IDIM   12530
INSTITUTO DE INVESTIGACIONES MEDICAS
Unidad Ejecutora - UE
artículos
Título:
Urinary Kallikrein and Blood Pressure Gender-Different Response to Potassium Supplementation in SHR
Autor/es:
E. ODDO V DE LUCA SAROBE R KRMAR R. MARTÍN F IBARRA, E ARRIZURIETA
Revista:
NEPHRON
Editorial:
Karger
Referencias:
Año: 2008 vol. 108 p. 37 - 45
ISSN:
0028-2766
Resumen:
crease in systolic blood pressure was seen in male SHR: 204.5
8 7.6 versus 173.5 8 7.9 (p ! 0.05); and 164.5 8 4.8 versus
156.8 8 5.5 in female rats (NS) at 12 weeks of age, concomitant
with an increase in UKa, particularly in male rats (29.357.6 versus 173.5 8 7.9 (p ! 0.05); and 164.5 8 4.8 versus
156.8 8 5.5 in female rats (NS) at 12 weeks of age, concomitant
with an increase in UKa, particularly in male rats (29.358 5.5 in female rats (NS) at 12 weeks of age, concomitant
with an increase in UKa, particularly in male rats (29.35
8 1.92 versus 36.54 8 2.61, p ! 0.05). As expected, plasma
aldosterone (pg/ml), increased markedly after potassium
treatment from 129 8 31.4 in untreated female and male
SHR and WKY to 528 8 180.7 in SHR and 473 8 88.4 in WKY
(p ! 0.05 in both cases). After potassium supplementation,
potassium excretion was significantly correlated with both
aldosterone levels and UKa (p ! 0.001 in both cases). No significantly
concurrent changes in plasma renin activity were
observed, but instead a significant decrease was seen in SHR
(p ! 0.01). The potassium blood pressure-lowering effect
was blunted by aldosterone receptor antagonist treatment
that also decreased UKa from 36.5 8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:1.92 versus 36.54 8 2.61, p ! 0.05). As expected, plasma
aldosterone (pg/ml), increased markedly after potassium
treatment from 129 8 31.4 in untreated female and male
SHR and WKY to 528 8 180.7 in SHR and 473 8 88.4 in WKY
(p ! 0.05 in both cases). After potassium supplementation,
potassium excretion was significantly correlated with both
aldosterone levels and UKa (p ! 0.001 in both cases). No significantly
concurrent changes in plasma renin activity were
observed, but instead a significant decrease was seen in SHR
(p ! 0.01). The potassium blood pressure-lowering effect
was blunted by aldosterone receptor antagonist treatment
that also decreased UKa from 36.5 8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:8 31.4 in untreated female and male
SHR and WKY to 528 8 180.7 in SHR and 473 8 88.4 in WKY
(p ! 0.05 in both cases). After potassium supplementation,
potassium excretion was significantly correlated with both
aldosterone levels and UKa (p ! 0.001 in both cases). No significantly
concurrent changes in plasma renin activity were
observed, but instead a significant decrease was seen in SHR
(p ! 0.01). The potassium blood pressure-lowering effect
was blunted by aldosterone receptor antagonist treatment
that also decreased UKa from 36.5 8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:8 180.7 in SHR and 473 8 88.4 in WKY
(p ! 0.05 in both cases). After potassium supplementation,
potassium excretion was significantly correlated with both
aldosterone levels and UKa (p ! 0.001 in both cases). No significantly
concurrent changes in plasma renin activity were
observed, but instead a significant decrease was seen in SHR
(p ! 0.01). The potassium blood pressure-lowering effect
was blunted by aldosterone receptor antagonist treatment
that also decreased UKa from 36.5 8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:! 0.05 in both cases). After potassium supplementation,
potassium excretion was significantly correlated with both
aldosterone levels and UKa (p ! 0.001 in both cases). No significantly
concurrent changes in plasma renin activity were
observed, but instead a significant decrease was seen in SHR
(p ! 0.01). The potassium blood pressure-lowering effect
was blunted by aldosterone receptor antagonist treatment
that also decreased UKa from 36.5 8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:! 0.001 in both cases). No significantly
concurrent changes in plasma renin activity were
observed, but instead a significant decrease was seen in SHR
(p ! 0.01). The potassium blood pressure-lowering effect
was blunted by aldosterone receptor antagonist treatment
that also decreased UKa from 36.5 8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:! 0.01). The potassium blood pressure-lowering effect
was blunted by aldosterone receptor antagonist treatment
that also decreased UKa from 36.5 8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:8 2.61 to 19.5 8 1.9, particularly
in male SHR. No attempt was made in this experimental
setting to block kallikrein or kinin receptors. Conclusions:Conclusions:
UKa increases as a consequence of aldosterone
stimulation by potassium load since an aldosterone receptor
blockade abolishes UKa increment and blood pressure fall.
