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|dc.creator||Gomez-Alamillo, C. (Carlos)||-|
|dc.creator||Sanchez-Casajus, A. (Angel)||-|
|dc.creator||Sierra, M. (Milagros)||-|
|dc.creator||Huarte, E. (Eduardo)||-|
|dc.creator||Diez-Martinez, J. (Javier)||-|
|dc.identifier.citation||Gomez-Alamillo C, Sanchez-Casajus A, Sierra M, Huarte E, Diez J. Vasoconstriction of the afferent arteriole and defective renal synthesis of nitric oxide in essential hypertension. Kidney Int Suppl 1996 Jun;55:S129-31.||es_ES|
|dc.description.abstract||This study was designed to investigate whether some relation exists between afferent arteriolar resistance (AAR) and the renal production of nitric oxide (NO) and prostacyclin (PGI2) in 21 patients with untreated essential hypertension and 20 normotensive controls. All subjects were studied in conditions of an unlimited Na+ diet both basally and after a four-hour amino acid infusion. AAR was calculated using Gomez's equations. Renal production of NO and PGI2 were assessed by radioimmunoassay of the urinary excretion of cGMP and 6-keto-PGF1 alpha, respectively. Baseline AAR was higher (P < 0.01) in hypertensives than in normotensives. The baseline urinary excretion of 6-keto-PGF1 alpha and cGMP were similar in the two groups of subjects. AAR diminished (P < 0.005) in normotensives and remained unchanged in hypertensives after amino acid infusion. Urinary excretion of 6-keto-PGF1 alpha was increased similarly in the two groups of subjects after infusion. Urinary excretion of cGMP remained unchanged in normotensives and decreased by 31% in hypertensives after infusion. These findings suggest that afferent vasoconstriction present in hypertensive patients is unresponsive to the vasodilatory manoeuvre of amino acid infusion. This lack of response may be due to a defective renal synthesis of NO in these patients.||es_ES|
|dc.publisher||Nature Publishing Group||es_ES|
|dc.title||Vasoconstriction of the afferent arteriole and defective renal synthesis of nitric oxide in essential hypertension||es_ES|
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