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Insulin attenuates alpha-adrenergic aortic contraction in normotensive but not borderline hypertensive rats.
Winecoff, A P; Tackett, R L; Fuchs, L C.
Afiliación
  • Winecoff AP; Department of Pharmacy Practice, College of Pharmacy, University of Georgia, Augusta, USA.
Clin Exp Hypertens ; 17(5): 787-801, 1995 Jul.
Article en En | MEDLINE | ID: mdl-7655448
Hyperinsulinemia can alter vasoconstrictor responses in normotensive and hypertensive rats, but the effects of insulin on vascular contraction have not been evaluated in borderline hypertension. This study determined the effects of insulin on alpha-adrenoceptor mediated aortic contraction in male and female borderline hypertensive rats (BHR) and normotensive Wistar Kyoto (WKY) rats. Dose-response curves to norepinephrine (NE) and phenylephrine (PE) were performed in thoracic aorta in the absence or presence of insulin (100 microU/ml) for 2 hrs. Contraction to NE and PE was reduced in aorta from female WKY rats incubated with insulin compared to control. In aorta from 6 of 13 male WKY rats (insulin responders), an attenuated response to NE and PE was observed in the presence of insulin. However, insulin did not alter responses to NE or PE in aorta from male or female BHR. These results indicate that insulin impairs alpha-adrenoceptor mediated contraction in the normotensive female WKY rat and in a group of responder male WKY rats, but not in BHR. This study supports the presence of a resistance to the vascular effects of insulin in BHR.
Asunto(s)
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vasoconstricción / Receptores Adrenérgicos alfa / Hipertensión / Insulina Límite: Animals Idioma: En Revista: Clin Exp Hypertens Año: 1995 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
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Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Vasoconstricción / Receptores Adrenérgicos alfa / Hipertensión / Insulina Límite: Animals Idioma: En Revista: Clin Exp Hypertens Año: 1995 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido