POTASSIUM SUPPLEMENTATION LOWERS BLOOD-PRESSURE AND INCREASES URINARY KALLIKREIN IN ESSENTIAL HYPERTENSIVES

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dc.contributor.authorVALDES, G
dc.contributor.authorVIO, CP
dc.contributor.authorMONTERO, J
dc.contributor.authorAVENDANO, R
dc.date.accessioned2025-01-23T19:22:42Z
dc.date.available2025-01-23T19:22:42Z
dc.date.issued1991
dc.description.abstractIn order to eludicate possible mechanism(s) involved in the blood pressure reduction induced by potassium (K) supplementation, we studied the changes of BP and of some of its regulatory systems, including levels of urinary kallikrein (UKal)-an index of renal kallikrein production. Twenty-four untreated essential hypertensives, with a basal BP of 147/96 +/- 13/7 mmHg and normal renal function, received in crossover, double-blind, randomised fashion, 64 mmol KCl or placebo during two periods of 4 weeks each. At the 4th week of potassium supplementation systolic, diastolic and mean BPs decreased by 6.3 +/- 2 (P < 0.01), 3.0 +/- 2 and 4.1 +/- 2 (P < 0.05) mmHg respectively for the supine position, and 5.0 +/- 2, 4.0 +/- 2 (P < 0.05) and 4.0 +/- 1 (P < 0.05) mmHg for the standing position. Urinary potassium (K) increased from 55 +/- 4 to 123 +/- 6 mmol/24 hours (P < 0.001) and UKal from 692 +/- 69 to 1052 +/- 141 mU/24 hours (P < 0.01). Serum K rose from 3.8 +/- 0.1 mEq/l to 4.1 +/- 0.1 mmol/l (P < 0.001) and PRA from 0.77 +/- 0.12 to 0.99 +/- 0.14 ng/ml/h (P < 0.05). Correlations were observed between UKal and urinary K (r = 0.44, P < 0.0001); between differences in UKal and urinary K and in UKal and urinary Na (r = 0.50, P < 0.0005 and r = 0.48, P < 0.001 respectively). Responders to KCl supplementation (n = 7) had a greater increase of urinary kallikrein (P < 0.005) and PRA (P < 0.05) than nonresponders (n = 8). The present study confirms the mild BP lowering effect and stimulation of UKal by KCl supplementation and shows that variations in UKal correlate with urinary K and characterise patients with potassium sensitivity. Further studies, that include determinations of the circulating components of the kallikrein-kinin system, are required to elucidate whether bradykinin, the enzymatic product of kallikrein and potent stimulator of endothelial protective factors, may be a mediator of the vascular effects described for a high K intake.
dc.fuente.origenWOS
dc.identifier.issn0950-9240
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/99083
dc.identifier.wosidWOS:A1991FN99500005
dc.issue.numero2
dc.language.isoen
dc.pagina.final96
dc.pagina.inicio91
dc.revistaJournal of human hypertension
dc.rightsacceso restringido
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titlePOTASSIUM SUPPLEMENTATION LOWERS BLOOD-PRESSURE AND INCREASES URINARY KALLIKREIN IN ESSENTIAL HYPERTENSIVES
dc.typeartículo
dc.volumen5
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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