Insulin-exacerbated hypertension in captopril-treated spontaneously hypertensive rats: Role of sympathoexcitation

Sanya Roysommuti, Mahmood S. Mozaffari, J. Micheal Wyss

Research output: Contribution to journalArticlepeer-review

1 Scopus citations


Insulin excess exacerbates hypertension in spontaneously hypertensive rats (SHR). This study examined the relative contribution of the renin-angiotensin system and the sympathetic nervous system in this phenomenon. In SHR, daily subcutaneous injections of insulin were initiated either before short-term angiotensin-converting enzyme inhibition with captopril or after lifetime captopril treatment. Insulin treatment resulted in significant increases in mean arterial pressure and heart rate and captopril treatment lowered arterial pressure, but captopril did not lower arterial pressure more in the insulin-treated compared with control rats. To test the contribution of the sympathetic nervous system to this form of hypertension, each rat was intravenously infused with either a ganglionic blocker (i.e., hexamethonium) or a centrally acting α2-adrenergic receptor agonist (i.e., clonidine). Administration of either agent largely eliminated the differences in mean arterial pressure and heart rate between the insulin-treated and saline-treated SHR, irrespective of captopril treatment. These data indicate that in SHR, the ability of insulin to increase blood pressure is closely related to sympathoexcitation, which is unresponsive to blockade of angiotensin-converting enzyme.

Original languageEnglish (US)
Pages (from-to)1036-1041
Number of pages6
JournalCanadian Journal of Physiology and Pharmacology
Issue number11
StatePublished - Nov 2003


  • Blood pressure
  • Captorpil
  • Clonidine
  • Hexamethonium
  • Insulin
  • Rat

ASJC Scopus subject areas

  • Physiology
  • Pharmacology
  • Physiology (medical)


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