Urinary Kallikrein Excretion in a Spontaneously Hypertensive Strain of Rats

Porcelli, G; Bianchi, Giuseppe; Croxatto, H.

doi:10.3181/00379727-149-38939

Cited by 25 publications

(13 citation statements)

References 5 publications

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“…Other genetically hypertensive rats, such as New Zealand strain rats (73), fawnhooded rats (74), and Milan hypertensive rats, also exhibit low excretion of urinary kallikrein (75).…”

Section: Genetically Hypertensive Rats and Dahl Salt-sensitive Ratsmentioning

confidence: 99%

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Katori

Murakami

2006

J Pharmacol Sci

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Abstract. It is widely accepted that a high sodium intake triggers blood pressure rise. However, only one-third of the normotensive subjects were reported to show salt-sensitivity in their blood pressure. Many factors have been proposed as causes of salt-sensitive hypertension, but none of them provides a satisfactory explanation. We propose, on the basis of accumulated data, that the reduced activity of the kallikrein-kinin system in the kidney may provide this link. Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron. Bradykinin generated is immediately destroyed by carboxypeptidase Y-like exopeptidase and neutral endopeptidase, both quite independent from the kininases in plasma, such as angiotensin converting enzyme. The salt-sensitivity of the blood pressure depends largely upon ethnicity and potassium intake. Interestingly, potassium and ATP-sensitive potassium (K ATP ) channel blockers accelerate renal kallikrein secretion and suppress blood pressure rises in animal hypertension models. Measurement of urinary kallikrein may become necessary in salt-sensitive normotensive and hypertensive subjects. Furthermore, pharmaceutical development of renal kallikrein releasers, such as K ATP channel blockers, and renal kininase inhibitors, such as ebelactone B, may lead to the development of novel antihypertensive drugs.

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“…Other genetically hypertensive rats, such as New Zealand strain rats (73), fawnhooded rats (74), and Milan hypertensive rats, also exhibit low excretion of urinary kallikrein (75).…”

Section: Genetically Hypertensive Rats and Dahl Salt-sensitive Ratsmentioning

confidence: 99%

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Katori

Murakami

2006

J Pharmacol Sci

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“…A number of studies in humans and experimental animals have attempted to determine the relationship between urinary kallikrein activity and blood pressure regulation (5)(6)(7)(8)(9). Although most investigators feel that kallikreins could influence blood pressure, the meaning of these findings is controversial.…”

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confidence: 99%

Urinary kallikrein and plasma renin activity as determinants of renal blood flow. The influence of race and dietary sodium intake.

