system in the fetal heart was sensitive to the actions of retinoic acid (RA), recognized as a major cardiac morphogen. RA treatment produced a significant increase (2-to 3-fold) both in the OT concentration and in the OT mRNA levels. Ex vivo, an OT antagonist inhibited RA-mediated cardiomyocyte differentiation of P19 embryonic stem cells. The decline of cardiac OT expression from infancy to adulthood of the rat and changes in cell types expressing OTR indicate a dynamic regulation of the OT system in the heart rather than constitutive expression. The results support the hypothesis that RA induces cardiomyogenesis by activation of the cardiac OT system. heart development ͉ oxytocin receptors ͉ retinoic acid ͉ oxytocin antagonist ͉ cardiomyocyte differentiation O xytocin (OT), recognized traditionally as a reproductive hormone with a major role in childbirth and lactation, is produced in high concentrations in the hypothalamic supraoptic nucleus and paraventricular nucleus, then transported from these source nuclei to the posterior pituitary by neurosecretion (1). Longitudinal studies of neural and hormonal circuits activated by experimental volume expansion have identified OT as a major regulator of cardiovascular functions (reviewed in refs. 2 and 3). OT, injected peripherally, causes a decrease of arterial pressure (4) while reducing both heart rate and the force of contractions in isolated atria (5). OT acts via neuroendocrine͞ endocrine͞paracrine pathways to release atrial natriuretic peptide (ANP) from the heart (6, 7). ANP is a potent diuretic, natriuretic, and vasorelaxant hormone that is also involved in cell growth regulation. In addition, we have demonstrated that in isolated, perfused hearts, an OT antagonist (OTA) blocks basal ANP release (7), suggesting the presence of local OT in the heart. Further study revealed cardiac OT synthesis (8), with OT being detected in the medium of cultured neonatal rat cardiomyocytes (9).Recently, we showed that P19 embryonic carcinoma cells, a model of mouse embryonic stem cells, express OT receptors (OTRs), and OT stimulates the differentiation of these cells into beating cell colonies expressing ...

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

See 2 more Smart Citations

Oxytocin in cardiac ontogeny

Jankowski

Danalache²,

Wang³

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

102

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“…In addition, using polymerase chain reaction (PCR) amplification of cDNA obtained from mRNA of both rat atria and ventricles, the presence of specific transcripts was also demonstrated. The OT and OT receptor transcripts were also shown by in situ hybridization in atrial and ventricular tissues using RT-PCR (22,43). Consequently, OT released from the neural lobe may reach the heart by the circulation to induce ANP release, but the intracardiac OT might also play a paracrine role in stimulating ANP release.…”

Section: Natriuretic Peptides and Hydromineral Balancementioning

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

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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...

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Neuroendocrine Regulation of Hydromineral Homeostasis

Mecawi

Ruginsk

Elias

et al. 2015

Comprehensive Physiology

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Since the crucial evolutionary change from an aqueous to a terrestrial environment, all living organisms address the primordial task of equilibrating the ingestion/production of water and electrolytes (primarily sodium) with their excretion. In mammals, the final route for the excretion of these elements is mainly through the kidneys, which can eliminate concentrated or diluted urine according to the requirements. Despite their primary role in homeostasis, the kidneys are not able to recover water and solutes lost through other systems. Therefore, the selective stimulation or inhibition of motivational and locomotor behavior becomes essential to initiate the search and acquisition of water and/or sodium from the environment. Indeed, imbalances affecting the osmolality and volume of body fluids are dramatic challenges to the maintenance of hydromineral homeostasis. In addition to behavioral changes, which are integrated in the central nervous system, most of the systemic responses recruited to restore hydroelectrolytic balance are accomplished by coordinated actions of the cardiovascular, autonomic and endocrine systems, which determine the appropriate renal responses. The activation of sequential and redundant mechanisms (involving local and systemic factors) produces accurate and self-limited effector responses. From a physiological point of view, understanding the mechanisms underlying water and sodium balance is intriguing and of great interest for the biomedical sciences. Therefore, the present review will address the biophysical, evolutionary and historical perspectives concerning the integrative neuroendocrine control of hydromineral balance, focusing on the major neural and endocrine systems implicated in the control of water and sodium balance.

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Rat heart: A site of oxytocin production and action

Cited by 171 publications

References 25 publications

Oxytocin in cardiac ontogeny

Oxytocin in cardiac ontogeny

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

Neuroendocrine Regulation of Hydromineral Homeostasis

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