Low urinary excretion of active and total kallikrein in developing spontaneously hypertensive rats and effect of long term converting enzyme inhibition.
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Age Factors↗
Biomedical subjects
F Praddaude
Publications and source records attributed to F Praddaude.
Reduced urinary kallikrein activity in rats developing spontaneous hypertension.
Urinary kallikrein activity, intake, and excretion of sodium and water were measured in metabolic balance studies on spontaneously hypertensive rats (SHR) of the Okamoto-Aoki strain and normotensive Wistar-Kyoto rats (WKY) on a normal sodium diet from 4 through 15 wk of age. Urinary excretion of active and total kallikrein was significantly lower in SHR at all ages examined and represented a stable percentage of the values in age-matched WKY throughout development, on the average 69.5 and 67.4%, respectively. SHR exhibited a lower urinary excretion of sodium and water than WKY, a higher cumulative sodium balance at all ages studied, and a higher cumulative water balance only at ages 7 and 8 wk. The slopes of the regression lines correlating urinary kallikrein to systolic arterial pressure and to urinary excretion and cumulative balance of sodium and water were always significantly less in SHR than in WKY. The results of the present study indicate that SHR developing hypertension exhibit a precocious and stable abnormality in renal excretion of kallikrein activity.
Animals↗
[Metabolic balances of sodium and water in young spontaneously hypertensive rats and the effects of chronic inhibition of the conversion enzyme].
In order to show in SHR to what extent the kidneys excrete salt and water in proper relation to intake and whether antihypertensive action of converting enzyme inhibition (CEI) involves changes in salt--and water--balance, metabolic studies were conducted during 12 weeks following weaning (wk 4 to 15) on 4 groups of 9 male rats: SHR, WKY and SHR.C, WKY.C (C: given 30 mg captopril/kg body wt every 12 hr by gavage), all fed a standard rat chow (sodium 104 +/- 3 meq/g) in metabolic cages with free access to distilled water. SHR exhibited a higher weekly sodium retention than WKY only up to the end of wk 9 (5.2 +/- 0.5 vs 3.4 +/- 0.6 mEq/wk, p less than 0.001). This was due to lower urinary excretion and greater intakes since fecal losses were higher. From ages 10 through 15 wk, weekly sodium retention was the same in both strains although urinary sodium excretion in SHR was still significantly lower. SHR also retained more water at 7 and 8 wk than age-matched WKY due to lower urinary excretion. From ages 4 to 15 wk, SHR exhibited a reduced relationship of urinary sodium and water excretion to systolic arterial pressure. From ages 4 to 15 wk, weekly sodium retention in SHR.C (2.9 +/- 0.9 mEq/wk) was below that in SHR (4.5 +/- 0.9 mEq/wk, p less than 0.05) and not different from that in WKY (3.7 +/- 0.8 mEq/wk). As intakes and fecal losses were unchanged by CEI, this was due to increased urinary sodium excretion in SHR.C over that in SHR (by 1.4 +/- 0.5 mEq/wk.(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin-Converting Enzyme Inhibitors↗
Change in cortical active kallikrein during the onset of Goldblatt hypertension in the rat.
In two-kidney, one clip hypertensive rats renal cortical kallikrein was studied one and two weeks following induction of the hypertension in comparison with sham time controls. Cortical active kallikrein was lower in hypertensive rats only at week 2, although blood pressure was significantly higher one week after clipping. Total cortical kallikrein was however never different in sham control and in hypertensive rats. This results provide evidence for a change in the activation of prekallikrein during the onset of Goldblatt hypertension.
Animals↗
[Normalization of active urinary kallikrein excretion by young spontaneously hypertensive rats by chronic inhibition of conversion enzyme].
This study was designed to investigate the decreased urinary kallikrein excretion (Ukall.V) in Okamoto-Aoki spontaneously hypertensive rats (SHR) and the effect of long-term converting enzyme inhibition. From ages 4 to 7 weeks, Ukall.V was determined (amidolytic assay: nanokatals/wk) in 4 groups of 6 male rats housed into individual metabolic cages and fed a normal sodium diet: SHR and normotensive Wistar-Kyoto rats (WKY); SHR-C and WKY-C which were given captopril: 30 mg/kg BW every 12 hours by gavage. Ukall.V was each time lower in SHR than in age-matched WKY, even at 4 wks of age (54.6 +/- 9.1 vs 108.5 +/- 16.1 nkat/wk; p less than .01) when systolic blood pressure (s.BP) was already higher. In SHR-C, s.BP was identical or slightly lower to that in WKY. Ukall.V was still lower at wk 4 when captopril was first administered (60.9 +/- 8.4 nkat/wk; p less than .01), but identical to that in WKY at each subsequent age (105.7 +/- 25.9 vs 114.1 +/- 5.6 nkat/wk at wk 5; 219.8 +/- 44.5 vs 253.4 +/- 22.4 nkat/wk at wk 7). Excretion of active kallikrein was highly correlated to s.BP in WKY (r = .87), SHR (r = 0.91) and SHR-C (r = 0.95). The slope of the regression line relating Ukall.V with s.BP was significantly less in SHR than WKY (1.33 +/- 0.35 vs 3.36 +/- 0.84 nkat/wk/mmHg; p less than .01); the slope in SHR-C (3.35 +/- 0.77 nkat/wk/mmHg) was significantly steeper than in SHR (p less than .01) and identical to that in WKY.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
[Decrease in urinary excretion of active kallikrein in conscious young and adult spontaneously hypertensive rats].
