Mesenteric arteries and saphenous veins of control and perinephritic hypertensive dogs were studied with light and electron microscopy. 2 weeks after surgery there are ultrastructural changes, both in arteries and veins which are thought to be of hydroelectrolytic origin. These alterations are more marked 7 weeks after surgery and disappear thereafter. There are signs of increased protein synthesis activity in the smooth muscle of the mesenteric arteries, but not of the saphenous veins obtained 7 and 14 weeks after surgery, leading to a progressive hypertrophy of the muscular cells. The connective tissue augmented proportionally. Degeneration of adrenergic nerves in the arteries, accompanied by a parallel decrease in their noradrenaline content, constituted an unexpected finding clearly deserving further study.

Tissue noradrenaline content as well as uptake and metabolism of tritiated exogenous noradrenaline were studied comparatively, in vitro in mesenteric arteries, and in saphenous veins of normotensive and perinephritic hypertensive dogs. The influence of cocaine, iproniazid and 3’-4’-dihydroxy-2-methyµ-propiophenone (U-0521) on these variables wasalso investigated. The concentration of (–)-7-³H-noradrenaline used was 1.084 µM. No changes were observed in noradrenaline content, uptake and metabolism in saphenous vein strips obtained from normotensive or hypertensive animals. However, in mesenteric artery strips obtained from hypertensive dogs, a marked reduction in endogenous noradrenaline content was observed as well as a reduction in noradrenaline accumulation (20 weeks after surgery). The deamination pattern was also modified in these strips: the formation of DOPEGwas markedly diminished and the formation of DOMA was increased. These results agree well with the degeneration of the sympathetic innervation of the mesenteric arteries of hypertensive dogs described by Azevedo et al. (1981).

Direct vascular effects of trimetaphan camsylate were studied in the dog mesenteric artery and lateral saphenous vein; vascular strips were suspended in normal Krebs-Henseleit solution and contraction produced by phenylephrine 2.4 X 10(-6) mol litre-1. Both vessels were relaxed by trimetaphan, maximal relaxation being obtained at the concentration of 1.3 X 10(-3) mol litre-1; this effect was more marked in the vein strips. Calculated ED50 for the relaxing effect of trimetaphan was not significantly different between artery and the vein. It is concluded that the sensitivity of arteries and veins to trimetaphan is similar, but that this effect cannot play a significant role in the production of controlled hypotension.

No abstract

Perinephritic hypertension was induced in mongrel dogs by cellophane encapsulation of one kidney and simultaneous contralateral nephrectomy. Systolic blood pressure began to rise before diastolic blood pressure and both reached maximal values 3 weeks after surgery, their levels becoming stable thereafter up to the end of the study (20 weeks). Cardiac contractility, measured by the index dp/dt/P₄₀ (rate of rise of isovolumic left intraventricular pressure at a developed left ventricular pressure of 40 mm Hg) was not altered during the evolution of hypertension; heart weight and left ventricular thickness were increased. Plasma renin activity markedly decreased in the chronic phase and plasma urea and creatinine levels rised initially in a moderate but significant way, thereafter remaining stable. The structure of the wrapped kidney remained normal 20 weeks after surgery, when microscopic arterial lesions were seen in other organs. The comparison of the evolution of this hypertensive model with other more commonly used renal experimental hypertension types allows us to conclude that cellophane perinephritic hypertension in the dog must be considered as an individual entity.