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.

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.

Intrarenal Distribution of Plasma Flow in Cirrhosis as Measured by Transit Renography: Relationship with Plasma Renin Activity, and Sodium and Water Excretion

1977 ◽  
Vol 52 (5) ◽  
pp. 469-475 ◽  
Author(s):  
S. P. Wilkinson ◽  
I. K. Smith ◽  
M. Clarke ◽  
V. Arroyo ◽  
J. Richardson ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Free Water ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Activity ◽  
Water Excretion ◽  
Transit Times ◽  
Abnormal Pattern ◽  
Intrarenal Distribution

1. The intrarenal distribution of plasma flow was determined with a technique based on the analysis of the transit time of sodium o-[131I]-iodohippurate through the kidney in 43 patients with cirrhosis with near-normal total renal perfusion. 2. Twenty-five of the patients had an abnormal pattern of transit times, suggesting a redistribution of plasma flow from outer cortical to juxtamedullary nephrons. 3. Plasma renin activity ranged from below normal to six times normal and high values were found only in patients showing an abnormal pattern of transit times. The latter was also found to be related to sodium retention and a reduced renal capacity to excrete free water.

Effects of indomethacin in dogs with acute and chronic renovascular hypertension

1981 ◽  
Vol 240 (4) ◽  
pp. H533-H538
Author(s):  
J. R. Dietz ◽  
J. O. Davis ◽  
J. M. DeForrest ◽  
R. H. Freeman ◽  
S. F. Echtenkamp ◽  
...  
Keyword(s):  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Acute Phase ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Arterial Blood ◽  
Renal Prostaglandins ◽  
High Level ◽  
Vascular Receptor

This study examines the role that prostaglandins play in both the developmental and chronic phases of renovascular hypertension. Two 5-mg/kg doses of indomethacin were given to conscious dogs with renal denervation and receiving propranolol during the acute and chronic phases of one-kidney (1-KHT) and the acute phase of two-kidney (2-KHT) renovascular hypertension. Indomethacin produced striking reductions in plasma renin activity from the high level observed during the acute phase of both 1-KHT and 2-KHT. However, plasma renin activity failed to return to normal, and the hypertensive level of pressure decreased only slightly. In the chronic 1-KHT dogs, indomethacin did not lower plasma renin activity or mean arterial blood pressure unless plasma renin activity was elevated above the normal level. Also, indomethacin failed to alter renal function during the acute phase of 1-KHT but effective renal plasma flow fell during chronic 1-KHT. These results suggest that, in the dog, renal prostaglandins are involved in the pathogenesis of both acute 1-KHT and 2-KHT, whereas the role of renal prostaglandins in the regulation of arterial pressure appears to be negligible in chronic 1-KHT except during superimposed sodium depletion or severe hypertension. The data indicate that prostaglandins are involved in renovascular hypertension in the dog only under conditions where plasma renin activity is elevated. It is suggested that the release of renin after renal artery constriction is mediated by the vascular receptor that is at least partially independent of renal prostaglandin synthesis.

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