HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Effects of streptozotocin-induced diabetes on the pharmacology of rat conduit and resistance intrapulmonary arteries.

AbstractBACKGROUND:
Poor control of blood glucose in diabetes is known to promote vascular dysfunction and hypertension. Diabetes was recently shown to be linked to an increased prevalence of pulmonary hypertension. The aim of this study was to determine how the pharmacological reactivity of intrapulmonary arteries is altered in a rat model of diabetes.
METHODS:
Diabetes was induced in rats by the beta-cell toxin, streptozotocin (STZ, 60 mg/kg), and isolated conduit and resistance intrapulmonary arteries studied 3-4 months later. Isometric tension responses to the vasoconstrictors phenylephrine, serotonin and PGF2alpha, and the vasodilators carbachol and glyceryl trinitrate, were compared in STZ-treated rats and age-matched controls.
RESULTS:
STZ-induced diabetes significantly blunted the maximum response of conduit, but not resistance pulmonary arteries to phenylephrine and serotonin, without a change in pEC50. Agonist responses were differentially reduced, with serotonin (46% smaller) affected more than phenylephrine (32% smaller) and responses to PGF2alpha unaltered. Vasoconstriction caused by K+-induced depolarisation remained normal in diabetic rats. Endothelium-dependent dilation to carbachol and endothelium-independent dilation to glyceryl trinitrate were also unaffected.
CONCLUSION:
The small resistance pulmonary arteries are relatively resistant to STZ-induced diabetes. The impaired constrictor responsiveness of conduit vessels was agonist dependent, suggesting possible loss of receptor expression or function. The observed effects cannot account for pulmonary hypertension in diabetes, rather the impaired reactivity to vasoconstrictors would counteract the development of pulmonary hypertensive disease.
AuthorsAlison M Gurney, Frank C Howarth
JournalCardiovascular diabetology (Cardiovasc Diabetol) Vol. 8 Pg. 4 (Jan 21 2009) ISSN: 1475-2840 [Electronic] England
PMID19159454 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Vasoconstrictor Agents
  • Vasodilator Agents
  • Phenylephrine
  • Serotonin
  • Streptozocin
  • Carbachol
  • Dinoprost
  • Nitroglycerin
  • Potassium
Topics
  • Animals
  • Calcium Signaling (drug effects)
  • Carbachol (pharmacology)
  • Diabetes Mellitus, Experimental (physiopathology)
  • Diabetic Angiopathies (complications, physiopathology)
  • Dinoprost (pharmacology)
  • Endothelium, Vascular (drug effects, physiopathology)
  • Hypertension, Pulmonary (etiology)
  • Male
  • Membrane Potentials (drug effects)
  • Muscle, Smooth, Vascular (drug effects, physiopathology)
  • Nitroglycerin (pharmacology)
  • Phenylephrine (pharmacology)
  • Potassium (pharmacology)
  • Pulmonary Artery (drug effects, physiopathology)
  • Pulmonary Circulation (drug effects)
  • Rats
  • Rats, Wistar
  • Serotonin (pharmacology)
  • Streptozocin
  • Vascular Resistance (drug effects, physiology)
  • Vasoconstrictor Agents (pharmacology)
  • Vasodilator Agents (pharmacology)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: