Effect of Neurotransmitters and Neuropeptides on Vasopressin Release

Sladek, Celia D.; Armstrong, William E.

doi:10.1007/978-1-4615-8129-1_7

Cited by 38 publications

(21 citation statements)

References 337 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ANG II is known to stimulate the synthesis of AVP and its release from the posterior pituitary (35). To eliminate any potential contribution of AVP to the attenuated renal SNA response to VE we observed in ANG II-infused animals, we blocked AVP V 1 receptors.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

LaGrange

Toney

Bishop

2003

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

In this study the hypothesis was tested that chronic infusion of ANG II attenuates acute volume expansion (VE)-induced inhibition of renal sympathetic nerve activity (SNA). Rats received intravenous infusion of either vehicle or ANG II (12 ng·kg −1 ·min −1 ) for 7 days. ANG II-infused animals displayed an increased contribution of SNA to the maintenance of mean arterial pressure (MAP) as indicated by ganglionic blockade, which produced a significantly (P < 0.01) greater decrease in MAP (75 ± 3 mmHg) than was observed in vehicle-infused (47 ± 8 mmHg) controls. Rats were then anesthetized, and changes in MAP, mean right atrial pressure (MRAP), heart rate (HR), and renal SNA were recorded in response to right atrial infusion of isotonic saline (20% estimated blood volume in 5 min). Baseline MAP, HR, and hematocrit were not different between groups. Likewise, MAP was unchanged by acute VE in vehicle-infused animals, whereas VE induced a significant bradycardia (P < 0.05) and increase in MRAP (P < 0.05). MAP, MRAP, and HR responses to VE were not statistically different between animals infused with vehicle vs. ANG II. In contrast, VE significantly (P < 0.001) reduced renal SNA by 33.5 ± 8% in vehicle-infused animals but was without effect on renal SNA in those infused chronically with ANG II. Acutely administered losartan (3 mg/kg iv) restored VEinduced inhibition of renal SNA (P < 0.001) in rats chronically infused with ANG II. In contrast, this treatment had no effect in the vehicle-infused group. Therefore, it appears that chronic infusion of ANG II can attenuate VE-induced renal sympathoinhibition through a mechanism requiring AT 1 receptor activation. The attenuated sympathoinhibitory response to VE in ANG II-infused animals remained after arterial barodenervation and systemic vasopressin V 1 receptor antagonism and appeared to depend on ANG II being chronically increased because ANG II given acutely had no effect on VE-induced renal sympathoinhibition. Keywordssympathetic nerve activity; cardiopulmonary reflex; body fluid balance; arterial baroreceptor reflex Numerous studies have investigated interactions between circulating ANG II and the arterial baroreceptor reflex. Whereas recent studies indicate that an acute increase in circulating ANG II can attenuate the increase in sympathetic nerve activity (SNA) that follows arterial baroreceptor unloading (34), chronic increases of ANG II have been repeatedly demonstrated to reset arterial baroreflex control of SNA (4, 6). The latter effect may permit SNA to rise relative to the prevailing level of arterial pressure. In addition to the arterial Copyright © 2003 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript baroreflex, the cardiopulmonary baroreflex is also an important determinant of sympathetic outflow as well as sodium and water balance. However, the extent to which chronic increases of ANG II might interact with this reflex to modify the SNA response to volume expansion (VE) is not known. This is surprising given that norma...

show abstract

Section: Discussionmentioning

confidence: 99%

“…After tracheal cannulation, rats were ventilated with oxygen-enriched room air. End-tidal PCO 2 was maintained within normal limits (35)(36)(37)(38)(39)(40) by adjusting ventilation rate (80-100 breaths/min) and/or tidal volume (2.0-3.0 ml). Body temperature was maintained at 37 ± 1°C by using a ventrally placed water-circulating pad.…”

Section: Methodsmentioning

confidence: 99%

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

LaGrange

Toney

Bishop

2003

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

show abstract

“…Integration of the haemodynamic and osmotic information probably occurs in the hypothalamus to allow the final signal to pass to the neurohypophysis. The neurotransmitters involved in this complex integration of afferent information are numerous and include biogenic amines, amino acids and peptides, and their discussion is beyond the scope of this article (for recent reviews see, Sklar & Schrier, 1983; Carter & Lightman, 1985; Sladek & Armstrong, 1987).…”

Section: Znjuences On Thirst and Vasopressin Osmoregulationmentioning

confidence: 99%

Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

Baylis

Thompson

1988

Clinical Endocrinology

137

View full text Add to dashboard Cite

“…VP synthesis and release is stimulated by increased plasma osmolarity and decreased blood pressure, or hypovolemia (Sladek and Armstrong 1987;Cunningham and Sawchenko 1991). These systemic changes modify the functional activity of VP neurons directly or via hormones and neurotransmitters, noradrenaline in particular (Sladek and Armstrong 1987;Falke 1991).…”

Section: Introductionmentioning

confidence: 99%

Vasopressinergic neurons of the supraoptic nucleus in perinatal rats: reaction to osmotic stimulation and its regulation

2010

View full text Add to dashboard Cite

Osmotic stimulation (OS) of vasopressin (VP) neurons of the supraoptic nucleus (SON) promotes VP secretion and tyrosine hydroxylase (TH) expression in adult mammals. VP secretion is under a noradrenaline control, whereas the regulation of TH expression remains uncertain. This study was aimed to determine at what period of ontogenesis: (1) VP neurons begin to react to OS by modifying simultaneously VP and TH gene expression and synthesis, (2) the noradrenergic control of VP neurons is established. Rats on the 21st embryonic day (E), third postnatal day (P), P13 were salt loaded or salt loaded and treated with an antagonist (prazosin) or agonist (phenylephrine) of α1-adrenoreceptors. According to our immunocytochemical and in situ hybridization data, OS resulted in an increased amount of VP mRNA in each age group and of VP on E21 and P3. TH gene and synthesis was initially expressed under OS on P3. The number of TH-expressing neurons diminished by threefold in salt loaded rats from P3 to P13. OS combined with prazosin administration resulted in an increased level of VP mRNA on P3 and P13, but not on E21 suggesting the onset of the noradrenaline inhibitory control after birth. OS together with prazosin treatment stimulated TH expression on P3 and P13, whereas phenylephrine provided an opposite effect. Thus, VP neurons begin to react to OS by an increased VP synthesis at the end of fetal life and by the onset of TH expression shortly after birth; the expression of both substances appears to be under the inhibitory control of noradrenaline.

show abstract

Effect of Neurotransmitters and Neuropeptides on Vasopressin Release

Cited by 38 publications

References 337 publications

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Chronic angiotensin II infusion attenuates the renal sympathoinhibitory response to acute volume expansion

Osmoregulation of Vasopressin Secretion and Thirst in Health and Disease

Vasopressinergic neurons of the supraoptic nucleus in perinatal rats: reaction to osmotic stimulation and its regulation

Contact Info

Product

Resources

About