ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2014
Intracarotid hypertonic sodium chloride differentially modulates sympathetic nerve activity to the heart and kidney.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Acute effects of salt on blood pressure are mediated by serum osmolality.Journal of clinical hypertension (Greenwich, Conn.) · 2018Trial
- Central regulation of body fluid homeostasis.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2022Review
- Neuroanatomical characterization of GαiPhysiological genomics · 2021Article
- Sympathetic Nervous System Contributions to Hypertension: Updates and Therapeutic Relevance.The Canadian journal of cardiology · 2020Review
- Hypothalamic Paraventricular Nucleus GαiHypertension (Dallas, Tex. : 1979) · 2020Article
- Article
- Functional-Optical Coherence Tomography: A Non-invasive Approach to Assess the Sympathetic Nervous System and Intrinsic Vascular Regulation.Frontiers in physiology · 2019Article
- The influence of acute elevations in plasma osmolality and serum sodium on sympathetic outflow and blood pressure responses to exercise.Journal of neurophysiology · 2018Article
- Role of the Sympathetic Nervous System and Its Modulation in Renal Hypertension.Frontiers in medicine · 2018Review
- NaCl and osmolarity produce different responses in organum vasculosum of the lamina terminalis neurons, sympathetic nerve activity and blood pressure.The Journal of physiology · 2017Article
- Recent Advances in Neurogenic Hypertension: Dietary Salt, Obesity, and Inflammation.Hypertension (Dallas, Tex. : 1979) · 2017Review
- Organum Vasculosum of the Lamina Terminalis Detects NaCl to Elevate Sympathetic Nerve Activity and Blood Pressure.Hypertension (Dallas, Tex. : 1979) · 2017Article
- Impaired sodium-evoked paraventricular nucleus neuronal activation and blood pressure regulation in conscious Sprague-Dawley rats lacking central Gαi2 proteins.Acta physiologica (Oxford, England) · 2016Article
- Cerebrospinal Fluid Hypernatremia Elevates Sympathetic Nerve Activity and Blood Pressure via the Rostral Ventrolateral Medulla.Hypertension (Dallas, Tex. : 1979) · 2015Article
- Activation of the hypothalamic paraventricular nucleus by forebrain hypertonicity selectively increases tonic vasomotor sympathetic nerve activity.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertonic NaCl infused into the carotid arteries increases mean arterial pressure (MAP) and changes sympathetic nerve activity (SNA) via cerebral mechanisms. We hypothesized that elevated sodium levels in the blood supply to the brain would induce differential responses in renal and cardiac SNA via sensors located outside the blood-brain barrier. To investigate this hypothesis, we measured renal and cardiac SNA simultaneously in conscious sheep during intracarotid infusions of NaCl (1.2 M), sorbitol (2.4 M), or urea (2.4 M) at 1 ml/min for 4 min into each carotid. Intracarotid NaCl significantly increased MAP (91 ± 2 to 97 ± 3 mmHg, P < 0.05) without changing heart rate (HR). Intracarotid NaCl was associated with no change in cardiac SNA (11 ± 5.0%), but a significant inhibition of renal SNA (-32.5 ± 6.4%, P < 0.05). Neither intracarotid sorbitol nor urea changed MAP, HR, central venous pressure, cardiac SNA, and renal SNA. The changes in MAP and renal SNA were completely abolished by microinjection of the GABA agonist muscimol (5 mM, 500 nl each side) into the paraventricular nucleus of the hypothalamus (PVN). Infusion of intracarotid NaCl for 20 min stimulated a larger increase in water intake (1,100 ± 75 ml) than intracarotid sorbitol (683 ± 125 ml) or intracarotid urea (0 ml). These results demonstrate that acute increases in blood sodium levels cause a decrease in renal SNA, but no change in cardiac SNA in conscious sheep. These effects are mediated by cerebral sensors located outside the blood-brain barrier that are more responsive to changes in sodium concentration than osmolality. The renal sympathoinhibitory effects of sodium are mediated via a pathway that synapses in the PVN.
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