scholarly journals Effects of vasopressin on baroreceptor reflex in the area postreme and nucleus tractus solitarius

1997 ◽  
Vol 73 ◽  
pp. 89
Author(s):  
Keisuke Migita ◽  
Nobuaki Hori ◽  
Ryou Saito ◽  
Kenji Yamamoto ◽  
Yukio Takano ◽  
...  
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Baroreceptor Reflex

Chronic nucleus tractus solitarius lesions do not prevent hypovolemia-induced vasopressin secretion in rats

1994 ◽  
Vol 267 (4) ◽  
pp. R965-R973 ◽  
Author(s):  
A. M. Schreihofer ◽  
E. M. Stricker ◽  
A. F. Sved
Keyword(s):  
Polyethylene Glycol ◽  
Plasma Volume ◽  
Nucleus Tractus Solitarius ◽  
Baroreceptor Reflex ◽  
Bilateral Vagotomy ◽  
Vasopressin Secretion ◽  
Bilateral Lesions ◽  
Alpha Chloralose ◽  
And Control ◽  
Arterial Baroreceptor

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS-lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.

Baroreceptor reflex modulation by circulating angiotensin II is mediated by AT1 receptors in the nucleus tractus solitarius

2007 ◽  
Vol 293 (6) ◽  
pp. R2267-R2278 ◽  
Author(s):  
Peter S. P. Tan ◽  
Suzanne Killinger ◽  
Jouji Horiuchi ◽  
Roger A. L. Dampney
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Area Postrema ◽  
Critical Role ◽  
Baroreceptor Reflex ◽  
Reflex Modulation ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Background Infusion ◽  
Continuous Background

Circulating ANG II modulates the baroreceptor reflex control of heart rate (HR), at least partly via activation of ANG II type 1 (AT1) receptors on neurons in the area postrema. In this study, we tested the hypothesis that the effects of circulating ANG II on the baroreflex also depend on AT1 receptors within the nucleus tractus solitarius (NTS). In confirmation of previous studies in other species, increases in arterial pressure induced by intravenous infusion of ANG II had little effect on HR in urethane-anesthetized rats, in contrast to the marked bradycardia evoked by equipressor infusion of phenylephrine. In the presence of a continuous background infusion of ANG II, the baroreflex control of HR was shifted to higher levels of HR but had little effect on the baroreflex control of renal sympathetic activity. The modulatory effects of circulating ANG II on the cardiac baroreflex were significantly reduced by microinjection of candesartan, an AT1 receptor antagonist, into the area postrema and virtually abolished by microinjections of candesartan into the medial NTS. After acute ablation of the area postrema, a background infusion of ANG II still caused an upward shift of the cardiac baroreflex curve, which was reversed by subsequent microinjection of candesartan into the medial NTS. The results indicate that AT1 receptors in the medial NTS play a critical role in modulation of the cardiac baroreflex by circulating ANG II via mechanisms that are at least partly independent of AT1 receptors in the area postrema.

scholarly journals Aldosterone-Sensitive Nucleus Tractus Solitarius Neurons Regulate Sensitivity of the Baroreceptor Reflex in High Sodium–Loaded Rats

2010 ◽  
Vol 112 (4) ◽  
pp. 482-486 ◽  
Author(s):  
Tomoharu Masuda ◽  
Yasutoshi Hirabara ◽  
Yusuke Nakamura ◽  
Akiko Chishaki ◽  
Mai Tsuruhisa ◽  
...  
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Baroreceptor Reflex ◽  
High Sodium

Baroreceptor reflex inhibition induced by the stimulation of serotonin3 receptors in the nucleus tractus solitarius of the rat

Neuroscience ◽  
1992 ◽  
Vol 46 (1) ◽  
pp. 91-100 ◽  
Author(s):  
N. Merahi ◽  
H.S. Orer ◽  
A.-M. Laporte ◽  
H. Gozlan ◽  
M. Hamon ◽  
...  
Keyword(s):  
Nucleus Tractus Solitarius ◽  
Baroreceptor Reflex ◽  
Reflex Inhibition ◽  
Stimulation Of

5-HT-mediated inhibition of cardiovagal baroreceptor reflex response during defense reaction in the rat

2004 ◽  
Vol 287 (4) ◽  
pp. H1641-H1649 ◽  
Author(s):  
Marie-Anne Comet ◽  
Caroline Sévoz-Couche ◽  
Naïma Hanoun ◽  
Michel Hamon ◽  
Raul Laguzzi
Keyword(s):  
Receptor Antagonist ◽  
Nucleus Tractus Solitarius ◽  
Inhibitory Effect ◽  
Baroreceptor Reflex ◽  
Chemical Stimulation ◽  
Cardiac Response ◽  
Reflex Response ◽  
Defense Reaction ◽  
Serotonin Synthesis ◽  
Stimulation Of

Previous studies showed that the cardiac response of the baroreceptor reflex (bradycardia) is inhibited during the defense reaction evoked by direct electrical or chemical stimulation of the periaqueductal gray (dPAG) in the rat. Whether central serotonin and nucleus tractus solitarius (NTS) serotonin3 (5-HT3) receptors might participate in this inhibition was investigated in urethane-anesthetized and atenolol-pretreated rats. Our results showed that both electrical and chemical stimulation of the dPAG produced a drastic reduction of the cardiovagal component of the baroreceptor reflex triggered by either intravenous administration of phenylephrine or aortic nerve stimulation. This inhibitory effect of dPAG stimulation on the baroreflex bradycardia was not observed in rats that had been pretreated with p-chlorophenylalanine (300 mg/kg ip daily for 3 days) to inhibit serotonin synthesis. Subsequent 5-hydroxytryptophan administration (60 mg/kg ip), which was used to restore serotonin synthesis, allowed the inhibitory effect of dPAG stimulation on both aortic and phenylephrine-induced cardiac reflex responses to be recovered in p-chlorophenylalanine-pretreated rats. On the other hand, in nonpretreated rats, the inhibitory effect of dPAG stimulation on the cardiac baroreflex response could be markedly reduced by prior intra-NTS microinjection of granisetron, a 5-HT3 receptor antagonist, or bicuculline, a GABAA receptor antagonist. These results show that serotonin plays a key role in the dPAG stimulation-induced inhibition of the cardiovagal baroreceptor reflex response. Moreover, they support the idea that 5-HT3 and GABAA receptors in the NTS contribute downstream to the inhibition of the baroreflex response caused by dPAG stimulation.

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