Why the study?
Does acetylcholine-induced endothelium-dependent vasodilatation differ in the kidneys of spontaneously hypertensive rats compared to normotensive rats?
Does acetylcholine-induced endothelium-dependent vasodilatation differ in the kidneys of spontaneously hypertensive rats compared to normotensive rats?
Endothelium-dependent vasodilatation in response to acetylcholine is impaired in the renal resistance vessels of spontaneously hypertensive rats.
Impaired renal endothelial vasodilatation in hypertensive rats supports endothelial dysfunction in hypertension pathogenesis; leaves open human translation.
The possible role of endothelium-derived relaxing factor (EDRF) was investigated in resistance vessels of the kidney obtained from spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. Kidneys were studied in parallel and perfused with Tyrode's solution at constant optimal flow rates. In the presence of indomethacin, during vasoconstriction (increase in perfusion pressure) produced by prostaglandin F2 alpha, acetylcholine caused a graded dilatation (pressure fall) that was greater in kidneys of WKY than of SHR. Methylene blue and hydroquinone, but not oxyhemoglobin, inhibited the decreases in perfusion pressure induced by acetylcholine, but not those by papaverine. The results suggest that part of the renal vasodilatation induced by acetylcholine is mediated by endothelium-derived relaxing factor, and that the response is impaired in the resistance vessels of the hypertensive rat kidney.
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Tuncer et al. (1993) studied this question.
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