Levy¹,

Lilley²,

Frigon³

et al. 1977

J. Clin. Invest.

233

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A B S T R A C T We investigated the relationship of the kallikrein-kinin system and the renin-angiotensin system in the regulation of blood pressure, salt and water excretion, and renal blood flow. Normotensive and hypertensive black and white men were studied during unrestricted sodium intake as well as on a 10-meq/day sodium intake; potassium intake was held constant throughout the study (80 meq/day).During unrestricted sodium intake, urinary kallikrein activity was greater in white normotensives than white hypertensives or black normotensives. There was no difference (P > 0.05) between white and black hypertensives or between black normotensives and black hypertensives. All groups had greater urinary kallikrein activity on low sodium vs. unrestricted sodium intake, but the increase in black hypertensives was small, and they excreted significantly less kallikrein than the other groups on the low sodium diet. Plasma renin activity showed similar increments after sodium restriction in all groups. Urinary kallikrein activity correlated with renal blood flow in all groups except the black normotensives on low sodium intake. Renal blood flow could be correlated uniformly with log (urinary kallikrein activity/supine plasma renin activity) in all groups on either diet. Urinary sodium and potassium excretion and urine volume were not different among the groups. We concluide: (a) support the concept that the kallikrein-kinin system and the renin-angiotensin system contribute to the regulation of renal blood flow and may account for racial differences in renal vascular resistance. INTRODUCTIONKallikrein is an enzyme that catalyzes the formation of the vasodilator hormones, lysyl-bradykinin (kallidin) and bradykinin, from a plasma alpha-2 globulin substrate, kininogen (1). Urinary kallikrein appears to be derived from the kidney and differs from the enzyme that circulates in plasma (2). It has been proposed that kallikrein exists in the renal cortex and may occupy a location that is juxtaposed to the enzyme renin (3). Although a physiologic function for lysyl-bradykinin, the enzymatic product, has not been established, pharmacologic infusion studies have shown that the peptide is a natriuretic and vasodilatory compound (4).A number of studies in humans and experimental animals have attempted to determine the relationship between urinary kallikrein activity and blood pressure regulation (5-9). Although most investigators feel that kallikreins could influence blood pressure, the meaning of these findings is controversial. Based on provocative preliminary observations (10) and the aforementioned studies, it seemed appropriate to examine the simultaneous influence of race and blood pressture on urinary kallikrein activity. In addition, we have examined the association between kallikrein in uirine and factors that have been related to blood pressure regulation including urinary volume, soditum excretion, plasma renin activity, and renal blood flow. These latter studies were designed to determine a possible physiologic role ...

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“…It has been agreed that renal KKS is also a depressor system based on the natriuresis [34], Actually, in human essential hypertension [35] and genetic hypertension models [36][37][38][39][40], decrease of renal KKS activity has been suggested to participate in the hypertension mechanism. In the present study, basal UKA level in the ND-BHN was significantly lower than that in the ND-control rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of Dietary Salt Restriction on Blood Pressure and the Renal Vasoactive System in the Congenitally Bilateral Hydronephrotic Rat

Kanehara

Tauchi²,

Ishitobi³

et al. 1996

Nephron

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We examined the responses on blood pressure when the renal vasoactive system such as renin-angiotensin-aldosterone system (RAAS) and kallikrein-kinin system (KKS) was activated by dietary salt restriction in the congenitally bilateral hydronephrotic rat (BHN). In a low salt diet (LS)-normotensive and normal kidney control rats after 8 weeks from initiating dietary salt restriction, the plasma sodium concentration (PNa) was retained at a level similar to that in the normal diet (ND)-control rats, and plasma renin activity (PRA), plasma aldosterone concentration (PAC) and urinary kallikrein activity (UKA) were about 1.8-, 9.4- and 1.7-fold higher, respectively, than those in the ND-control rats. In addition, LS-control rats had a significantly (p < 0.001) high systolic blood pressure (163 ± 2.0 mm Hg) compared with that (136 ± 5.8) of ND-control rats. These results suggest that the activated renal vasoactive system acted for not only sodium retention but also for elevation of blood pressure in LS-control rats. In LS-BHN at week 8, PNa was also retained at a nearly normal level. However, the renal vasoactive system activation for sodium retention was higher than that of LS-control rats; that is, increase of PRA, PAC and UKA were about 3.8-, 24.7- and 10.0-fold, respectively, than in ND-BHN. The higher activation of RAAS, nevertheless, does not affect blood pressure in BHN; that is, both hypertension of BHN fed LS and ND developed similarly. These findings suggest that dietary salt restriction could markedly activate the renal vasoactive system for sodium retention without elevating blood pressure in BHN different from control rats.

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Urinary Kallikrein Excretion in a Spontaneously Hypertensive Strain of Rats

Cited by 25 publications

References 5 publications

A Missing Link Between a High Salt Intake and Blood Pressure Increase

A Missing Link Between a High Salt Intake and Blood Pressure Increase

Urinary kallikrein and plasma renin activity as determinants of renal blood flow. The influence of race and dietary sodium intake.

Effects of Dietary Salt Restriction on Blood Pressure and the Renal Vasoactive System in the Congenitally Bilateral Hydronephrotic Rat

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