1 Altered vasoreactivity may contribute signi®cantly to the pathogenesis of diabetic vascular complications. This study investigated the eect of (a) insulin-treated diabetes, and (b) chronic in vivo administration of N o -nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, on mean arterial pressure and in vitro vascular reactivity to noradrenaline in mesenteric arterial bed preparations from spontaneously diabetic, insulin-dependent and treated BB rats, the best animal model of insulin-dependent mellitus (IDDM) currently available. Four groups of animals from the Edinburgh colony (BB/E) of spontaneously diabetic BB rats were studied: age-matched (mean+s.e.mean=156+2d) non-diabetic (glycated haemoglobin=3.8+0.1%) and insulin-treated diabetic (glycated haemoglobin=6.2+0.5%; duration of diabetes=56+4 d) groups were either L-NAME treated (oral dose=27+1 mg kg 71 d 71 ; duration of treatment from 30 until 153 days of age) or untreated. Although our diabetic BB/E rats do not achieve overall normoglycaemia, individual adjustment of the daily insulin dose administered to every diabetic rat achieves better glycaemic control than previous groups studying altered vascular reactivity and endothelial dysfunction in this animal model of diabetes. 2 Mean arterial pressure (measured directly via indwelling carotid arterial cannulae) was not signi®cantly dierent between non-diabetic (116+3 mmHg; n=10) and diabetic (122+2 mmHg; n=12) BB/E rats. L-NAME treatment signi®cantly (P50.001) increased mean arterial pressure in both groups (165+6 mmHg; n=9 and 142+4 mmHg; n=6 respectively) but the degree of hypertension observed in L-NAME-treated diabetic rats was signi®cantly (P50.01) attenuated compared to nondiabetic rats treated with L-NAME. 3 Mesenteric arterial bed preparations were cannulated under anaesthesia, excised and intralumenally perfused ex vivo with noradrenaline (0.2 ± 20 mM). Basal perfusion pressures were not signi®cantly dierent in mesentery preparations from non-diabetic (27.0+2.6 mmHg) and diabetic (27.1+3.2 mmHg) BB/E rats. There was no signi®cant dierence in maximal response above basal perfusion pressure (MAX) or pEC 50 , de®ned as the negative log of the agonist concentration required to give 50% of the maximal response above basal perfusion pressure, to noradrenaline in untreated non-diabetic (166+7 mmHg and 5.74+0.05 respectively) and diabetic (170+11 mmHg and 5.59+0.05) BB/E rats. 4 In vivo treatment of non-diabetic and diabetic BB/E rats with L-NAME had no signi®cant eect on basal perfusion pressure (25.9+4.8 mmHg and 28.5+3.9 mmHg respectively). L-NAME treatment in vivo increased (P50.001) MAX to noradrenaline of non-diabetic rats (224+8 mmHg) but did not aect the value for diabetic rats (178+14 mmHg). L-NAME treatment did not alter the pEC 50 values in either group (5.71+0.05 and 5.65+0.05). 5 Consistent with previous studies using vascular preparations from spontaneously diabetic BB rats, mesentery preparations from diabetic BB/E rats (n=12) exhibited a signi®cantly reduced vas...
Biochemical and biophysical properties of umbilical arteries from normotensive and preeclamptic pregnancies were examined. The production of prostaglandins E and F, 6-keto-PGF1 alpha, and thromboxane B2 by umbilical arteries from normotensive, mildly preeclamptic, and severely preeclamptic pregnancies were measured in incubation media at baseline and after addition of arachidonic acid. The initial baseline values of 6-keto-PGF1 alpha were decreased in the severely preeclamptic patients with intrauterine growth retardation (IUGR) but not in any of the other groups. Addition of arachidonic acid resulted in a significant increase in 6-keto-PGF1 alpha production over initial baseline in all groups except in the severely preeclamptic pregnancies without IUGR. These results suggest a differential defect in the 6-keto-PGF1 alpha metabolic pathway in severely preeclamptic patients with IUGR compared with those without IUGR. The stretch response curve to serotonin was decreased in the severely preeclamptic group with IUGR compared with the control group. The contractile response to individual vasoactive agents (serotonin, prostaglandin F2, norepinephrine, angiotensin II, and arachidonic acid) showed no significant difference between the normotensive and preeclamptic groups.
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