Urinary kallikrein and systemic prostacyclin synthesis during sodium chloride infusion in normal man

1985 ◽  
Vol 68 (5) ◽  
pp. 537-543 ◽  
Author(s):  
M. L. Watson ◽  
A. D. Cumming ◽  
A. T. Lambie ◽  
J. A. Oates
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Urine Flow ◽  
Renin Activity ◽  
Urinary Kallikrein ◽  
Plasma Protein Concentration

1. An intravenous infusion of 3 litres of sodium chloride solution (saline: 150 mmol/l) was given over 1 h to normal subjects. 2. During and immediately after the infusion, renal plasma flow increased in the majority of subjects, but the rise was not statistically significant. Significant increases in urine flow, sodium excretion, urinary kallikrein excretion and urinary excretion of dinor-6-keto prostaglandin (PG) F1α, a measure of systemic PGI2 synthesis, were noted. Plasma renin activity and plasma protein concentration were significantly lowered by the infusion. 3. At 2 h after the end of the infusion, although urine flow fell significantly, sodium excretion had not decreased. The reduction in plasma renin activity and plasma proteins persisted, and excretion of kallikrein and the PGI2 metabolite returned to control values. 4. Overall, urinary kallikrein excretion correlated significantly with urine flow and with sodium excretion. Peak kallikrein excretion occurred in the second 30 min of the infusion, and preceded maximal urine flow and sodium excretion. 5. The results suggest that increased systemic synthesis of PGI2 occurs in response to an acute infusion of sodium chloride, and may be an adaptive response of the vasculature to volume expansion. They support a role for the renal kallikrein-kinin system in the early diuretic and natriuretic response to saline infusion; the reduction in plasma renin activity and plasma protein concentration may be involved in both the early response and the persistent natriuresis 2 h after the infusion.

Effects of hypoproteinemia on fluid volumes and arterial pressure

1983 ◽  
Vol 245 (2) ◽  
pp. H284-H293 ◽  
Author(s):  
R. D. Manning ◽  
A. C. Guyton
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Protein ◽  
Plasma Volume ◽  
Protein Concentration ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Protein Concentration

The effects of both moderate and large decreases in plasma protein concentration on arterial pressure and fluid volumes were studied in 23 conscious dogs. In experiment 1, plasma protein concentration decreased 33% during a 5-day plasmapheresis period. During this time sodium space increased 11%, mean arterial pressure decreased slightly, and neither blood volume nor plasma volume decreased. Experiment 2 was performed to see if blockade of the alpha-sympathetic and angiotensin systems could prevent the blood volume homeostasis during moderate hypoproteinemia. Sodium space increased; however, blood volume was unchanged. During experiment 3 plasma protein concentration decreased 68% over a 12-day plasmapheresis period. By the last day of plasmapheresis, plasma protein concentration was 2.4 g/100 ml, mean arterial pressure had decreased 26 mmHg, sodium space had increased 12%, plasma renin activity had increased 11-fold, and blood volume and plasma volume were 63.9 +/- 4.0 and 66.9 +/- 2.5% of control, respectively. We conclude that the maintenance of a normal blood volume during moderate hypoproteinemia does not require active participation of the renin-angiotensin and alpha-sympathetic systems and large decreases in plasma protein concentration are accompanied by marked hypovolemia, hypotension, and hyperreninemia.

Urinary Kallikrein and Plasma Renin during the Reversal of Renovascular Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 263s-266s
Author(s):  
O. P. Gulati ◽  
O. A. Carretero ◽  
T. Morino ◽  
N. B. Oza
Keyword(s):  
Plasma Renin Activity ◽  
Renal Artery ◽  
Renovascular Hypertension ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Renin Activity ◽  
Experimental Hypertension ◽  
Urinary Kallikrein ◽  
Sodium Potassium ◽  
Water Excretion

1. Urinary kallikrein, sodium, potassium and water excretion, and plasma renin activity were measured before and during the reversal of experimental hypertension produced by unclamping the renal artery in rats. 2. Kallikrein excretion decreased significantly after unclamping, suggesting that it does not play a significant role in the reversal of hypertension. 3. A decrease in plasma renin activity coupled with a slight increase of sodium excretion was observed, indicating that these might participate in the reversal of hypertension.

Effect of arachidonic acid and indomethacin on renal function of dogs with pericardial tamponade

1981 ◽  
Vol 59 (6) ◽  
pp. 586-594 ◽  
Author(s):  
Robert J. Boudreau ◽  
Henry Mandin
Keyword(s):  
Blood Flow ◽  
Arachidonic Acid ◽  
Arterial Pressure ◽  
Plasma Protein ◽  
Sodium Excretion ◽  
Protein Concentration ◽  
Venous Pressure ◽  
Pericardial Tamponade ◽  
Renin Activity ◽  
Plasma Protein Concentration

Previous studies revealed persistent sodium retention in dogs with chronic pericardial tamponade (induced by injection of Freund adjuvant into pericardial sacs) and pericardiocentesis, revealed in increased sodium excretion. Three groups of dogs were studied. Group 1 was treated with indomethacin (2.5 mg/kg, iv) prior to pericardiocentesis. Compared with experiments without indomethacin, sodium excretion did not increase following pericardiocentesis in animals treated with indomethacin despite similar changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity. This effect of indomethacin was presumably mediated through prostaglandin (PG) synthesis inhibition. Group 2 dogs received an infusion of arachidonic acid (AA) (to increase PG synthesis) into the left renal artery (20 μg∙kg−1∙min−1). Sodium excretion increased after AA infusion during tamponade (11.2 to 30.9 mequiv∙min−1) with a further increase occurring after pericardiocentesis (84.4 mequiv.∙min−1). Animals in group 3 were infused with both 20 and 80 μg∙kg−1∙min−1 doses of AA. Although sodium excretion following 80 μg∙kg−1∙min−1 AA (21 mequiv.∙min−1) was higher than that seen during 20 μg∙kg−1∙min−1 (14.2 mequiv.∙min−1), a further increase in sodium excretion to 45.6 mequiv.∙min−1 followed pericardiocentesis. During tamponade, AA did not change any of the measured parameters other than sodium excretion, a result compatible with the proposed distal tubular site of action of PG. Absolute but not fractional cortical blood flow distribution increased during the time sodium excretion increased following pericardiocentesis in all experiments. It is proposed that increased PG synthesis may be one possible mechanism involved in the natriuresis seen following pericardiocentesis. One cannot exclude the possibility that increased absolute blood flow to the superficial cortex also contributes to the observed natriuresis. Changes in arterial pressure, venous pressure, hematocrit, plasma protein concentration, and renin activity appear to contribute to the observed natriuresis but only when PG synthesis is not blocked.

PLASMA RENIN ACTIVITY IN CONGENITAL VIRILIZING ADRENAL HYPERPLASIA

PEDIATRICS ◽  
1968 ◽  
Vol 41 (5) ◽  
pp. 897-904
Author(s):  
Masashi Imai ◽  
Yoshio Igarashi ◽  
Hirofumi Sokabe
Keyword(s):  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Adrenal Hyperplasia ◽  
Peripheral Plasma

Peripheral plasma renin activity was markedly elevated in two cases of the salt-losing form of congenital virilizing adrenal hyperplasia. The renin activity was reduced after treatment with deoxycorticosterone and sodium chloride. In the hypertensive form of the plasma renin activity was suppressed.

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.

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