Renal artery clamping

Spontaneously hypertensive rats can be used to screen compounds for antihypertensive effects and for effects on heart rate. The animals are dosed for one or a few days. Blood pressure and heart rate are measured by means of an inflatable cuff around the tail. Most classes of antihypertensives will be detected. Agents such as beta-adrenergic antagonists will be detected by decreased heart rate. Other rat models include deoxycorticosterone acetate (DOCA)-induced hypertensive, renal hypertensive (one or both renal arteries clamped), and stroke-prone spontaneously hypertensive rats. Hypertensive dogs produced by clamping one or both renal arteries may also be used to test or verify antihypertensive activity in a second species. 

Ischemic AKI may be induced by intrarenal norepinephrine injection or by renal artery clamping. There are similarities between these two models of ischemic renal failure. In the norepinephrine model of renal failure, as in the arterial clamping model, there is the same degree of tubular injury except for a slightly greater frequency of tubular casts at 48 hours in ischemic model [32]. In both models, calcium channel-blockers, improve renal function [33, 34]. The major difference is that in the renal artery clamping model, morphology at 48 hours showed smooth muscle necrosis in half of the resistance vessels, but in less than 10% of those in norepinephrine-induced model. 

Renal artery and vein had been clamped 2 hours previously... 

Apoptosis was observed in the rat renal tubular cells after clamping the renal artery for 30 min and two hours of reperfusion (Toronyi et al. 1999). Calcium chaimel blockers given into the carotid artery at the beginning of reperfusion decreased the number of apoptotic cells. 

In the Goldblatt method hypertension is induced by moderate constriction of both main renal arteries (by adjustable silver clamps) or by the constriction of one main renal artery and extirpation of the contralateral kidney. The Goldblatt procedure is applicable not only to dogs, but also to the monkey, rat, rabbit, goat, and sheep. Historically, it is interesting that Katzenstein (100) in 1905 had already observed a slight temporary elevation of blood pressure after partial occlusion of the renal arteries in dogs. 

In order to produce persistent hypertension in animals, it is necessary to restrict the blood flow in both kidneys or to clamp one renal artery and remove the contralateral normal kidney. The presence of a normal kidney seems to have a protective action against the development of severe hypertension. Tigerstedt and Bergman (176) pointed out that the pressor effect of renin was more marked and prolonged in rabbits which had undergone nephrectomy than in normal rabbits. Merrill, Williams, and Harrison (114) found that this increased sensitivity to renin did not appear immediately after removal of the kidneys but developed several days later. The hypothesis was advanced that the body normally contains some substance elaborated by the kidneys which antagonizes the pressor action of renin and which gradually disappears from the body after nephrectomy. 

Hypertension can be produced by partial constriction of both renal arteries, by constriction of one renal artery and extirpation of the contralateral kidney, and by a variety of other procedures (127), which all seem to result in a reduction of the expansile pulsation of the kidney. The fact that hypertension can also be produced by transplanted kidneys (24,51), that it may be produced or persist after denervation of the kidneys or after extensive sympathectomy (40), indicates that the nervous system plays no part in establishing this hypertension. However, no rise in blood pressure is observed if the renal vein is clamped simultaneously with the con-... 

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