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Vascular endothelin-1 expression and effect of an endothelin ETA antagonist on structure and function of small arteries from stroke-prone spontaneously hypertensive rats.
J Cardiovasc Pharmacol. 1998; 31 Suppl 1:S309-12.JC

Abstract

There is some evidence that the endothelin (ET) system may participate in blood pressure elevation and in vascular hypertrophy in stroke-prone spontaneously hypertensive rats (SHR-SP). To further understand the involvement of the ET system in this hypertensive model, we examined preproendothelin-1 (preproET-1) mRNA abundance in blood vessels of 5-week and 18-week SHR-SP in comparison to SHR, and treated 12-week old SHR-SP with the ETA-selective receptor antagonist A-127722.5 (30 mg/kg/day in the drinking water) for 10 weeks. Abundance of preproET-1 mRNA by Northern blot analysis was increased more than twofold in aorta and mesenteric arteries of SHR-SP relative to SHR at 18 weeks but not at 5 weeks of age. SHR-SP treated with A-127722.5 had a tail-cuff systolic blood pressure at 22 weeks of age of 241 +/- 2 mm Hg vs. 251 +/- 3 mm Hg in untreated SHR-SP (p < 0.05). Heart:body weight ratio was no different in both groups, but aortic segment:body weight ratio was slightly but significantly smaller in treated SHR-SP (p < 0.05). Pressurized mesenteric small arteries from treated SHR-SP had a smaller media width (12.6 +/- 0.6 microns vs. 14.9 +/- 0.5 microns; p < 0.05) and media:lumen ratio (5.8 +/- 0.2% vs. 7.3 +/- 0.3%; p < 0.01), whereas media cross-sectional area and lumen diameter tended to decrease and increase, respectively, without achieving statistical significance. Acetylcholine-induced relaxation was improved in treated SHR-SP (99.6 +/- 0.6% vs. 90.0 +/- 3.6%; p < 0.05), whereas relaxation responses to sodium nitroprusside were similar in both groups. These results show increases of preproET-1 expression in blood vessels that appear to be secondary to blood pressure elevation. There is a small ET-dependent component in blood pressure elevation and in conduit and resistance artery changes in adult stroke-prone SHR.

Authors+Show Affiliations

MRC Multidisciplinary Research Group on Hypertension, Clinical Research Institute of Montreal, University of Montreal, Quebec, Canada.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9595467

Citation

Sharifi, A M., et al. "Vascular Endothelin-1 Expression and Effect of an Endothelin ETA Antagonist On Structure and Function of Small Arteries From Stroke-prone Spontaneously Hypertensive Rats." Journal of Cardiovascular Pharmacology, vol. 31 Suppl 1, 1998, pp. S309-12.
Sharifi AM, He G, Touyz RM, et al. Vascular endothelin-1 expression and effect of an endothelin ETA antagonist on structure and function of small arteries from stroke-prone spontaneously hypertensive rats. J Cardiovasc Pharmacol. 1998;31 Suppl 1:S309-12.
Sharifi, A. M., He, G., Touyz, R. M., & Schiffrin, E. L. (1998). Vascular endothelin-1 expression and effect of an endothelin ETA antagonist on structure and function of small arteries from stroke-prone spontaneously hypertensive rats. Journal of Cardiovascular Pharmacology, 31 Suppl 1, S309-12.
Sharifi AM, et al. Vascular Endothelin-1 Expression and Effect of an Endothelin ETA Antagonist On Structure and Function of Small Arteries From Stroke-prone Spontaneously Hypertensive Rats. J Cardiovasc Pharmacol. 1998;31 Suppl 1:S309-12. PubMed PMID: 9595467.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vascular endothelin-1 expression and effect of an endothelin ETA antagonist on structure and function of small arteries from stroke-prone spontaneously hypertensive rats. AU - Sharifi,A M, AU - He,G, AU - Touyz,R M, AU - Schiffrin,E L, PY - 1998/5/22/pubmed PY - 1998/5/22/medline PY - 1998/5/22/entrez SP - S309 EP - 12 JF - Journal of cardiovascular pharmacology JO - J Cardiovasc Pharmacol VL - 31 Suppl 1 N2 - There is some evidence that the endothelin (ET) system may participate in blood pressure elevation and in vascular hypertrophy in stroke-prone spontaneously hypertensive rats (SHR-SP). To further understand the involvement of the ET system in this hypertensive model, we examined preproendothelin-1 (preproET-1) mRNA abundance in blood vessels of 5-week and 18-week SHR-SP in comparison to SHR, and treated 12-week old SHR-SP with the ETA-selective receptor antagonist A-127722.5 (30 mg/kg/day in the drinking water) for 10 weeks. Abundance of preproET-1 mRNA by Northern blot analysis was increased more than twofold in aorta and mesenteric arteries of SHR-SP relative to SHR at 18 weeks but not at 5 weeks of age. SHR-SP treated with A-127722.5 had a tail-cuff systolic blood pressure at 22 weeks of age of 241 +/- 2 mm Hg vs. 251 +/- 3 mm Hg in untreated SHR-SP (p < 0.05). Heart:body weight ratio was no different in both groups, but aortic segment:body weight ratio was slightly but significantly smaller in treated SHR-SP (p < 0.05). Pressurized mesenteric small arteries from treated SHR-SP had a smaller media width (12.6 +/- 0.6 microns vs. 14.9 +/- 0.5 microns; p < 0.05) and media:lumen ratio (5.8 +/- 0.2% vs. 7.3 +/- 0.3%; p < 0.01), whereas media cross-sectional area and lumen diameter tended to decrease and increase, respectively, without achieving statistical significance. Acetylcholine-induced relaxation was improved in treated SHR-SP (99.6 +/- 0.6% vs. 90.0 +/- 3.6%; p < 0.05), whereas relaxation responses to sodium nitroprusside were similar in both groups. These results show increases of preproET-1 expression in blood vessels that appear to be secondary to blood pressure elevation. There is a small ET-dependent component in blood pressure elevation and in conduit and resistance artery changes in adult stroke-prone SHR. SN - 0160-2446 UR - https://www.unboundmedicine.com/medline/citation/9595467/Vascular_endothelin_1_expression_and_effect_of_an_endothelin_ETA_antagonist_on_structure_and_function_of_small_arteries_from_stroke_prone_spontaneously_hypertensive_rats_ L2 - https://doi.org/10.1097/00005344-199800001-00086 DB - PRIME DP - Unbound Medicine ER -