Journal of Applied Physiology AJP: Heart and Circulatory Physiology
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J Appl Physiol (September 6, 2002). doi:10.1152/japplphysiol.00477.2002
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Articles in PresS, published online ahead of print September 6, 2002
J Appl Physiol, 10.1152/jap.00477.2002
Submitted on May 31, 2002
Accepted on August 29, 2002

Insulin sensitivity and big endothelin-1 conversion to endothelin-1 after ETA or ETB receptor blockade in humans

Gunvor Ahlborg1* and Jonas Lindstrom1

1 Department of Medical Laboratory Sciences and Techonology, Division of Clinical Physiology, Huddinge University Hospital, Karolinska Institutet, Stockholm, Sweden

* To whom correspondence should be addressed. E-mail: Gunvor.Ahlborg{at}labtek.ki.se.

Cardiovascular diseases are characterized by insulin resistance and elevated endothelin-1 (ET-1) levels. Further, ET-1 induces insulin resistance. To elucidate this mechanism six healthy subjects were studied during a hyperinsulinemic euglucemic clamp during infusion of (the ET-1 precursor) big ET-1 alone or after ETA or ETB receptor blockade. Insulin levels rose after big ET-1± the ETB antagonist BQ788 (p<0.05), but were unchanged after the ETA antagonist BQ123+big ET-1. M/I (infused glucose devided by insulin) fell after big ET-1± BQ788 (p<0.05). Insulin and M/I values were normalized by ETA blockade. Mean arterial blood pressure rose during big ET-1±BQ788 (p<0.001) but was unchanged after BQ123. Skeletal muscle, splanchnic and renal blood flow responses to big ET-1 were abolished by BQ123. ET-1 levels rose after big ET-1 (p<0.01) in a similar way after BQ123 or BQ788, despite higher elimination capacity after ETA blockade. Conclusion: ET-1 induced reduction in insulin sensitivity and clearance as well as splanchnic and renal vasoconstriction are ETA mediated. ETA receptor stimulation seems to inhibit the conversion of big ET-1 to ET-1.




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