Effect of nephrectomy on the reactivity of arteries from the Wistar rats

BACKGROUND. Cardiovascular diseases are the main cause of death in patients with chronic kidney disease (CKD). The study of the mechanisms of vascular dysfunction in CKD is relevant. To simulate CKD, a decrease in the mass of functioning nephrons is used in the experiments.

THE AIM. The effect of nephrectomy on the dilator and constrictor properties of the arteries was studied in experiments on segments of the superior mesenteric artery (SMA) and internal carotid artery (ICA) of Wistar rats.

MATERILS AND METHODS. Nephrectomy in rats was performed by resection of 5/6 of the mass of renal tissue. Vascular segment reactivity was assessed under isometric conditions. In isolated segments of vessels precontracted with phenylephrine, dilation was induced using acetylcholine or sodium nitroprusside before and during the action of tetraethylammonium or glibenclamide as potassium channel blockers, or methylene blue as a guanylate cyclase inhibitor.

RESULTS. Nephrectomy was shown to increase the contractile response of the arteries to phenylephrine to the greatest extent in SMA (more than 2 times). The dilatation of the arteries to sodium nitroprusside in nephrectomized and control rats was the same. The reaction of SMA and ICA to acetylcholine in most cases consisted of a dilatation and a much smaller constrictor phase. In nephrectomized rats, the magnitude of both the dilator and constrictor phases of the arterial reaction to acetylcholine was significantly lower than in control animals. Tetraethylammonium significantly decreased acetylcholine-induced dilation of the SMA and ICA, and methylene blue reduced this dilation in nephrectomized rats significantly less than in control animals. This, as well as the significant decrease in the dilatation of SMA to nitroprusside in the presence of methylene blue in control rats and an increase in nephrectomized rats, may indicate a malfunction of guanylate cyclase after nephrectomy.

CONCLUSIONS. CKD causes vascular dysfunction, in which arterial constrictor responses mediated by α1-adrenergic receptors are enhanced and endothelium-dependent dilator responses are weakened, which may cause, in particular, an increase in blood pressure.

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