Chronological changes in renal vascular reactivity in portal hypertensive rats.

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    • Subject Terms:
      LABORATORY rats; HYPERTENSION; CARDIOVASCULAR diseases; VASODILATION; VASOCONSTRICTORS; HEMODYNAMICS; NITRIC-oxide synthases
    • Abstract:
      Background Circulatory dysfunction in portal hypertension is characterized by increased cardiac output, decreased systemic vascular resistance, a fall in mean arterial pressure secondary to splanchnic and systemic vasodilation and hence renal hypoperfusion. Previous studies have disclosed that renal vasculatures of portal hypertensive rats had lower perfusion pressure and hyporesponsiveness to endogenous vasoconstrictors. However, the sequences of altered renal haemodynamics have never been described. This study aimed to explore the evolution of renal vascular hyporeactivity and associated mechanisms during portal hypertension. Materials and methods All rats were randomized into partial portal vein ligation ( PVL) or shamed surgery. Isolated kidney perfusion was performed at postoperative day 1, 4, 7 and 14, respectively, to evaluate chronologically renal vascular response to endothelin-1. Renal arteries and kidneys were harvested for further analysis. Results Impaired renal vascular reactivity to endothelin-1 developed 1 week following PVL. There were extensive up-regulations of vasodilative nitric oxide synthase ( NOS) and cyclooxygenase-2 in renal arteries of PVL rats. Among them, the changes in endothelial NOS paralleled with the evolution of renal vascular hyporesponsiveness. Preincubation of NOS inhibitor attenuated the renal vascular hyporeactivity in PVL rats. Up-regulated NOS and down-regulated cyclooxygenase-2 in kidneys of PVL rats might play a critical role to maintain renal circulation and body fluid homoeostasis in response to systemic hypotension. Conclusions This investigation highlights the versatile nature of renal vasculatures in portal hypertension, which is replete with compensatory mechanisms. It may help to unveil potential mechanisms of severe renal dysfunction in advanced liver disease. [ABSTRACT FROM AUTHOR]