Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Completely inactive renin was isolated from normal human plasma by DEAE-Sepharose column chromatography and Blue-Sepharose column chromatography. This inactive renin had a molecular weight of 54,000 daltons as determined by gel filtration on Ultrogel AcA 44. When the inactive renin was activated by trypsin, its molecular weight decreased to 48,000 daltons. The trypsin-activated renin differed from a native form of active renin in plasma with respect to molecular weight (active renin, 43,000), pI value (active renin, 5.20; trypsin-activated renin, 5.06), km value (active renin, 60 nmoles/liter; trypsin-activated renin, 89 nmoles/liter), Ki value for pepstatin A (active renin, 2.6 mumoles/liter; trypsin-activated renin 5.0 mumoles/liter) and pH profile for angiotensin formation. Glandular kallikrein (human urinary or pig pancreatic) did not activate the inactive renin. When the trypsin-activated renin was treated with glandular kallikrein, its activity was unchanged, but its molecular and kinetic properties except pI value (trypsin-activated kallikrein-treated renin, 4.82) coincided with those of a native form of active renin in plasma. These results indicate that glandular kallikrein does not directly activate inactive renin but participates in the activation process of inactive renin. The results also suggest that inactive renin in human plasma is a renin precursor.
Hypertension
PMID:Role of glandular kallikrein in the activation process of human plasma inactive renin. 633 49

To determine whether maneuvers known to modify immunoreactive urinary kallikrein excretion (iUKK) also alter the concentration of immunoreactive glandular kallikrein (iGKK) in plasma, we measured iGKK in the plasma and urine of rats before, at 1 week, and at 3 weeks after induction of two-kidney, one clip hypertension, low sodium intake, and DOCA-salt hypertension. Glandular kallikrein in plasma and urine was measured by radioimmunoassay. Clipping of a renal artery decreased iUKK from 11.7 +/- 0.5 microgram/24 hr/100 g body weight (BW) to 7.8 +/- 0.5 and 8.2 +/- 0.5 at 1 and 3 weeks after surgery without significantly changing iGKK in plasma. The level of iGKK in the plasma did not correlate significantly with iUKK in the clipped group. Low sodium intake significantly increased iUKK, which rose from 6.6 +/- 0.3 microgram/24 hr/100 g BW to 9.6 +/- 0.5 and 13.9 +/- 0.7 after 1 and 3 weeks. In addition, low sodium intake appeared to increase iGKK in plasma, and a significant positive correlation was observed between iUKK and iGKK in plasma in the group on low sodium diet (r = 0.65, p less than 0.01). DOCA-salt treatment increased iUKK significantly from 10.4 +/- 0.6 microgram/24 hr/100 g BW to 17.1 +/- 1.4 and 22.6 +/- 2.3 at 1 and 3 weeks after. The iGKK in plasma increased from 13.8 +/- 0.5 to 15.4 +/- 0.7 ng/ml (p less than 0.05) at 1 week after the DOCA-salt treatment began, but it returned to pretreatment levels 3 weeks later (14.5 +/- 0.7 ng/ml, n.s.).(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:Immunoreactive glandular kallikrein in plasma during alterations of urinary kallikrein excretion. 655 3