Hepatic Elimination of Renin in Man

1978 ◽  
Vol 55 (4) ◽  
pp. 377-382 ◽  
Author(s):  
B. Hesse ◽  
Ellen Damgaard Andersen ◽  
H. Ring-Larsen
Keyword(s):  
Plasma Renin Activity ◽  
Hepatic Vein ◽  
Plasma Flow ◽  
Control Period ◽  
Elimination Rate ◽  
Plasma Renin ◽  
Extraction Ratio ◽  
Renin Activity ◽  
Hepatic Elimination ◽  
Arterial Plasma

1. Hepatic elimination of renin was measured in 10 well-compensated cardiac patients with normal liver function during a control period and during a period of reduced hepatic plasma flow, induced by physical exercise (seven patients) or intravenous infusion of lysine vasopressin (three patients). 2. Hepatic renin elimination rate (hepatic plasma flow × arterial-hepatic vein difference of plasma renin activity) was found to be linearly correlated with arterial plasma renin activity (r = 0.986, P < 0.001). 3. When hepatic plasma flow fell by 45% the hepatic extraction ratio of renin (arterial-hepatic vein plasma renin activity difference/arterial plasma renin activity) increased by 75%. Hepatic renin clearance (hepatic plasma flow × extraction ratio) remained constant. 4. The results indicate that changes in the hepatic elimination rate of renin do not contribute to changes in plasma renin activity during these events.

Plasma renin activity and forearm blood flow in paraplegic humans

1985 ◽  
Vol 59 (3) ◽  
pp. 924-927 ◽  
Author(s):  
P. R. Freund ◽  
G. L. Brengelmann
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Forearm Blood Flow ◽  
Control Period ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
The Body ◽  
Renin Activity ◽  
Angiotensin System ◽  
Renin Angiotensin

We recently found that paraplegic humans respond to hyperthermia with subnormal increase in skin blood flow (SkBF), based on measurements of forearm blood flow (FBF). Is this inhibition of SkBF a defect in thermoregulation or a cardiovascular adjustment necessary for blood pressure control? Since high resting plasma renin activity (PRA) is found in unstressed individuals with spinal cord lesions and since PRA increases during hyperthermia in normal humans, we inquired whether the renin-angiotensin system is responsible for the attenuated FBF in hyperthermic resting paraplegics. Five subjects, 28–47 yr, with spinal transections (T1-T10), were heated in water-perfused suits. Blood samples for PRA determinations were collected during a control period and after internal temperature reached approximately 38 degrees C. Some subjects with markedly attenuated FBF had little or no elevation of PRA; those with the best-developed FBF response exhibited the highest PRA. Clearly, circulating angiotensin is not the agent that attenuates SkBF. Rather, increased activity of the renin-angiotensin system may be a favorable adaptation that counters the locally mediated SkBF increase in the lower body and thus allows controlled active vasodilation in the part of the body subject to centrally integrated sympathetic effector outflow.

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.

Influence of Sodium on Experimental Renovascular Hypertension in Rats

1980 ◽  
Vol 59 (s6) ◽  
pp. 149s-151s ◽  
Author(s):  
C. M. Taquini ◽  
A. Gallo ◽  
N. Basso ◽  
A. C. Taquini
Keyword(s):  
Plasma Renin Activity ◽  
Control Period ◽  
Plasma Renin ◽  
Diet Group ◽  
Renin Activity ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Group 2 ◽  
Group 1

1. Rats on normal sodium diet (group 1) and on chronically maintained low sodium diet (group 2) were studied during a control period, after clipping the renal artery (two-kidney, one-clip hypertension) and after nephrectomy (one-kidney, one-clip hypertension). 2. The low sodium diet neither prevented the development nor changed the severity of two-kidney, one-clip hypertension, and the latter was not accompanied by an increase in plasma renin activity. 3. After nephrectomy arterial pressure further increased and plasma renin activity decreased in group 1, and both remained unchanged in group 2. 4. Blood volume was the same in both groups 10 days before and 10 days after nephrectomy. 5. Sodium does not seem to be ‘necessary’ in the two-kidney, one-clip hypertension although it may play an enhancing role in the one-kidney model.

Familial Hypertension and Hormonal Profile, Renal Haemodynamics and Body Fluids of Young Normotensive Subjects

1978 ◽  
Vol 55 (s4) ◽  
pp. 367s-371s ◽  
Author(s):  
G. Bianchi ◽  
G. B. Picotti ◽  
G. Bracchi ◽  
D. Cusi ◽  
M. Gatti ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Significant Negative Correlation ◽  
Renin Activity ◽  
Compensatory Mechanism ◽  
Normotensive Subjects

1. Almost all the factors that may cause a rise in blood pressure are, in turn, influenced by the increase in blood pressure per se. Thus any primary involvement of one or more of these factors in the pathogenesis of essential hypertension must be evaluated before or during the development of hypertension. 2. Young normotensive subjects both of whose parents are hypertensive have a much higher probability of developing hypertension than those whose parents are both normotensive. 3. The following measurements were made in 56 subjects of the first group (both parents hypertensive) and 35 of the second group (both parents normotensive), matched for age, sex and body surface area: renal plasma flow and glomerular filtration rate, using p-aminohippurate and inulin clearance; 24 h urinary excretion of aldosterone, protein and electrolytes; plasma renin activity; plasma volume. Plasma catecholamines and cardiac index were also measured in 26 subjects of the first group and 25 subjects of the second group using a radioenzymic method and echocardiography. 4. All these factors were similar in the two groups except that renal plasma flow was higher in the first group (767·2 ± 30 versus 650·7 ± 17 ml/min, P < 0·01). Plasma renin activity tended to be lower in subjects with a higher renal plasma flow, but there was no significant negative correlation between the two factors. 5. The possibility that the higher renal plasma flow in subjects with a high probability of developing hypertension is a compensatory mechanism for a primary intrarenal defect is discussed.

