Neuronostatin acts in brain to biphasically increase mean arterial pressure through sympatho-activation followed by vasopressin secretion: the role of melanocortin receptors
Open accessAbstract
Neuronostatin is a recently described neuropeptide that is derived from the somatostatin preprohormone. We have shown previously that neuronostatin led to a biphasic, dose-related increase in mean arterial pressure when injected into the lateral cerebroventricle of adult, male rats. Because neuronostatin depolarized both magnocellular and parvocellular, paraventricular nucleus neurons in hypothalamic slice preparations, we hypothesized that neuronostatin elevated mean arterial pressure first by stimulating sympathetic nervous system activity followed by the release of a pressor hormone, specifically vasopressin. We found that the first phase of neuronostatin-induced increase in mean arterial pressure was reversed by pretreatment with phentolamine, indicating that phase 1 was, indeed, due to an increase in sympathetic activity. We also found that centrally injected neuronostatin led to a dose-related increase in vasopressin secretion in a time course consistent with the peak of the second phase. Furthermore, the second phase of arterial pressure elevation was reversed by pretreatment with a vasopressin 1 receptor antagonist, indicating that phase 2 was likely due to an increase in vasopressin secretion. We previously have shown that the anorexigenic and antidipsogenic effects of neuronostatin were reversed by pretreatment with the melanocortin 3/4 receptor antagonist, SHU9119, so we evaluated the ability of SHU9119 to reverse the effects of neuronostatin on MAP and vasopressin secretion. We found that SHU9119 abrogated the second phase of neuronostatin-induced increase in MAP and neuronostatin-induced vasopressin secretion, indicating that neuronostatin acts through the central melanocortin system to increase vasopressin release, ultimately leading to an elevation in MAP.
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The blood pressure-increasing effects of neuronostatin and nesfatin 1 were diminished by MC4R blockade.
“The BP-increasing effects of the hormones neuronostatin and nesfatin 1, which are elevated in obesity, were diminished203,204, and hypertension induced by inhibition of NO synthesis was attenuated by MC4R blockade205.”
From Obesity, kidney dysfunction and hypertension: mechanistic links (2019) · cites this paper as [203]
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- Authors
- Yosten, G. L. C., Pate, A. T., & Samson, W. K.
- Affiliations
- Saint Louis University (US)
- Corresponding author
- Yosten, Gina L. C.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2011-05
- Volume
- 300
- Issue
- 5
- Pages
- R1194-R1199
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- PMC
- PMC3094032
- OpenAlex
- W2064784255
- Cited by
- 35
- References
- 30
- Citations by year
- 2023: 1 · 2022: 1 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 3 · 2014: 7 · 2013: 4 · 2012: 5
- FWCI
- 2.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL-66023, R01HL066023)
- National Institute of General Medical Sciences (T32GM008306)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Health Sciences › Medicine › Surgery › Cardiovascular, Neuropeptides, and Oxidative Stress Research
- Keywords
- mean arterial pressure, vasopressin release, sympathetic activation, melanocortin receptors, melanocortin 3/4 receptor, SHU9119, hypothalamic paraventricular nucleus, phentolamine, anorectic effect, central blood pressure regulation
- MeSH terms
- Adrenergic alpha-Antagonists, Animals, Blood Pressure, Brain, Dose-Response Relationship, Drug, Hormone Antagonists, Injections, Intraventricular, Male, Melanocyte-Stimulating Hormones, Peptide Fragments, Phentolamine, Somatostatin, Sympathetic Nervous System, Time Factors, Vasopressins, Receptors, Vasopressin, Receptors, Melanocortin, Rats
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