Chronic Central Nervous System MC3/4R Blockade Attenuates Hypertension Induced by Nitric Oxide Synthase Inhibition but Not by Angiotensin II Infusion
Open accessAbstract
We examined whether central melanocortin 3 and 4 receptor (MC3/4R) blockade attenuates the blood pressure (BP) responses to chronic L-NAME or angiotensin II (Ang II) infusion in Sprague–Dawley rats implanted with telemetry transmitters, venous catheters, and intracerebroventricular cannula into the lateral ventricle. After 5 days of control measurements, L-NAME (10 μg/kg/min IV, groups 1 and 2) or Ang II (10 ng/kg/min IV, groups 3 and 4) were infused for 24 days, and starting on day 7 of L-NAME or Ang II infusion, the MC3/4R antagonist SHU-9119 (24 nmol/d, n=6/group; groups 1 and 3) or vehicle (saline 0.5 μL/h, n=6/group; groups 2 and 4) was infused intracerebroventricularly for 10 days. A control normotensive group also received SHU-9119 for 10 days (n=5). L-NAME and Ang II increased BP by 40±3 and 56±5 mm Hg, respectively, although heart rate was slightly reduced. MC3/4R blockade doubled food intake and reduced heart rate (≈40 to ≈50 bpm) in all groups. MC3/4R blockade caused only a small reduction in BP in normotensive group (4 mm Hg) and no change in rats receiving Ang II, although markedly reducing BP by 21±4 mm Hg in L-NAME–treated rats. After SHU-9119 infusion was stopped, food intake, heart rate, and BP gradually returned to values observed before SHU-9119 infusion was started. Ganglionic blockade at the end of L-NAME or Ang II infusion caused similar BP reduction in both groups. These results suggest that the brain MC3/4R contributes, at least in part, to the hypertension induced by chronic L-NAME infusion but not by Ang II.
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Hypertension induced by inhibition of nitric oxide synthesis was attenuated 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 [205]
Blockade of endogenous MC4R activity reduced blood pressure in several non-obese experimental models of hypertension, especially those associated with increased sympathetic nervous system activity.
“Blockade of endogenous MC4R activity also reduced BP in several non-obese experimental models of hypertension, especially those associated with increased SNS activity [42, 57] (Figure 2).”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [57]
MC4R blockade failed to lower blood pressure in angiotensin-II-induced hypertension, an experimental model with baroreflex mediated reductions in sympathetic nervous system activity.
“However, MC4R blockade failed to lower BP in angiotensin-II-induced hypertension, an experimental model with baroreflex mediated reductions in SNS activity [57].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [57]
The brain melanocortin system plays a key role in maintenance of sympathetic nervous system activity and blood pressure in normotensive subjects as well as in non-obese forms of hypertension that have increased sympathetic activity.
“These findings highlight the key role of the brain melanocortin system in maintenance of SNS activity and BP in normotensive subjects as well as in non-obese forms of hypertension that have increased sympathetic activity [41, 42, 57, 58].”
From Role of the brain melanocortins in blood pressure regulation (2017) · cites this paper as [57]
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Backgroundda Silva, A. A., do Carmo, J. M., Kanyicska, B., Dubinion, J., Brandon, E., & Hall, J. E. (2008) · Hypertension · doi:10.1161/hypertensionaha.107.100636 · Cited by 79 · cited 3× · see citing works
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“These differential effects on renal SNA could be particularly important if suppression of renal SNA mediates most of the chronic BP lowering effect of MC3/4R antagonism.(31) We, however, are not certain of the precise mechanism by which central MC3/4R blockade reduced BP in L-NAME but not -100 -80 -60 -40 -20 0 20 40…”
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“Although the brain areas where MC3/4R exert their effects on the autonomic nervous system and BP regulation are still poorly understood, MC4R are abundant in the paraventricular nucleus of the hypothalamus and in brain stem areas involved in autonomic regulation, as well as in the intermediolateral medulla.(32,33) For…”
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“We also found marked accentuated sympathetically mediated hypertension induced by chronic MC3/4R activation in rats treated with L-NAME.17 However, Hilzendeger et al30 showed that blockade of brain AT1 receptors failed to alter the increase in renal SNA elicited by the MC3/4R agonist, MTII.”
BackgroundInfluentialSelf-citationSympathetic activity is not increased in l -NAME hypertensive rats
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“These findings highlight the key role of the brain melanocortin system in maintenance of SNS activity and BP in normotensive subjects as well as in non-obese forms of hypertension that have increased sympathetic activity [41,42,57,58].”
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- Authors
- da Silva, A. A., do Carmo, J. M., Dubinion, J. H., Bassi, M., Mokhtarpouriani, K., Hamza, S. M., & Hall, J. E.
- Affiliations
- From the Department of Physiology and Biophysics, Mississippi Center for Obesity Research, Center of Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson.
- University of Mississippi Medical Center (US)
- Venue
- Hypertension
- Published
- 2015-01
- Volume
- 65
- Issue
- 1
- Pages
- 171-177
- ISSN
- 0194-911X (ISSN-L)
- 1524-4563
- PMC
- PMC4267912
- OpenAlex
- W2129899139
- Cited by
- 18
- References
- 34
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 1 · 2016: 3 · 2015: 3
- FWCI
- 1.60
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Hypertension (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (P01-HL-51971, P01HL051971)
- National Institute of General Medical Sciences (P20GM104357)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Keywords
- melanocortin 3/4 receptor, central nervous system, L-NAME, nitric oxide synthase inhibition, angiotensin II, blood pressure regulation, dietary intake, heart rate, ganglionic blockade, intracerebroventricular infusion
- MeSH terms
- Angiotensin II, Animals, Blood Pressure, Central Nervous System, Disease Models, Animal, Enzyme Inhibitors, Hypertension, Infusions, Intravenous, Male, Rats, Sprague-Dawley, Nitric Oxide Synthase, Receptor, Melanocortin, Type 3, Receptor, Melanocortin, Type 4, Rats
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