Renal Kallikrein Activity and Urinary Kallikrein Excretion in Rats with Experimental Renal Hypertension

1982 ◽  
Vol 63 (4) ◽  
pp. 349-354 ◽  
Author(s):  
M. Marin-Grez ◽  
G. Schaechtelin ◽  
G. Bönner ◽  
G. Speck ◽  
D. Ganten ◽  
...  
Keyword(s):  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Hypertensive Rats ◽  
Control Value ◽  
Urinary Kallikrein Excretion ◽  
Renal Kallikrein ◽  
Experimental Renal Hypertension ◽  
Kallikrein Activity

1. Rats were made hypertensive by ligating the aorta between the origins of both renal arteries. Sham-operated animals served as controls. Urinary and renal kallikrein activities, as well as plasma and renal renin activities, were measured 8 and 90 days after surgery. 2. Blood pressure was 155 ± 6 mmHg on day 8 after aortic ligature and 142 ± 6 mmHg on day 90; in controls pressures were 107 ± 3 and 110 ± 5 mmHg respectively. 3. Eight days after aortic ligature, kallikrein activity in the ischaemic kidneys was about 6·5 times, and in the non-ischaemic kidneys almost 2 times, that in controls. After 90 days the kallikrein activity was reduced to one-half of that in the controls in the ischaemic kidneys and it was normal in the contralateral. 4. The urinary kallikrein excretion of hypertensive rats was about one-third of that of the controls at both 8 and 90 days after aortic ligature. 5. The plasma renin activity in hypertensive rats was approximately seven times that in control animals 8 days after aortic ligature and did not differ from the control value after 90 days. Renin activity in the kidneys showed the same pattern as in other models of renovascular hypertension: elevation in the ischaemic kidney and reduction in the non-ischaemic one.

Renin—angiotensin and Kallikrein—kinin Systems in Sodium Homeostasis and Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 283s-286s
Author(s):  
C. I. Johnston ◽  
P. G. Matthews ◽  
E. Dax
Keyword(s):  
Plasma Renin Activity ◽  
Kinetic Method ◽  
Plasma Renin ◽  
Significant Rise ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Urinary Kallikrein Excretion ◽  
Sodium Load ◽  
Renal Hypertensive Rats ◽  
Goldblatt Hypertension

1. Urinary kallikrein excretion was measured in rats by an enzyme kinetic method employing radioimmunoassay of generated bradykinin. 2. Rats given a sodium load (NaCl solution, 20 g/l, to drink) for 28 days showed acute and prolonged significant falls in urinary kallikrein excretion associated with suppression of plasma renin and angiotensin. 3. Conversely sodium-depleted rats showed increases in urinary kallikrein excretion, associated with rises in plasma renin and angiotensin. 4. A close and significant direct relation between plasma renin activity and urinary kallikrein excretion was demonstrated. 5. The diuresis and natriuresis induced by frusemide in rats was associated with increased urinary kallikrein excretion and acute rises in plasma renin. 6. In chronic renal hypertensive rats urinary kallikrein excretion was increased only in the animals with two-kidney Goldblatt hypertension. This group was also the only group that demonstrated a significant rise in plasma renin activity.

Changes in Renal and Urinary Kallikrein Activity by Mannitol-Induced Osmotic Diuresis

1981 ◽  
Vol 61 (1) ◽  
pp. 47-51 ◽  
Author(s):  
G. Bönner ◽  
M. Marin-Grez ◽  
D. Beck ◽  
M. Deeg ◽  
F. Gross
Keyword(s):  
Renal Cortex ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Osmotic Diuresis ◽  
Plasma Aldosterone Concentration ◽  
Urinary Kallikrein Excretion ◽  
Short Period ◽  
Urinary Potassium ◽  
Renal Kallikrein ◽  
Kallikrein Activity

1. Osmotic diuresis was induced in male Sprague-Dawley rats by a 30% (w/v) mannitol solution injected three times at 15-min intervals. Kallikrein excretion increased for a short period after the first two injections, but, despite marked diuresis, the increment of kallikrein excretion after the second injection was less marked than after the first and no enhanced kallikrein excretion was observed after the third injection of mannitol. 2. Urinary kallikrein excretion correlated only with urinary potassium excretion. No correlation was found with either urine volume or urinary sodium excretion. 3. At the end of the osmotic diuresis kallikrein activity was significantly reduced both in the urine and in the renal cortex. At that time plasma aldosterone concentration was slightly greater in the mannitol-treated than that in the control group, but the difference did not reach statistical significance. 4. In this experiment no relationship was observed between the activity of the renal kallikrein-kinin system and the plasma aldosterone concentration. 5. The transient increase in urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein, which is followed by a diminished kallikrein activity in urine and in renal cortex.