Urinary excretion of active kallikrein was determined every day (amidolytic assay) in 6 male Okamoto-Aoki spontaneously hypertensive rats (SHR) and 6 male normotensive Wistar-Kyoto rats (WKY) from ages 4 to 7 weeks and from 12 to 15 weeks. The rats were housed in individual metabolic cages and were allowed free access to food having normal sodium content and to tap water. Urinary kallikrein excretion was lower in 4-week-old SHR than in age-matched WKY (7.8 +/- 1.4 vs. 15.5 +/- 2.3 nkat/24 h respectively, P less than 0.01) at a moment when systolic blood pressure (BP) in SHR was already higher than in WKY. The slope of the increase in active kallikrein excretion from week 4 to 7 was not different for SHR and WKY (6.34 +/- 1.05 vs. 7.50 +/- 1.02 nkat/24 h-1 . wk-1 respectively). In contrast, from week 12 to 15, this slope was not significant for SHR (1.67 +/- 2.55 nkat/24 h-1 . wk-1) while it remained positive in WKY (7.36 +/- 3,44 nkat/24 h-1 . wk-1). In both SHR and WKY, urinary kallikrein excretion was directly related to BP from week 4 to 7 but the slope of the regression line was less for SHR than for WKY (0.19 +/- 0.05 vs. 0.48 +/- 0.12 nkat/24 h-1 . mm Hg respectively). From ages 12 to 15 weeks, kallikrein excretion was still related to pressure in WKY (y = 1.92 x - 180.8; r = 0.93) but not in SHR (y = 0.71 x - 81.48; r = 0.52).(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
[Urinary kallikrein activity in conscious spontaneously-hypertensive rats: development as a function of age].
Urinary excretion of active kallikrein was determined every day (amidolytic assay) in 6 male Okamoto-Aoki spontaneously hypertensive rats (SHR) and in 6 male normotensive Wistar-Kyoto rats (WKY) from ages 3 to 6 weeks and from 12 to 16 weeks. The rats were placed into individual metabolic cages and allowed free access to food having normal sodium content and to tap water. Urinary kallikrein excretion (UKall V, nKat/24 h) was lower in 3-week-old SHR (7.8 +/- 1.4 nKat/24 h) than in WKY (15.5 +/- 2.3 nKat/24 h, p less than 0.01) at a moment when systolic blood pressure (BP) in SHR (85.5 +/- 4.0 mmHg) was already higher than in WKY (76.3 +/- 4.6 mmHg, p less than 0.01). The slope of the increase in kallikrein excretion from week 3 to week 6 was not different for SHR and WKY (y = 6.39 x - 12.09, r = 0.95 vs y = 7.49 x - 9.40, r = 0.93). In contrast, from week 12 to week 15, this slope was slightly negative for SHR (y = 1.08 x + 59.38, r = 0.66) and became significantly different (p less than 0.05) from the slope in WKY which remained positive (y = 5.09 x + 7.05, r = 0.48). The relation between kallikrein excretion and systolic BP was an exponential curve for both SHR and WKY. But the curve of SHR (y = 1.22.e0.03x, r = 0.91) was significantly different (p less than 0.01) from the curve of WKY (y = 1.08.e0.03x, r = 0.95). For each identical systolic BP, UKall V was always lower in SHR than in WKY.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
[Changes in the activity of renal intracortical kallikrein during induction of Goldblatt arterial hypertension of the 2 kidney--1 clip type in the rat].
Renal tissue kallikrein and proteins were measured in two kidney-one clip Goldblatt hypertensive rats both in the stenotic and the controlateral kidney and in sham operated rats at either 1 or 2 weeks after clipping. Activity was assessed by the amidolytic activity and by the kininogenase activity. Kallikrein in normotensive controls was 97.4 +/- 13 ng of bradykinin min-1 mg-1 of protein at week 1 and increased up to 116 +/- 18. Kallikrein in the GH rats was 83 +/- 12 in the stenotic kidney and 85,6 +/- 14 in the controlateral one at week 1, these values remained unchanged at week 2. As a consequence renal tissue kallikrein became significantly lower in the GH rats only at week 2 when compared to controls both the clipped and unclipped kidney showed the same magnitude decrease. Protein concentration remained at a steady level through out the 2 weeks of study. The results suggest that the lower renal kallikrein activity secondary to hypertension found in GH rats result from a decreased activation of prekallikrein in both kidney.
