Why the study?
Does experimental renal failure alter vascular relaxation in rat resistance vessels?
Does experimental renal failure alter vascular relaxation in rat resistance vessels?
Experimental renal failure in rats impairs beta-adrenergic relaxation but preserves endothelium-dependent relaxation in resistance vessels.
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Impaired beta-adrenergic relaxation in uremic rat vessels should not yet inform clinical practice; leaves open selective adrenergic mechanisms in human CKD.
Chronic renal failure is associated with increased cardiovascular morbidity and reduced arterial elasticity. Only little information is available on the functional effects of uraemia on resistance arteries. Therefore, we studied the influence of renal failure on rat small mesenteric vessels. The responses of arterial rings were investigated in a Mulvany myograph 6 weeks after 5/6 nephrectomy or sham operation. The subtotal nephrectomy resulted in a 1.9-fold elevation of plasma urea nitrogen but was without significant effect on blood pressure. Endothelium-dependent relaxations, largely mediated via arterial K(+) channels, were preserved in the resistance vessels of uraemic rats. Endothelium-independent vasorelaxations, mediated via exogenous nitric oxide and the opening of ATP-sensitive K(+) channels, were also unchanged. However, the responses induced by isoprenaline were slightly reduced, indicating impaired relaxation via beta-adrenoceptors in experimental renal failure.
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Jolma et al. (2002) studied this question.
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