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      Effects of Insulin on Coronary Blood Flow in Anesthetized Pigs

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          Insulin can influence the vasculature by a sympathetically mediated vasoconstriction and a vasodilatation; the latter effect predominates in the renal circulation of anesthetized pigs. We determined the effect of intravenous infusion of insulin on coronary blood flow in pentobarbitone-anesthetized pigs at constant heart rate, arterial pressure and blood levels of glucose and potassium. In 6 pigs, infusion of 0.004 IU kg<sup>–1</sup> min<sup>–1</sup> of insulin decreased coronary flow despite increasing left ventricular d P d t<sub>max</sub><sup>–1</sup>; when the latter was abolished by propranolol, the coronary flow response was augmented. The mechanisms of this response were examined in 22 pigs given propranolol. Phentolamine changed coronary flow response to an increase (6 pigs) and this was abolished by intracoronary injection of N<sup>ω</sup>-nitro- L-arginine methyl ester (L-NAME; 5 pigs). L-NAME augmented coronary flow response (6 pigs) and this was abolished by phentolamine (5 pigs). In 18 pigs given propranolol, three incremental doses of insulin caused graded coronary flow decreases whether L-NAME was given (6 pigs) or not (6 pigs) beforehand, and caused graded coronary flow increases after phentolamine (6 pigs). Thus insulin caused a coronary vasoconstriction mediated by sympathetic α-adrenergic effects and a vasodilatation related to the release of nitric oxide. The net effect was a coronary vasoconstriction.

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          Insulin-Induced Increment of Coronary Flow Reserve Is Not Abolished by Dexamethasone in Healthy Young Men

           H LAINE (2000)
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            Mechanisms of the renal vasodilation caused by insulin in anesthetized pigs

            The present study was planned to determine the mechanisms involved in the renal vasodilation caused by insulin. Changes in flow caused by the intravenous infusion of 0.004 IU/kg/min of insulin at constant heart rate, aortic blood pressure, left ventricular contractility and blood levels of glucose and potassium in the left renal artery were assessed using an electromagnetic flowmeter. In ten pigs, infusion of insulin caused an increase in renal blood flow which averaged 12.8% of the control values. After hemodynamic variables had returned to control values, insulin infusion was repeated in five pigs following blockade of alpha-adrenergic receptors with injection of phentolamine into the renal artery and in the other five pigs following blockade of nitric oxide formation with injection in the same artery of Nomega-nitro-L-arginine methyl ester (L-NAME). After blockade of alpha-adrenergic receptors, insulin infusion caused an increase in renal blood flow which averaged 18.1% of the control values, being significantly enhanced with respect to the increase previously obtained in the same pigs. On the contrary, after blockade of nitric oxide formation insulin infusion caused a decrease in renal blood flow which averaged 6.5% of the control values. These responses were respectively abolished by the subsequent injection into the renal artery of L-NAME and phentolamine. The present study showed that the renal vasodilation caused by insulin in the anesthetized pig was the result of two opposite effects which involved a predominant vasodilation mediated by the release of nitric oxide from the endothelium and a sympathetic vasoconstrictor mechanism mediated by alpha-adrenergic receptors.

              Author and article information

              J Vasc Res
              Journal of Vascular Research
              S. Karger AG
              December 2002
              17 January 2003
              : 39
              : 6
              : 504-513
              Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia, Università del Piemonte Orientale ‘A. Avogadro’, Novara, Italia
              67203 J Vasc Res 2002;39:504–513
              © 2002 S. Karger AG, Basel

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              Page count
              Figures: 5, Tables: 1, References: 28, Pages: 10
              Research Paper


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