Time course of vascular prostanoid production in the fructose-hypertensive rat

A. M. PUYÓ; M. ZABALZA; M. A. MAYER; A. CARRANZA; H. A. PEREDO

Autonomic & Autacoid Pharmacology

Año: 2009 p. 135 - 139

1 There is a relationship between hypertension, insulin resistance and an altered plasmaticlipid profile known as metabolic syndrome’. Fructose (F) overload induces in the rat a mildhypertension associated with metabolic alterations such as hyperglycemia, hypertriglyceride-mia and insulin resistance, resembling such syndrome.2 Prostanoids (PR), metabolites of arachidonic acid, include vasoactive substances synthesizedand released by the vessel wall. An altered pattern of PR release has been previously found inmesenteric vessels of experimental diabetic rats.3 This study analyzed the effects of F-overload during different periods (4, 9, 15 and 22 weeks)on PR release in aorta (A) and mesenteric vascular beds (MVB). Animals received tap water(control) or F solution (10% w ⁄ v) to drink.4 Rats with F overload showed significantly higher systolic blood pressure, glycemia andtriglyceridemia than controls; but no differences in this parameters were found among periodsof treatment either in controls or experimental animals.5 In A, prostacyclin was decreased at 9, 15 and 22 weeks of treatment when compared to 4weeks and controls. In MVB, prostacyclin showed different patterns of release in the studiedperiods of F overload. Prostaglandin (PG) E2 diminish inMVB at the same extent in all periods.No changes were observed in A. The vasoconstrictor thromboxane was elevated in the MVB at9 weeks. PGF2a, also a vasoconstrictor, remains unchanged.6 In conclusion, F overload provokes in the rat a decrease in the vascular production ofvasodilator PR and, in one of the studied periods, an increase in the release of thevasoconstrictor thromboxane, leading to a negative imbalance in the prostacylin ⁄ thromboxaneratio. This could be involved in the blood pressure alterations found in this experimental modelof metabolic syndrome.