Why the study?
Chronic kidney disease is accompanied by cardiovascular complications, prompting a comparison of the reactivity of skin microcirculatory bed vessels and mesenteric arteries in 5/6 nephrectomy rats.
Does experimental kidney dysfunction (5/6 nephrectomy) impair vascular reactivity in skin microvessels and mesenteric arteries in rats?
Does experimental kidney dysfunction (5/6 nephrectomy) impair vascular reactivity in skin microvessels and mesenteric arteries in rats?
Experimental kidney dysfunction in rats induces endothelial dysfunction and alters microcirculatory tone, reducing vascular reactivity in both skin and mesenteric beds.
May inform microvascular models in experimental CKD; leaves open whether skin LDF tracks mesenteric reactivity in patients.
Chronic kidney disease is accompanied by cardiovascular complications, including endothelial dysfunction, arterial hypertension, and atherosclerosis. The aim of this work was to compare the reactivity of skin microcirculatory (MCR) bed vessels, assessed via laser Doppler flowmetry (LDF), and mesenteric arteries in 5/6 nephrectomy rats. Wistar rats were divided into two groups: NE (nephrectomy) group included rats with 5/6 kidney tissue resected (n = 15), while SO (sham operated) group comprised sham operated rats (n = 15). After 8 weeks, the reactivity of rat skin microvessels to acetylcholine (ACh) and sodium nitroprusside (NP) iontophoresis was assessed. A week later, the effect of NE on the reactivity of phenylephrine-preconstricted mesenteric arteries was assessed in vivo using microphotographic and video recording of the vascular diameter. NE had no effect on average values of resting blood perfusion in the skin, however, altered the structure of the frequency spectrum of skin microcirculatory index (SMI) fluctuations, increasing the value of endothelial, neurogenic, and myogenic tone. NE led to the development of endothelial dysfunction of mesenteric arteries and skin MCR vessels, as manifested in a decrease in vascular reactivity to endothelium-dependent (ACh) and endothelium-independent (NP) vasodilators. Thus, experimental kidney dysfunction entailed changes in the spectral components of SMI fluctuations in the skin, suggesting an increase in tonic vascular effects of various genesis. NE was accompanied by a decrease in the reactivity of skin microvessels and mesenteric arteries, however, there was no correlation between an increase in the SMI and dilation of the mesenteric arteries in response to vasodilatory agonists at this follow-up period.
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Иванова et al. (2023) studied this question.
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