Cardiovascular effects of lesions of the rostral ventrolateral medulla and the nucleus reticularis parvocellularis in rats

Cochrane, Karen L.; Nathan, Marc A.

doi:10.1016/0165-1838(93)90323-m

Cited by 15 publications

(4 citation statements)

References 43 publications

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“…The RVLM located in the medulla oblongata contains adrenergic (TH-containing) neurons that are thought to be of critical importance for maintaining sympathetic vasomotor tone and blood pressure (Cochrane and Nathan, 1993;Guyenet et al, 1989;Lipski et al, 1995). RVLM neurons project to the sympathetic pre-ganglionic neurons located in the intermediolateral cell column of the spinal cord that control the sympathetic nerves to the heart, blood vessel and kidneys (Lipski et al, 1995;Dampney 1994).…”

Section: Discussionmentioning

confidence: 99%

Intra-carotid angiotensin II activates tyrosine hydroxylase-expressing rostral ventrolateral medulla neurons following blood–brain barrier disruption in rats

Yao

May

2013

Neuroscience

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Angiotensin II (Ang II) in the periphery and within the brain plays important roles in blood pressure control. Circulating angiotensin is normally excluded from the brain by the blood-brain barrier (BBB), but there is evidence that in some diseases there is disruption of the BBB that could allow circulating Ang II to access nuclei from which it is normally excluded, such as the rostral ventrolateral medulla (RVLM). We therefore investigated whether disruption of the BBB leads to increased activation by circulating Ang II of tyrosine hydroxylase (TH)-containing neurons in the RVLM. In anaesthetised rats, in which the BBB was disrupted with intracarotid hypertonic mannitol (1.6M, 2mL/kg), subsequent intracarotid infusion of a subpressor dose of Ang II (5ng/kg) activated ∼24% of TH-containing RVLM neurons whereas saline only activated ∼8% of TH neurons. Intracarotid pretreatment with the Ang II receptor type 1 (AT1R) blocker, losartan (20μg/kg), significantly reduced the number of TH cells activated to ∼11% (P<0.05, one-way analysis of variance, n=5). In summary, disruption of the BBB resulted in increased activation by circulating Ang II of TH-containing cells in the RVLM. The activation was reduced by losartan indicating a specific action on AT1Rs. These results suggest that disruption of the BBB allows entry of circulating Ang II into the RVLM, which could increase sympathetic outflow. This potential source of Ang II within the RVLM might be an important consideration when assessing sympathetic nerve activity in disease states associated with a compromised BBB.

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Section: Discussionmentioning

confidence: 99%

Intra-carotid angiotensin II activates tyrosine hydroxylase-expressing rostral ventrolateral medulla neurons following blood–brain barrier disruption in rats

Yao

May

2013

Neuroscience

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“…) could be taken to imply that physiologists and anatomists were as one in establishing the fundamental organization of CNS sympathetic control. In fact such a simplistic view is clearly incorrect since lesion studies in the rat have shown that only transient changes in both blood pressure and sympathetic activity accompany destruction of the RVLM (Cochrane & Nathan, 1993). Further studies have revealed that the IML is richly innervated by axons descending from numerous brainstem nuclei in addition to the RVLM (see Fig.…”

Section: The Vasomotor Centre Revisitedmentioning

confidence: 98%

Annual review prize lecture. Central nervous mechanisms contributing to cardiovascular control.

Spyer¹

1994

The Journal of Physiology

400

308

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“…[ 44 ] Ventral medullo-hypothalamic projections from neurons of the medullary lateral tegmental field (nucleus reticularis parvocellularis) neurons may synergistically enhance the release of vasopressin and excitatory peptidergic synaptic drive conveyed to rostral ventrolateral medullary presympathetic and intermediolateral cell column preganglionic sympathetic neurons. [ 45 ] Vasopressin (and angiotensin II) humorally conveyed to nucleus tractus solitarius or area postrema neurons via the blood or cerebrospinal fluid blunts the baroreflex. [ 46 – 48 ] Vasopressin ligand-effector coupling to G q -coupled vascular smooth muscle V1 a and V1 b receptors generates arterioconstriction and venoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Trimethoprim-sulfamethoxazole-induced hyponatremia in an elderly lady with Achromobacter xylosoxidans pneumonia

Ghali

Kim

2020

Medicine

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Rationale: Hyponatremia occurs frequently in the hospital setting and may be attributable to a host of etiologies. Drugs are frequently implicated. Trimethoprim-sulfamethoxazole (TMP/SMX) represents a well-recognized pharmacologic precipitant of drug-induced hyponatremia, with several reports extant in the retrievable literature. Nephrologists thus debate the mechanisms giving rise to TMP/SMX-induced hyponatremia and the precise mechanism by which treatment with TMP/SMX generates reductions of serum sodium concentration remain controversial. The agent has a well-known effect of antagonizing the effects of aldosterone upon the distal nephron. Renal salt wasting and the syndrome of inappropriate antidiuretic hormone secretion represent implicated mechanistic intermediaries in TMP/SMX-induced hyponatremia. Patient concerns: The patient endorsed no explicit concerns. Diagnoses: We describe the case of an 83-year-old female clinically diagnosed with pneumonia found to have an initial serum sodium in the range of 130 to 134 mEq/L consistent with mild hyponatremia upon admission. Sputum cultures grew Achromobacter xylosoxidans susceptible to TMP/SMX. The patient's serum sodium concentration precipitously decline following institution of treatment with TMP/SMX to 112 to 114 mEq/L during the course of 5 days. Interventions: Severe hyponatremia proved recalcitrant to initial therapy with supplemental salt tabs and standard doses of the vasopressin receptor antagonist tolvaptan. Outcomes: Escalating doses of tolvaptan increased the patient's sodium to 120 to 124 mEq/L. The patient was transferred to another hospital for further management. During her stay, the patient did not exhibit frank or obvious clinical features consistent with hyponatremia nor readily appreciable evidence of volume depletion. Lessons: TMP/SMX represents a frequent, though underreported cause of hyponatremia in the hospital setting several authors believe natriuresis may represent the most common mechanism underlying TMP/SMX-induced hyponatremia. Evidence implicating natriuresis to be mechanistic in TMP/SMX-induced hyponatremia include clinically appreciable hypovolemia and resolution of hyponatremia with oral or intravenous salt repletion. Salt repletion failed to monotherapeutically enhance our patient's hyponatremiadisfavoring renal salt wasting as originately mechanistic. Contemporaneous refractoriness of serum sodium to fluid restriction nor standard doses of tolvaptan confounded our initial attempts to mechanistically attribute the patient's hyponatremia to a specific cause. Clinical euvolemia and rapid response of hyponatremia to exceptionally high doses of tolvaptan strongly favors syndrome of inappropriate antidiuretic hormone to represent the chief mechanism by which TMP/SMX exacerbates hyponatremia.

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Cardiovascular effects of lesions of the rostral ventrolateral medulla and the nucleus reticularis parvocellularis in rats

Cited by 15 publications

References 43 publications

Intra-carotid angiotensin II activates tyrosine hydroxylase-expressing rostral ventrolateral medulla neurons following blood–brain barrier disruption in rats

Intra-carotid angiotensin II activates tyrosine hydroxylase-expressing rostral ventrolateral medulla neurons following blood–brain barrier disruption in rats

Annual review prize lecture. Central nervous mechanisms contributing to cardiovascular control.

Trimethoprim-sulfamethoxazole-induced hyponatremia in an elderly lady with Achromobacter xylosoxidans pneumonia

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