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Berg T. α2-Adrenoreceptor Constraint of Catecholamine Release and Blood Pressure Is Enhanced in Female Spontaneously Hypertensive Rats. Front Neurosci. 2016;10:130doi: 10.3389/fnins.2016.00130.
Berg, T. (2016). α2-Adrenoreceptor Constraint of Catecholamine Release and Blood Pressure Is Enhanced in Female Spontaneously Hypertensive Rats. Frontiers in neuroscience, 10130. https://doi.org/10.3389/fnins.2016.00130
Berg, Torill. "α2-Adrenoreceptor Constraint of Catecholamine Release and Blood Pressure Is Enhanced in Female Spontaneously Hypertensive Rats." Frontiers in neuroscience vol. 10 (2016): 130. doi: https://doi.org/10.3389/fnins.2016.00130
Berg T. α2-Adrenoreceptor Constraint of Catecholamine Release and Blood Pressure Is Enhanced in Female Spontaneously Hypertensive Rats. Front Neurosci. 2016 Mar 30;10:130. doi: 10.3389/fnins.2016.00130. eCollection 2016. PMID: 27065790; PMCID: PMC4812064.
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Front Neurosci. 2016 Mar 30;10:130. doi: 10.3389/fnins.2016.00130. eCollection 2016.

α2-Adrenoreceptor Constraint of Catecholamine Release and Blood Pressure Is Enhanced in Female Spontaneously Hypertensive Rats.

Frontiers in neuroscience

Torill Berg

Affiliations

  1. Division of Physiology, Department of Molecular Medicine, Institute of Basic Medical Sciences, University of Oslo Oslo, Norway.

PMID: 27065790 PMCID: PMC4812064 DOI: 10.3389/fnins.2016.00130

Abstract

UNLABELLED: α2-adrenoceptors (α2AR) lower central sympathetic output and peripheral catecholamine release, and may therefore prevent sympathetic hyperactivity and hypertension. The α2AR are dysfunctional in male spontaneously hypertensive rats (SHR). Premenopausal females are less hypertensive than males. The purpose of this study was to test if this difference could be explained by functional α2AR in the female SHR. A 15-min tyramine-infusion was used to stimulate norepinephrine release through the re-uptake transporter, consequently preventing re-uptake. Presynaptic control of vesicular release will therefore be reflected as differences in overflow to plasma. The surgical trauma activates secretion of epinephrine, also subjected to α2AR auto-inhibition. Blood pressure was monitored through a femoral artery catheter and cardiac output by ascending aorta flow in 12-14 weeks-old (early hypertension) SHR and normotensive rats (WKY). Total peripheral vascular resistance (TPR) was calculated. Female SHR, unlike male, were close to normotensive. Pre-treatment with none-selective (clonidine) or non-A-selective (ST-91) α2AR agonist reduced, and none-selective α2AR antagonist (L-659,066) increased tyramine-induced norepinephrine overflow in female WKY and SHR. L-659,066 also increased secretion of epinephrine. The L-659,066-induced increase in catecholamine release was further enhanced by additional pre-treatment with ST-91 or angiotensin AT1 receptor antagonist (losartan) in SHR only. L-659,066 eliminated the tyramine-induced rise in TPR in both strains in female rats.

CONCLUSION: α2AR-mediated control of catecholamine release and vascular tension was therefore functional in female SHR, unlike that previously observed in male SHR. Functional α2AR is likely to have a protective function and may explain the lack of hypertension in the young female SHR.

Keywords: angiotensin AT1 receptor; epinephrine; female rats; norepinephrine; spontaneously hypertensive rats; sympathetic nervous system; total peripheral vascular resistance; α2-adrenoceptors

References

  1. Front Neurol. 2013 Feb 28;4:19 - PubMed
  2. Eur J Pharmacol. 2002 Oct 11;452(3):325-37 - PubMed
  3. Eur J Pharmacol. 1992 Sep 4;219(3):465-8 - PubMed
  4. J Neurochem. 2001 Aug;78(4):685-93 - PubMed
  5. J Pharmacol Exp Ther. 1988 Apr;245(1):32-40 - PubMed
  6. J Hypertens. 2003 Jul;21(7):1363-9 - PubMed
  7. Circ Res. 1991 Mar;68(3):827-35 - PubMed
  8. Br J Pharmacol. 2007 May;151(2):186-94 - PubMed
  9. Naunyn Schmiedebergs Arch Pharmacol. 2003 Dec;368(6):504-12 - PubMed
  10. Nature. 1999 Nov 11;402(6758):181-4 - PubMed
  11. Am J Physiol Heart Circ Physiol. 2004 Jan;286(1):H59-67 - PubMed
  12. Br J Pharmacol. 2000 Mar;129(6):1095-102 - PubMed
  13. J Pharmacol Exp Ther. 2005 Aug;314(2):804-10 - PubMed
  14. J Cardiovasc Pharmacol. 1997 Jan;29(1):93-6 - PubMed
  15. Hypertension. 2004 May;43(5):918-23 - PubMed
  16. Clin Exp Pharmacol Physiol. 2005 Jan-Feb;32(1-2):35-9 - PubMed
  17. Br J Pharmacol. 2003 Apr;138(8):1389-402 - PubMed
  18. Am Heart J. 1986 Feb;111(2):383-90 - PubMed
  19. Fundam Clin Pharmacol. 1996;10(6):493-503 - PubMed
  20. Am J Physiol Heart Circ Physiol. 2000 Apr;278(4):H1075-83 - PubMed
  21. Front Neurol. 2012 Nov 08;3:160 - PubMed
  22. Science. 1996 Aug 9;273(5276):803-5 - PubMed
  23. Hypertension. 1993 Apr;21(4):498-503 - PubMed
  24. Front Neurol. 2011 Nov 23;2:71 - PubMed
  25. Front Physiol. 2014 Dec 19;5:499 - PubMed
  26. Hypertension. 1999 Sep;34(3):403-7 - PubMed
  27. Am J Physiol Heart Circ Physiol. 2007 Sep;293(3):H1955-61 - PubMed
  28. Trends Pharmacol Sci. 1997 Jun;18(6):211-9 - PubMed
  29. Am J Physiol. 1971 Dec;221(6):1629-39 - PubMed
  30. J Physiol. 2000 Nov 1;528(Pt 3):407-17 - PubMed
  31. J Pharmacol Exp Ther. 2011 Apr;337(1):256-66 - PubMed
  32. Eur J Pharmacol. 1992 Feb 11;211(2):257-61 - PubMed
  33. Biol Cell. 2004 Jun;96(5):343-8 - PubMed
  34. Biochemistry. 2006 Apr 18;45(15):4760-7 - PubMed
  35. Front Neurol. 2013 Jun 10;4:70 - PubMed
  36. J Med Chem. 2007 Aug 9;50(16):3964-8 - PubMed

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