TY - JOUR
T1 - Urinary kallikrein A marker of blood pressure sensitivity to salt
AU - Madeddu, Paolo
AU - Varoni, Maria Vittoria
AU - Demontis, Maria Piera
AU - Pinna-Parpaglia, Paolo
AU - Glorioso, Nicola
AU - Anania, Vittorio
PY - 1996
Y1 - 1996
N2 - We evaluated if a rat strain inbred for low urinary kallikrein excretion differs from normal-kallikrein Wistar rats regarding blood pressure levels in basal conditions and during alterations in sodium balance. Blood pressure was measured in unanesthetized rats on normal sodium intake. Then, blood pressure sensitivity to salt was evaluated over a period of 20 days of high sodium diet (0.84 mmol per g chow). Low-kallikrein rats showed greater systolic blood pressure levels (125 ± 3 vs. 114 ± 2 mm Hg in controls, P <0.01) at nine weeks of age. Systolic blood pressure was increased after sodium loading in the low-kallikrein group and remained unchanged in controls (150 ± 6 vs. 112 ± 2 mm Hg, P <0.01). This effect was associated with a reduced cumulative urinary excretion of sodium in the low-kallikrein rats. No group difference was found in the clearance of endogenous creatinine in basal conditions. Urinary creatinine excretion decreased during sodium loading, particularly in the low-kallikrein group. The group-difference in urinary kallikrein excretion found in basal conditions (6.85 ± 0.31 vs. 20.74 ± 1.71 nkat/24 hr in controls, P <0.01) was enhanced by high salt diet (2.96 ± 0.67 vs. 22.07 ± 2.47 nkat/24 hr in controls, P <0.01). In addition, renal kallikrein activity and content were reduced in low-kallikrein rats. The latter group showed a greater ratio of heart weight to body wt both in basal conditions and after sodium loading. The ratio of kidney weight to body wt was reduced after sodium loading. These results indicate that a genetically-determined defect in urinary kallikrein excretion is associated with a greater blood pressure sensitivity to salt, possibly due to altered renal sodium handling.
AB - We evaluated if a rat strain inbred for low urinary kallikrein excretion differs from normal-kallikrein Wistar rats regarding blood pressure levels in basal conditions and during alterations in sodium balance. Blood pressure was measured in unanesthetized rats on normal sodium intake. Then, blood pressure sensitivity to salt was evaluated over a period of 20 days of high sodium diet (0.84 mmol per g chow). Low-kallikrein rats showed greater systolic blood pressure levels (125 ± 3 vs. 114 ± 2 mm Hg in controls, P <0.01) at nine weeks of age. Systolic blood pressure was increased after sodium loading in the low-kallikrein group and remained unchanged in controls (150 ± 6 vs. 112 ± 2 mm Hg, P <0.01). This effect was associated with a reduced cumulative urinary excretion of sodium in the low-kallikrein rats. No group difference was found in the clearance of endogenous creatinine in basal conditions. Urinary creatinine excretion decreased during sodium loading, particularly in the low-kallikrein group. The group-difference in urinary kallikrein excretion found in basal conditions (6.85 ± 0.31 vs. 20.74 ± 1.71 nkat/24 hr in controls, P <0.01) was enhanced by high salt diet (2.96 ± 0.67 vs. 22.07 ± 2.47 nkat/24 hr in controls, P <0.01). In addition, renal kallikrein activity and content were reduced in low-kallikrein rats. The latter group showed a greater ratio of heart weight to body wt both in basal conditions and after sodium loading. The ratio of kidney weight to body wt was reduced after sodium loading. These results indicate that a genetically-determined defect in urinary kallikrein excretion is associated with a greater blood pressure sensitivity to salt, possibly due to altered renal sodium handling.
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M3 - Article
C2 - 8731109
AN - SCOPUS:0030004306
VL - 49
SP - 1422
EP - 1427
JO - Kidney International
JF - Kidney International
SN - 0085-2538
IS - 5
ER -