Animals↗
Bilateral urinary kallikrein excretion in the Goldblatt hypertensive rat.
Separate kallikrein excretions [RIA of generated Bradykinins (BK)] and renal functions were measured in 32 two-kidney, one-clip Goldblatt hypertensive (GH) and in 16 sham-operated (SO) rats either one, two, three or four weeks after operation. Mean blood pressure and plasma renin activity were higher in GH rats than in the respective controls. In GH rats, kallikrein excretion was lower from the clipped kidney than from the controlateral one (114 +/- 63 vs 220 +/- 87 ng BK min-1 per 30 min urine collection at week 1, P less than 0.05; 151 +/- 94 vs 425 +/- 125 ng BK min-1 per 30 min urine volume at week 4, P less than 0.01). While the excretion was normal from the controlateral kidney, GH rats had lower total kallikrein excretions than SO rats (335 +/- 138 vs 476 +/- 81 ng BK min-1 per 30 min urine volume at week 1, P less than 0.05; 556 +/- 179 vs 1078 +/- 191 ng BK min-1 per 30 min urine volume at week 4, P less than 0.01). Urinary kallikrein excretion is decreased in 2K-1C Goldblatt hypertension from one week to four weeks after clipping on account of an exclusive reduction in that from the stenotic kidney.
Animals↗
Effect of dietary fiber on gastrointestinal motility and jejunal transit time in dogs.
Strain gauge recordings of the motility of the antrum, duodenum, and jejunum were made in 10 dogs receiving a daily meal of canned food. Addition of 30 g of either wheat bran, cellulose, or guar gum increased the duration of the postprandial pattern of motility by 41-54% in the duodenum. Only cellulose and gum caused increases in the duration of the postprandial pattern of motility in the jejunum. The normal postprandial pattern of duodenojejunal contractions consisted of bursts of 4-10 rhythmic contractions. When bran or cellulose were added, the bursts were prolonged (12-15 contractions per burst) with 4-15 min intervals between bursts. In contrast, when gum was added, contractions occurred continuously at a rate of 7-8/min, but their amplitude was one-half that seen with the other fibers. The increased number of low amplitude contractions when gum was added caused the postprandial motility index to double. There was no change in the motility index when cellulose was added. Guar gum also increased the frequency of antral contractions by 129%, while bran and cellulose had no effect. Jejunal transit time and flow of digesta were measured in four dogs 2 h after the meal. Addition of bran or gum increased the transit time by 28% and 51%, respectively, but cellulose caused a 900% increase in transit time associated with a 50% reduction in the flow of digesta. Addition of different fibers causes different alterations in postprandial motility. Jejunal transit of digesta appears unrelated to the pattern of contractions.
Animals↗
Propagation of electrical spiking activity along the small intestine: intrinsic versus extrinsic neural influences.
1. The electrical activity of the small intestine of conscious dog, recorded by means of chronically implanted electrodes, was related to the transit time estimated by phenol red infusion and its propagation observed after a single or double transection and following either isolation or removal of a 50 cm jejunal loop. 2. In the fasted dog, the activity was characterized by the propagation of myoelectric complexes at a velocity of 4 cm/min during which the mean transit time averaged 13 min/m. About 2/3 of these complexes were seen to pass beyond a single section and anastomosis of the jejunum with a delay of 15 min. This number was reduced to 1/3 and the delay doubled when a second section was performed 50 cm distally. 3. In dog with an isolated jejunal loop, most of the myo-electric complexes were seen to pass from the proximal intestine to the loop and then to the intestine beyond the sit of anastomosis within 37 min. Some complexes however passed directly through the anastomosis within 30-32 min, affecting or not the loop. Others started on the loop and/or on the intestine beyond the anastomosis. Finally, the total number of complexes recorded on the distal jejunum was greater than on the duodenum, an effect which disappeared after removal of the isolated loop. 4. The propagation of the complexes occurred at a lower velocity after denervation of a jejunal segment in situ but was arrested in the case of an isolated-denervated jejunal loop. 5. It is concluded that continuity of structures in the bowel is essential for the propagation of a myo-electric complex which is stopped and replaced by another complex at the level of an anastomosis, the number os complexes reorganized beyond an anastomosis and their velocity of propagation depending upon both intrinsic and extrinsic neural influences.
Action Potentials↗
[Propagation of myoelectric complexes and intestinal resection in dogs].
The velocity of propagation of the myoelectric complexes was studied in dogs after a single and a double transection of the jejunum. Results were compared with those obtained when a 50 cm segment of the bowel was isolated or removed. After a single transection, the passage through the anastomosis occurred with a delay of 15 min. The delay at this level was more than doubled when a second transection was performed 50 cm aborally, the total delay being then 65 min for the passage through the two anastomoses. After removal or isolation of a 50 cm jejunal segment, the delay was reduced to 45 and 49 min respectively.
Animals↗