Vasopressinergic mechanisms in the nucleus reticularis lateralis in blood pressure control

Gómez, Roberto; Cannata, M. A.; Milner, Teresa A.; Anwar, Mumtaz Ali; Reis, Donald J.; Ruggiero, David A.

doi:10.1016/0006-8993(93)90356-r

Cited by 37 publications

(22 citation statements)

References 37 publications

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“…However, exogenously applied VP and stress significantly increased BP, and this effect could be inhibited by higher doses of the V 1a and also V 1b , but not by the V 2 antagonist pretreatment, in line with a previous report (30). Centrally administered VP does not always increase HR, and even bradycardia was reported (7,10). In our experiments, the effect of intracerebroventricularly applied VP on HR was inconsistent; all types of HR response occurred, including tachycardia, bradycardia, and a biphasic one.…”

Section: Discussionsupporting

confidence: 89%

The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study

Milutinović¹,

Murphy²,

Japundžić‐Žigon³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Although it has been suggested that vasopressin (VP) acts within the central nervous system to modulate autonomic cardiovascular controls, the mechanisms involved are not understood. Using nonpeptide, selective V 1a, V1b, and V2 antagonists, in conscious rats, we assessed the roles of central VP receptors, under basal conditions, after the central application of exogenous VP, and after immobilization, on cardiovascular short-term variability. Equidistant sampling of blood pressure (BP) and heart rate (HR) at 20 Hz allowed direct spectral analysis in very-low frequency (VLF-BP), low-frequency (LF-BP), and highfrequency (HF-BP) blood pressure domains. The effect of VP antagonists and of exogenous VP on body temperature (Tb) was also investigated. Under basal conditions, V 1a antagonist increased HF-BP and Tb, and this was prevented by metamizol. V1b antagonist enhanced HF-BP without affecting Tb, and V2 antagonist increased VLF-BP variability which could be prevented by quinapril. Immobilization increased BP, LF-BP, HF-BP, and HF-HR variability. V1a antagonist prevented BP and HR variability changes induced by immobilization and potentiated tachycardia. V1b antagonist prevented BP but not HR variability changes, whereas V2 antagonist had no effect. Exogenous VP increased systolic arterial pressure (SAP) and HF-SAP variability, and this was prevented by V1a and V1b but not V2 antagonist pretreatment. Our results suggest that, under basal conditions, VP, by stimulation of V1a, V1b, and cognate V2 receptors, buffers BP variability, mostly due to thermoregulation. Immobilization and exogenous VP, by stimulation of V1a or V1b, but not V2 receptors, increases BP variability, revealing cardiorespiratory adjustment to stress and respiratory stimulation, respectively. temperature; heart rate; V1a; V1b; V2 antagonist VASOPRESSIN (VP) IS A NEUROHYPOPHYSEAL peptide that acts both as neurohormone and central neurotransmitter/modulator. Peripherally, VP exerts a variety of biological effects in mammals: body fluid balance, blood pressure (BP) control, platelet aggregation, ACTH, aldosterone and clothing factor VIII secretion, liver glycogenolysis, and uterine motility. Centrally, VP affects learning, memory, behavior, and autonomic functions such as BP, body temperature (T b ), and respiration. The role of VP is particularly important in stress (14,25,27), and VP dysfunction was found to contribute to the pathogenesis of cardiovascular disease (28, 35) and to underlie central diabetes insipidus.So far, three types of G protein-linked membrane-bound VP receptor subtypes, V 1a , V 1b , and V 2 , have been cloned and characterized by their primary structure, gene localization, mRNA distribution, physiological function, and pharmacology (4,12,41,47). V 2 receptors have been found only in the periphery; they are positively coupled to adenylcyclase and play a dominant role in the antidiuretic response to VP. V 1a and V 1b receptors have been found both peripherally and in the central nervous system (CNS), where they mediate phospholi...

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Section: Discussionsupporting

confidence: 89%

The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study

Milutinović¹,

Murphy²,

Japundžić‐Žigon³

2006

American Journal of Physiology-Regulatory, Integrative and Comp

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“…However, we did not observe any RVLM-projecting neurons that were immunoreactive for VP-NP. This result is consistent with Gomez et al, (1993) who reported very few VP-ir neurons in PVH retrogradely labeled from RVLM injections of FluoroGold and observed that the VP-ir neurons were in a different compartment of PVH than the retrogradely labeled neurons. The predominance of OT-NP-ir neurons with RVLM projections in comparison to the lack of VP-NP-ir neurons projecting to RVLM is also in agreement with other evidence that oxytocin is overwhelmingly predominant over vasopressin in the brainstem (Nilaver et al, 1980;Lang et al, 1983).…”

Section: Most Rvlm-projecting Pvh Neurons Are Glutamatergicsupporting

confidence: 92%

“…According to several studies, these peptidergic PVH neurons project to the spinal cord and/or to the dorsomedial medulla (Nilaver et al, 1980;Sawchenko and Swanson, 1982;Hallbeck and Blomqvist, 1999;Hallbeck et al, 2001) or the ventrolateral medulla (Hancock and Nicholas, 1987;Gomez et al, 1993;Mack et al, 2002). We found a few OT-NP-ir PVH neurons with projections to RVLM (2.2% of CTB-labeled neurons in PVH).…”