EFFECTS OF EXPERIMENTAL RENAL HYPERTENSION ON ALDOSTERONE BIOSYNTHESIS BY RAT ADRENAL TISSUE

1969 ◽  
Vol 60 (4) ◽  
pp. 669-680 ◽  
Author(s):  
J. Müller ◽  
F. Gross
Keyword(s):  
Renal Artery ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Deficiency ◽  
Marked Rise ◽  
Contralateral Kidney ◽  
Aldosterone Production ◽  
Experimental Renal Hypertension

ABSTRACT Aldosterone biosynthesis by quartered adrenal glands from rats with different forms of experimental renal hypertension due to clamping of one renal artery, was studied under various in vitro conditions. During incubation without aldosterone-stimulating substances, the adrenals of rats with one renal artery clamped and the other kidney left intact produced 200 % more aldosterone from endogenous precursors and converted 50 % more added tritium-labelled pregnenolone, progesterone or corticosterone to aldosterone than adrenals of control animals. The difference in aldosterone production was less marked when serotonin, KCl or ACTH was added to the incubation medium. The production of corticosterone and of deoxycorticosterone, respectively, was almost the same in adrenals of both groups of rats under most in vitro conditions. The marked rise in aldosterone production seen in the presence of an intact contralateral kidney was partially or completely inhibited, when simultaneously with renal artery constriction, the contralateral kidney was removed or the ureter of either the clamped or the contralateral kidney was ligated. These results indicate that in rats with experimental renal hypertension, increases in aldosterone production are correlated with increases of plasma renin activity and of the renin content of the clamped kidney, but are independent of changes in blood pressure. Since chronically elevated levels of plasma or renal renin activity act mainly in the early stages of aldosterone biosynthesis, it is concluded that the marked activation in the final stages of aldosterone biosynthesis observed in sodium deficiency is not mediated by the renin-angiotensin system.

Plasma renin activity and urinary kallikrein excretion in lead-exposed workers as related to hypertension and nephropathy

Life Sciences ◽  
1981 ◽  
Vol 28 (2) ◽  
pp. 175-184 ◽  
Author(s):  
P. Boscolo ◽  
G. Galli ◽  
A. Iannaccone ◽  
F. Martino ◽  
G. Porcelli ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Urinary Kallikrein Excretion ◽  
Exposed Workers

Plasma renin activity and urinary kallikrein excretion in response to intravenous furosemide in diabetic patients

1990 ◽  
Vol 27 (4) ◽  
pp. 337-342 ◽  
Author(s):  
Shyam Bala Lall ◽  
Shanti Kunchaparty ◽  
Hefazat Husain Siddiqui ◽  
Jasbir Singh Bajaj
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Diabetic Patients ◽  
Urinary Kallikrein ◽  
Urinary Kallikrein Excretion

Changes in the Renin-Angiotensin-Aldosterone System and in Sodium and Potassium Balance during Development of Renal Hypertension in Rats

1975 ◽  
Vol 48 (1) ◽  
pp. 17-26 ◽  
Author(s):  
F. H. H. Leenen ◽  
J. W. Scheeren ◽  
D. Omylanowski ◽  
J. D. Elema ◽  
B. Van Der Wal ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Systolic Blood Pressure ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Potassium Balance ◽  
Peripheral Plasma ◽  
Sodium And Potassium

