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Renal medullary blood flow (MBF) is believed today to have a potent role in blood pressure control through its influence on sodium and water excretion. The present article reviews: (i) the study of MBF in two experimental models of heritable hypertension, namely spontaneously hypertensive rats (SHR) and Lyon genetically hypertensive (LH) rats selected, respectively, from Wistar and Sprague-Dawley rats; and (ii) the regulation of MBF by the renin–angiotensin system (RAS) in these animals and the interaction between angiotensin (Ang) II and nitric oxide, prostaglandins and reactive oxygen species in the renal medulla.

Although numerous renal disorders are observed during or after the development of hypertension, the reduced pressure–natriuresis function is an early apparent and common abnormality found in SHR and LH rats. This abnormality is associated with a blunted increase in MBF in response to elevations in renal perfusion pressure. Moreover, both SHR and LH rats exhibit an exaggerated medullary vasoconstriction and/or a reduced medullary vasodilatation under stimulation with AngII.

Chronic RAS blockade prevents the development of hypertension in both SHR and LH rats. This effect involves an improved response of MBF to increasing renal perfusion pressure and to AngII.

Medullary blood flow is inappropriately regulated in genetically hypertensive rats; a decreased MBF caused by the disequilibrium of local vasodilator/vasoconstrictor systems may favour the prohypertensive role of the RAS in genetic hypertension.
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Keywords: angiotensin II; genetic hypertension; pressure natriuresis; renal medullary circulation

Document Type: Research Article

Publication date: May 1, 2009

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