ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2015
Activation of the hypothalamic paraventricular nucleus by forebrain hypertonicity selectively increases tonic vasomotor sympathetic nerve activity.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 21 citations in OpenAlex.
- Neuronal Sik1 in the Hypothalamic Paraventricular Nucleus Decreases Blood pressure Elevation Following a High-Salt Diet.Molecular neurobiology · 2026Article
- Paraventricular nucleus projections to the nucleus tractus solitarii are essential for full expression of hypoxia-induced peripheral chemoreflex responses.The Journal of physiology · 2023Article
- The damaging duo: Obesity and excess dietary salt contribute to hypertension and cardiovascular disease.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023Review
- Article
- Oxytocin Receptor Activation Rescues Opioid-Induced Respiratory Depression by Systemic Fentanyl in the Rat.The Journal of pharmacology and experimental therapeutics · 2021Article
- Intermittent hypercapnic hypoxia induces respiratory hypersensitivity to fentanyl accompanied by tonic respiratory depression by endogenous opioids.The Journal of physiology · 2020Article
- Central AT1 receptor signaling by circulating angiotensin II is permissive to acute intermittent hypoxia-induced sympathetic neuroplasticity.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Article
- Carotid bodies contribute to sympathoexcitation induced by acute salt overload.Experimental physiology · 2019Article
- Glutamatergic neurons of the paraventricular nucleus are critical contributors to the development of neurogenic hypertension.The Journal of physiology · 2018Article
- Sympathoexcitation following intermittent hypoxia in rat is mediated by circulating angiotensin II acting at the carotid body and subfornical organ.The Journal of physiology · 2018Article
- Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Burst patterning of hypothalamic paraventricular nucleus-driven sympathetic nerve activity in ANG II-salt hypertension.American journal of physiology. Heart and circulatory physiology · 2018Article
- Sympathetic neural and hemodynamic responses to head-up tilt during isoosmotic and hyperosmotic hypovolemia.Journal of neurophysiology · 2017Article
- ATP stimulates rat hypothalamic sympathetic neurons by enhancing AMPA receptor-mediated currents.Journal of neurophysiology · 2015Article
- Hypothalamic signaling mechanisms in hypertension.Current hypertension reports · 2015Review
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2 authors at 1 institution in 1 country.
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Abstract
We recently reported that mean arterial pressure (MAP) is maintained in water-deprived rats by an irregular tonic component of vasomotor sympathetic nerve activity (SNA) that is driven by neuronal activity in the hypothalamic paraventricular nucleus (PVN). To establish whether generation of tonic SNA requires time-dependent (i.e., hours or days of dehydration) neuroadaptive responses or can be abruptly generated by even acute circuit activation, forebrain sympathoexcitatory osmosensory inputs to PVN were stimulated by infusion (0.1 ml/min, 10 min) of hypertonic saline (HTS; 1.5 M NaCl) through an internal carotid artery (ICA). Whereas isotonic saline (ITS; 0.15 M NaCl) had no effect (n = 5), HTS increased (P < 0.001; n = 6) splanchnic SNA (sSNA), phrenic nerve activity (PNA), and MAP. Bilateral PVN injections of muscimol (n = 6) prevented HTS-evoked increases of integrated sSNA and PNA (P < 0.001) and attenuated the accompanying pressor response (P < 0.01). Blockade of PVN NMDA receptors with d-(2R)-amino-5-phosphonovaleric acid (AP5; n = 6) had similar effects. Analysis of respiratory rhythmic bursting of sSNA revealed that ICA HTS increased mean voltage (P < 0.001) without affecting the amplitude of inspiratory or expiratory bursts. Analysis of cardiac rhythmic sSNA likewise revealed that ICA HTS increased mean voltage. Cardiac rhythmic sSNA oscillation amplitude was also increased, which is consistent with activation of arterial baroreceptor during the accompanying pressor response. Increased mean sSNA voltage by HTS was blocked by prior PVN inhibition (muscimol) and blockade of PVN NMDA receptors (AP5). We conclude that even acute glutamatergic activation of PVN (i.e., by hypertonicity) is sufficient to selectively increase a tonic component of vasomotor SNA.
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