These results further support the hypothesis that the kallikrein
kinin system plays a role in blood pressure regulation
and they also show a gender different response to potassium
load in relation to UKa and blood pressure.
Copyright © 2008 S. Karger AG, Basel
Key Words
Hypertension, sexual dimorphism Sexual dimorphism
Potassium supplementation Urinary kallikrein activity,
sexual dimorphism Mineralocorticoids Spontaneous
hypertensive ratSexual dimorphism
Potassium supplementation Urinary kallikrein activity,
sexual dimorphism Mineralocorticoids Spontaneous
hypertensive ratUrinary kallikrein activity,
sexual dimorphism Mineralocorticoids Spontaneous
hypertensive ratMineralocorticoids Spontaneous
hypertensive rat
Abstract
Aims: To test whether blood pressure is affected by potassium
supplementation which modifies urinary kallikrein
(UK) in SHR of either sex, and to elucidate the mechanisms
involved. Design: In SHR and WKY blood pressure, renal
function and hormonal profile were studied after 1% oral
potassium supplementation starting at 4 weeks of age and
throughout until 12 weeks of age. Results were compared
with those of untreated SHR and WKY of either sex. Results:To test whether blood pressure is affected by potassium
supplementation which modifies urinary kallikrein
(UK) in SHR of either sex, and to elucidate the mechanisms
involved. Design: In SHR and WKY blood pressure, renal
function and hormonal profile were studied after 1% oral
potassium supplementation starting at 4 weeks of age and
throughout until 12 weeks of age. Results were compared
with those of untreated SHR and WKY of either sex. Results:Design: In SHR and WKY blood pressure, renal
function and hormonal profile were studied after 1% oral
potassium supplementation starting at 4 weeks of age and
throughout until 12 weeks of age. Results were compared
with those of untreated SHR and WKY of either sex. Results:Results:
Systolic blood pressure (mm Hg) started to rise in SHR and
was significantly different at 68 weeks of age: 153.5 8 7.9
versus 100 8 5.6 in female and 157 8 7.7 versus 98.4 8 6.8
in male rats (p ! 0.01). Systolic blood pressure increased progressively
in female and male rats reaching 164.5 8 4.8 and
204.5 8 7.6, respectively, at 12 weeks of age. At this time systolic
blood pressure was higher in male than in female SHR
(p ! 0.01) and UK activity (UKa; nkat/day/100 g body weight)
was slightly lower in male SHR. After 1% oral potassium supplementation
administered from 4 to 12 weeks of age, a de-8 7.9
versus 100 8 5.6 in female and 157 8 7.7 versus 98.4 8 6.8
in male rats (p ! 0.01). Systolic blood pressure increased progressively
in female and male rats reaching 164.5 8 4.8 and
204.5 8 7.6, respectively, at 12 weeks of age. At this time systolic
blood pressure was higher in male than in female SHR
(p ! 0.01) and UK activity (UKa; nkat/day/100 g body weight)
was slightly lower in male SHR. After 1% oral potassium supplementation
administered from 4 to 12 weeks of age, a de-8 5.6 in female and 157 8 7.7 versus 98.4 8 6.8
in male rats (p ! 0.01). Systolic blood pressure increased progressively
in female and male rats reaching 164.5 8 4.8 and
204.5 8 7.6, respectively, at 12 weeks of age. At this time systolic
blood pressure was higher in male than in female SHR
(p ! 0.01) and UK activity (UKa; nkat/day/100 g body weight)
was slightly lower in male SHR. After 1% oral potassium supplementation
administered from 4 to 12 weeks of age, a de-! 0.01). Systolic blood pressure increased progressively
in female and male rats reaching 164.5 8 4.8 and
204.5 8 7.6, respectively, at 12 weeks of age. At this time systolic
blood pressure was higher in male than in female SHR
(p ! 0.01) and UK activity (UKa; nkat/day/100 g body weight)
was slightly lower in male SHR. After 1% oral potassium supplementation
administered from 4 to 12 weeks of age, a de-8 4.8 and
204.5 8 7.6, respectively, at 12 weeks of age. At this time systolic
blood pressure was higher in male than in female SHR
(p ! 0.01) and UK activity (UKa; nkat/day/100 g body weight)
was slightly lower in male SHR. After 1% oral potassium supplementation
administered from 4 to 12 weeks of age, a de-8 7.6, respectively, at 12 weeks of age. At this time systolic
blood pressure was higher in male than in female SHR
(p ! 0.01) and UK activity (UKa; nkat/day/100 g body weight)
was slightly lower in male SHR. After 1% oral potassium supplementation
administered from 4 to 12 weeks of age, a de-! 0.01) and UK activity (UKa; nkat/day/100 g body weight)
was slightly lower in male SHR. After 1% oral potassium supplementation
administered from 4 to 12 weeks of age, a de-