Key result
In isolated perfused rat kidneys, the enhanced vascular reactivity to vasoconstrictors seen in the hypertensive state was blunted by simultaneously occurring diabetes mellitus.
Why the study?
Do diabetes and hypertension cause additive effects on vascular responsiveness to vasoconstrictor and vasodilator agents in isolated perfused rat kidneys?
Do diabetes and hypertension cause additive effects on vascular responsiveness to vasoconstrictor and vasodilator agents in isolated perfused rat kidneys?
In isolated perfused rat kidneys, the enhanced vascular reactivity associated with hypertension is blunted by concurrent diabetes mellitus, without affecting vasorelaxation.
Suggests opposing rather than additive vascular effects in comorbidity; leaves open human translation from rat models.
OBJECTIVE: The aim of this study was to investigate whether diabetes and hypertension cause additive effects in the responses to various vasoconstrictor and vasodilator agents, in isolated perfused kidneys obtained from streptozotocin (STZ)-diabetic Wistar-Kyoto (WKY) rats and from diabetic spontaneously hypertensive rats (SHR). METHODS: SHR and WKY rats were administered STZ 55 mg/kg by intravenous injection into a lateral tail vein at age 12 weeks. Eight weeks later the kidneys were isolated and perfused via the left renal artery with a physiological salt solution. Renal perfusion pressure was measured continuously. Concentration response curves were plotted for various vasoconstrictor and vasodilator agents. RESULTS: Both the diabetic and the hypertensive state were associated with an increased wet kidney weight. The contractile responses of the renal arterial system to phenylephrine (PhE), serotonin (5-HT) and angiotensin II (Ang II) in terms both of the maximal rise in perfusion pressure (mmHg) and of the sensitivity (log EC50) were the same in preparations from diabetic WKY rats and in those from normoglycaemic WKY rats. The maximal contractile responses both to PhE and to Ang II were enhanced in kidneys from SHR compared with those in kidneys from their normotensive controls, whereas simultaneously occurring diabetes impaired this sensitization. After precontraction with 3 x 10(-6) mol/l PhE both endothelium-dependent (methacholine) and endothelium-independent (sodium nitroprusside) vasodilator drugs caused the same vasodilator response in the preparations taken from the four groups of animals. CONCLUSION: In isolated perfused kidneys obtained from STZ-diabetic WKY rats and SHR, the isolated diabetic state did not influence the vasoconstriction caused by various agonists. However, the enhanced vascular reactivity in the hypertensive state was blunted by simultaneously occurring diabetes mellitus. Endothelium-dependent and -independent vasorelaxation in this model was not affected neither by the hypertensive nor by the diabetic state.
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Beenen et al. (1996) studied Diabetes and hypertension (animal model). Diabetes (STZ-induced) and hypertension vs. Normoglycaemic and normotensive control rats was evaluated on Contractile responses of the renal arterial system to vasoconstrictors and vasodilators. In isolated perfused rat kidneys, the enhanced vascular reactivity to vasoconstrictors seen in the hypertensive state was blunted by simultaneously occurring diabetes mellitus.
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