Section: Most Rvlm-projecting Pvh Neurons Are Glutamatergicsupporting

confidence: 52%

“…Previous reports suggest that some parvocellular PVH neurons with descending projections to the hindbrain may be oxytocinergic or vasopressinergic (Sawchenko and Swanson, 1982;Hallbeck and Blomqvist, 1999;Hallbeck et al, 2001;Mack et al, 2002;Kc et al, 2002). In this regard, microinjection of vasopressin or oxytocin into the RVLM increases arterial blood pressure (Andreatta-Van Leyen et al, 1990;Gomez et al, 1993;Mack et al, 2002;Kc et al, 2002) and vasopressin-and oxytocin-immunoreactive fibers have been found in close proximity to spinally-projecting RVLM neurons (Hancock and Nicholas, 1987;Gomez et al, 1993). Moreover, blockade of vasopressin-type 1 receptors attenuates PVH-evoked increases in RVLM unit discharge (Yang et al, 2001;Yang and Coote, 2003).…”

Section: Introductionmentioning

confidence: 97%

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Water deprivation activates a glutamatergic projection from the hypothalamic paraventricular nucleus to the rostral ventrolateral medulla

Stocker

Simmons

Stornetta

et al. 2005

J of Comparative Neurology

122

133

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Elevated sympathetic outflow contributes to the maintenance of blood pressure in water-deprived rats. The neural circuitry underlying this response may involve activation of a pathway from the hypothalamic paraventricular nucleus (PVH) to the rostral ventrolateral medulla (RVLM). We sought to determine whether the PVH-RVLM projection activated by water deprivation is glutamatergic and/or contains vasopressin-or oxytocin-neurophysins. Vesicular glutamate transporter2 (VGLUT2) mRNA was detected by in situ hybridization in the majority of PVH neurons retrogradely labeled from the ipsilateral RVLM with cholera-toxin subunit B (CTB; 85% on average with regional differences). Very few RVLM-projecting PVH neurons were immunoreactive for oxytocin-or vasopressin-associated neurophysin. Injection of biotinylated dextran amine (BDA) into the PVH produced clusters of BDA-positive nerve terminals within the ipsilateral RVLM that were immunoreactive (ir) for the VGLUT2 protein. Some of these terminals made close appositions with tyrosine-hydroxylase-ir dendrites (presumptive C1 cells). In waterdeprived rats (n=4), numerous VGLUT2 mRNA-positive PVH neurons retrogradely labeled from the ipsilateral RVLM with CTB were c-Fos-ir (16-40% depending on PVH region). In marked contrast, few glutamatergic, RVLM-projecting PVH neurons were c-Fos-ir in control rats (n=3; 0-3% depending on PVH region). Most (94 ± 4%) RVLM-projecting PVH neurons activated by water deprivation contained VGLUT2 mRNA. In summary, the majority of PVH neurons that innervate the RVLM are glutamatergic and this population includes the neurons that are activated by water deprivation. One mechanism by which water deprivation may increase the sympathetic outflow is the activation of a glutamatergic pathway from the PVH to the RVLM.

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“…Several other neurotransmitters have been shown to increase blood pressure when injected into the RVLM [33], but there is little, if any, evidence for their involvement in the control of baseline blood pressure. For example, vasopressin injected into the RVLM increased blood pressure, though similar injections of a vasopressin receptor antagonist, in a dose required to block the actions of vasopressin, had no effect on baseline blood pressure [34].…”

Section: Can Changes In the Activity Of Rostral Ventrolateral Medullamentioning

confidence: 96%

Brainstem mechanisms of hypertension: Role of the rostral ventrolateral medulla

Sved

Ito²,

Sved³

2003

Current Science Inc

114

106

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The central nervous system plays a key role in the regulation of cardiovascular function, and alterations in the central neural mechanisms that control blood pressure may underlie the vast majority of cases of primary hypertension. The well-studied baroreceptor reflex powerfully regulates arterial pressure, though its involvement in the pathogenesis of chronic hypertension is likely to be only of minor importance. Supraspinal maintenance of sympathetic vasomotor outflow appears to emanate from neurons in the rostral ventrolateral medulla, and the tonic drive exerted on sympathetic vasomotor activity by the rostral ventrolateral medulla appears to be increased in several animal models of hypertension. In particular, the excitation of the rostral ventrolateral medulla by excitatory amino acid neurotransmitters and by stimulation of AT(1) angiotensin receptors appears to be increased in experimental hypertension. The current data support the view that neurogenic hypertension is mediated by increased excitatory drive of rostral ventrolateral medulla sympathoexcitatory neurons.

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Vasopressinergic mechanisms in the nucleus reticularis lateralis in blood pressure control

Cited by 37 publications

References 37 publications

The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study

The role of central vasopressin receptors in the modulation of autonomic cardiovascular controls: a spectral analysis study

Water deprivation activates a glutamatergic projection from the hypothalamic paraventricular nucleus to the rostral ventrolateral medulla

Brainstem mechanisms of hypertension: Role of the rostral ventrolateral medulla

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