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Impaired sodium-evoked paraventricular nucleus neuronal activation and blood pressure regulation in conscious Sprague-Dawley rats lacking central Gαi2 proteins.
Acta Physiol (Oxf) 2016; 216(3):314-29AP

Abstract

AIM

We determined the role of brain Gαi2 proteins in mediating the neural and humoral responses of conscious male Sprague-Dawley rats to acute peripheral sodium challenge.

METHODS

Rats pre-treated (24-h) intracerebroventricularly with a targeted oligodeoxynucleotide (ODN) (25 μg per 5 μL) to downregulate brain Gαi2 protein expression or a scrambled (SCR) control ODN were challenged with an acute sodium load (intravenous bolus 3 m NaCl; 0.14 mL per 100 g), and cardiovascular parameters were monitored for 120 min. In additional groups, hypothalamic paraventricular nucleus (PVN) Fos immunoreactivity was examined at baseline, 40, and 100 min post-sodium challenge.

RESULTS

In response to intravenous hypertonic saline (HS), no difference was observed in peak change in mean arterial pressure between groups. In SCR ODN pre-treated rats, arterial pressure returned to baseline by 100 min, while it remained elevated in Gαi2 ODN pre-treated rats (P < 0.05). No difference between groups was observed in sodium-evoked increases in Fos-positive magnocellular neurons or vasopressin release. V1a receptor antagonism failed to block the prolonged elevation of arterial pressure in Gαi2 ODN pre-treated rats. A significantly greater number of Fos-positive ventrolateral parvocellular, lateral parvocellular, and medial parvocellular neurons were observed in SCR vs. Gαi2 ODN pre-treated rats at 40 and 100 min post-HS challenge (P < 0.05). In SCR, but not Gαi2 ODN pre-treated rats, HS evoked suppression of plasma norepinephrine (P < 0.05).

CONCLUSION

This highlights Gαi2 protein signal transduction as a novel central mechanism acting to differentially influence PVN parvocellular neuronal activation, sympathetic outflow, and arterial pressure in response to acute HS, independently of actions on magnocellular neurons and vasopressin release.

Authors+Show Affiliations

Department of Pharmacology & Experimental Therapeutics and the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.Department of Pharmacology & Experimental Therapeutics and the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.Department of Pharmacology & Experimental Therapeutics and the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.Department of Integrative Physiology & Anatomy, University of North Texas Health Science Center, Fort Worth, TX, USA.Department of Pharmacology & Experimental Therapeutics and the Whitaker Cardiovascular Institute, Boston University School of Medicine, Boston, MA, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26412230

Citation

Carmichael, C Y., et al. "Impaired Sodium-evoked Paraventricular Nucleus Neuronal Activation and Blood Pressure Regulation in Conscious Sprague-Dawley Rats Lacking Central Gαi2 Proteins." Acta Physiologica (Oxford, England), vol. 216, no. 3, 2016, pp. 314-29.
Carmichael CY, Carmichael AC, Kuwabara JT, et al. Impaired sodium-evoked paraventricular nucleus neuronal activation and blood pressure regulation in conscious Sprague-Dawley rats lacking central Gαi2 proteins. Acta Physiol (Oxf). 2016;216(3):314-29.
Carmichael, C. Y., Carmichael, A. C., Kuwabara, J. T., Cunningham, J. T., & Wainford, R. D. (2016). Impaired sodium-evoked paraventricular nucleus neuronal activation and blood pressure regulation in conscious Sprague-Dawley rats lacking central Gαi2 proteins. Acta Physiologica (Oxford, England), 216(3), pp. 314-29. doi:10.1111/apha.12610.
Carmichael CY, et al. Impaired Sodium-evoked Paraventricular Nucleus Neuronal Activation and Blood Pressure Regulation in Conscious Sprague-Dawley Rats Lacking Central Gαi2 Proteins. Acta Physiol (Oxf). 2016;216(3):314-29. PubMed PMID: 26412230.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Impaired sodium-evoked paraventricular nucleus neuronal activation and blood pressure regulation in conscious Sprague-Dawley rats lacking central Gαi2 proteins. AU - Carmichael,C Y, AU - Carmichael,A C T, AU - Kuwabara,J T, AU - Cunningham,J T, AU - Wainford,R D, Y1 - 2015/10/19/ PY - 2015/07/17/received PY - 2015/08/08/revised PY - 2015/09/01/revised PY - 2015/09/20/accepted PY - 2015/9/29/entrez PY - 2015/9/29/pubmed PY - 2016/12/22/medline KW - Gα-subunit proteins KW - blood pressure regulation KW - central nervous system KW - paraventricular nucleus KW - sodium SP - 314 EP - 29 JF - Acta physiologica (Oxford, England) JO - Acta Physiol (Oxf) VL - 216 IS - 3 N2 - AIM: We determined the role of brain Gαi2 proteins in mediating the neural and humoral responses of conscious male Sprague-Dawley rats to acute peripheral sodium challenge. METHODS: Rats pre-treated (24-h) intracerebroventricularly with a targeted oligodeoxynucleotide (ODN) (25 μg per 5 μL) to downregulate brain Gαi2 protein expression or a scrambled (SCR) control ODN were challenged with an acute sodium load (intravenous bolus 3 m NaCl; 0.14 mL per 100 g), and cardiovascular parameters were monitored for 120 min. In additional groups, hypothalamic paraventricular nucleus (PVN) Fos immunoreactivity was examined at baseline, 40, and 100 min post-sodium challenge. RESULTS: In response to intravenous hypertonic saline (HS), no difference was observed in peak change in mean arterial pressure between groups. In SCR ODN pre-treated rats, arterial pressure returned to baseline by 100 min, while it remained elevated in Gαi2 ODN pre-treated rats (P < 0.05). No difference between groups was observed in sodium-evoked increases in Fos-positive magnocellular neurons or vasopressin release. V1a receptor antagonism failed to block the prolonged elevation of arterial pressure in Gαi2 ODN pre-treated rats. A significantly greater number of Fos-positive ventrolateral parvocellular, lateral parvocellular, and medial parvocellular neurons were observed in SCR vs. Gαi2 ODN pre-treated rats at 40 and 100 min post-HS challenge (P < 0.05). In SCR, but not Gαi2 ODN pre-treated rats, HS evoked suppression of plasma norepinephrine (P < 0.05). CONCLUSION: This highlights Gαi2 protein signal transduction as a novel central mechanism acting to differentially influence PVN parvocellular neuronal activation, sympathetic outflow, and arterial pressure in response to acute HS, independently of actions on magnocellular neurons and vasopressin release. SN - 1748-1716 UR - https://www.unboundmedicine.com/medline/citation/26412230/Impaired_sodium_evoked_paraventricular_nucleus_neuronal_activation_and_blood_pressure_regulation_in_conscious_Sprague_Dawley_rats_lacking_central_Gαi2_proteins_ L2 - https://doi.org/10.1111/apha.12610 DB - PRIME DP - Unbound Medicine ER -