1. The relationships between the renin-angiotensin-aldosterone system, sodium and potassium balance and systolic blood pressure were studied during development of moderate (160–180 mmHg; clip i.d. 0.25 mm) and severe (200–230 mmHg; clip i.d. 0.20 mm) renal hypertension in rats with an undisturbed contralateral kidney. 2. In severely hypertensive rats renin activity in the peripheral plasma increased from day 9, by which time the systolic blood pressure was elevated to 160–180 mmHg. The rate of total corticosteroid and aldosterone production in vitro increased from day 14 and plasma renin substrate concentration increased from day 24. In moderately hypertensive rats, none of these changes occurred. 3. During the first 10 days after the application of 0.25 and 0.20 mm clips, sodium and potassium retention/g gain in body weight were higher than in sham-operated controls. During the next 10 days, the positive balance stabilized in animals with a 0.25 mm clip whereas, in animals with a 0.20 mm clip, sodium and potassium balance returned to the level of the sham-operated controls through increased renal losses. Despite these changes the systolic pressure rose further in animals with a 0.20 mm clip. 4. The initial sodium retention could be a factor in the early rise of blood pressure and could account for the delay in the rise of peripheral plasma renin activity. The subsequent loss of the retained sodium and potassium during the development of severe hypertension could have facilitated the rise in peripheral plasma renin activity, but did not initiate this rise.

Alpha 1-adrenoceptor blockade in renal hypertensive rats with low and high renin levels

1984 ◽  
Vol 246 (4) ◽  
pp. H573-H578
Author(s):  
B. Waeber ◽  
J. Nussberger ◽  
H. R. Brunner
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Norepinephrine ◽  
Hypertensive Rats ◽  
Blood Pressure Elevation ◽  
Significant Difference ◽  
Renal Hypertensive Rats

A total of 75 male Wistar rats with one-kidney, one-clip renal hypertension was maintained on either a regular (RNa) or a low-salt (LNa) diet for 3 wk after clipping. Blood pressure in the unanesthetized rats was equally elevated independent of sodium intake. Plasma renin activity was higher in LNa animals, and blood pressure was renin dependent only in this group, as evidenced by the blood pressure response to 10 mg/kg captopril iv. There was no significant difference in plasma catecholamines between RNa and LNa rats, although in the former the sympathetic nervous system is believed to play a major role in sustaining high blood pressure. The acute intravenous administration of 0.5 mg/kg prazosin did not induce a more pronounced blood pressure fall in the RNa rats. Prazosin enhanced plasma norepinephrine levels similarly in both groups, but epinephrine levels only rose in the LNa animals. Prazosin also markedly stimulated plasma renin activity rendering blood pressure renin dependent even in RNa rats. Thus, using alpha 1-adrenoceptor blockade, it has not been possible to demonstrate that the blood pressure elevation of salt-repleted one-kidney, one-clip renal hypertensive rats is due to an enhanced sympathetic nerve activity. Data obtained with sympatholytic agents must be interpreted with great caution if renin activity cannot be kept unchanged.

Urinary Kallikrein Excretion and Plasma Renin Activity in Patients with Essential Hypertension and Primary Aldosteronism

1978 ◽  
Vol 55 (1) ◽  
pp. 51-55 ◽  
Author(s):  
A. Lechi ◽  
G. Covi ◽  
C. Lechi ◽  
A. Corgnati ◽  
E. Arosio ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Primary Aldosteronism ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Hypertensive Patients ◽  
Urinary Kallikrein Excretion ◽  
Low Renin Hypertension

1. The 24 h urinary excretion of kallikrein has been studied in 40 normotensive control subjects and in 74 age-matched patients with essential hypertension under similar conditions. By use of the renin-sodium index, hypertensive patients were divided into two subgroups: low-renin hypertension and normal-renin hypertension patients. Urinary kallikrein determinations were also obtained from six hypertensive patients with primary aldosteronism. 2. Urinary kallikrein was significantly lower both in patients with normal-renin and low-renin essential hypertension. Urinary kallikrein excretion was very high in the patients with primary aldosteronism. 3. In nine hypertensive patients β-adrenoreceptor-blocking therapy caused a significant decrease of plasma renin activity, but had no significant effect on urinary kallikrein excretion. 4. The results support the concept that low urinary kallikrein is likely to be a marker of essential hypertension. Under certain conditions its excretion is positively related to mineralocorticoid hormone concentrations but it is not primarily related to the renin-angiotensin system.

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