ABSTRACTS PRESENTADOS AL 11th INTERNATIONAL SYMPOSIUM "RADIONUCLIDES IN NEPHRO-UROLOGY", REALIZADO EN MONTEREY, CALIFORNIA, 13-17 MAYO 2001.
17. SYMMETRICAL CORTICAL NEPHRON BLOOD FLOW REDUCTION:IS THIS THE PHENOTYPIC EXPRESSION OF THE GENOMIC ANGIOTENSINOGEN, AGT, POLYMORPHISM IN ESSENTIAL HYPERTENSION.
Britton
KE, Nimmon CC, Caulfield M. Departments of Nuclear Medicine and Clinical
Pharmacology, St Bartholomew's Hospital London.
Essential Hypertension EH is a familial disorder associated with a symmetrical reduction of effective renal plasma flow (1). We have demonstrated using bimodal transit time distribution in man that this reduction is due to a similar reduction of cortical nephron CN plasma flow with no change in juxta medullary nephron plasma flow in both kidneys (2,3) and that this is reversible by the action of angiotensin converting enzyme inhibitors (2,4). Caufield has shown a strong linkage and association of the AGT gene locus with EH in white British families (5) and in sib pairs of Afro Caribbean origin (6). A strong correlation has been shown between the plasma AGT concentration and blood pressure (7). The non-modulation phenotype seen in 40% of EH shows altered angiotensin 2 responsiveness to a high salt intake, interpreted as increased intra renal A2 production (8) and recently they showed a correlation between the AGT gene locus and non-modulator status. Increased Angiotensinogen in the Juxtaglomerular apparatus may cause an over autorregulation and overcontraction of the cortical nephron afferent arterioles accounting for the symmetrical reduction in CN plasma flow seen in essential hypertension. This can be tested using our improved technique of intrarenal flow measurement(9).
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2. Lancet 1981; ii:900-903.
3. Clin. Sci 1981; 61:385-389.
4. Nephron 1990; 54: 47-53.
5. N Engl J Med 1994; 330:1629-1633.
6. J Clin Invest 1995; 96: 687-692.
7. Hypertension 1979; 1:287-291.
8. Hypertension 1992; 20:788-796.
9. Eur J Nucl Med 2000: 27; 994.
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