Renal Effects of Angiotensin I-Receptor Blockade and Angiotensin Convertase Inhibition in Man

1996 ◽  
Vol 90 (3) ◽  
pp. 205-213 ◽  
Author(s):  
Francois Schmitt ◽  
Svetlozar Natov ◽  
Frank Martinez ◽  
Bernard Lacour ◽  
Thierry P. Hannedouche
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renin Activity ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibition

1. The objective was to compare two means of inhibition of the renin—angiotensin system [angiotensin-converting enzyme inhibition and selective antagonism of angiotensin II subtype 1 (AT1) receptor] on renal function in 10 healthy normotensive volunteers on a normal sodium diet. Since mechanisms of action may differ between both drugs, a synergistic action was further studied by combining the two drugs. 2. The design was a double-blind randomized acute administration of either placebo or a single oral dose of enalapril, 20 mg, followed in each case by administration of the AT1 selective antagonist losartan potassium, 50 mg orally. 3. The methods included measurements of hormones (plasma renin activity, plasma aldosterone), blood pressure and renal function from 45 to 135 min after administration of placebo or enalapril, and from 45 to 135 min after losartan and placebo or losartan and enalapril. Renal function was studied using clearance of sodium, lithium, uric acid, inulin and para-aminohippuric acid. To examine further the determinants of glomerular filtration at the microcirculation level, fractional clearance of neutral dextran was determined and sieving curves were applied on a hydrodynamic model of ultrafiltration. 4. Losartan did not change plasma renin activity, blood pressure or glomerular filtration rate, but increased significantly renal plasma flow and urinary excretion of sodium and uric acid. Enalapril increased plasma renin activity and renal plasma flow, and decreased blood pressure without natriuretic, lithiuretic or uricosuric effects. The renal vasodilatation was potentiated when losartan and enalapril were combined, despite a further rise in plasma renin. In contrast to enalapril, losartan either alone or in combination with enalapril significantly depressed fractional clearances of dextran of small radii (34–42 Å). These changes in fractional clearances of dextran were presumably related to the rise in glomerular plasma flow since the other major determinants of filtration, i.e. transcapillary glomerular pressure gradient, ultrafiltration coefficient and membrane property, were computed as unchanged by either losartan, enalapril or a combination of both. 5. In conclusion, these findings suggest that in normal sodium-repleted man the renal, hormonal and blood pressure effects of AT1 antagonism and angiotensin-converting enzyme inhibition are not strictly similar and could be synergistic.

scholarly journals Effect of Hemorrhage on Arterial Plasma Renin Activity in the Rabbit

1966 ◽  
Vol 19 (2) ◽  
pp. 269-273 ◽  
Author(s):  
JOHN K. MCKENZIE ◽  
MICHAEL R. LEE ◽  
WILLIAM F. COOK
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Arterial Plasma

Effect of the Converting-Enzyme Inhibitor SQ 14 225 (captopril) in Early One-Kidney, One-Clip Hypertension in the Rat

1981 ◽  
Vol 60 (4) ◽  
pp. 387-392 ◽  
Author(s):  
R. Vandongen ◽  
Anne Tunney ◽  
Patricia Martinez
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Enzyme Inhibitor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Converting Enzyme ◽  
Hypotensive Action ◽  
Converting Enzyme Inhibitor ◽  
Restore Blood Pressure ◽  
Arterial Plasma

1. Arterial plasma renin activity was significantly elevated in rats with one-kidney, one-clip hypertension of less than 3 weeks duration. 2. Intraperitoneal injection of the angiotensin-converting enzyme inhibitor SQ 14 225 (captopril) caused a dose-related decrease in systolic blood pressure in hypertensive rats. The lowest dose of captopril used (3.5 mg/kg) inhibited conversion of exogenous angiotensin I and maximally potentiated the depressor response to bradykinin, but failed to restore blood pressure to that of the normotensive controls. 3. Removal of the solitary clipped kidney also did not restore blood pressure to normal. Injection of captopril (3.5 mg/kg) 24 h after nephrectomy, when no circulating renin activity was detectable, lowered blood pressure further in hypertensive but not in similarly nephrectomized controls. 4. These results indicate that raised blood pressure in early one-kidney, one-clip hypertension in the rat cannot be entirely attributed to the renin-angioterisin system, even when plasma renin activity is significantly increased. 5. This study has also confirmed a hypotensive action of captopril in anephric rats when plasma renin activity is undetectable.

Effect of KCl infusion on renin secretory rates and aldosterone excretion in dogs

1975 ◽  
Vol 229 (2) ◽  
pp. 370-375 ◽  
Author(s):  
W Flamenbaum ◽  
JG Kleinman ◽  
JS McNeil ◽  
RJ Hamburger ◽  
TA Kotchen
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Flow Distribution ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renin Activity ◽  
Secretory Rate ◽  
Arterial Plasma ◽  
Renal Blood Flow Distribution

The effects of unilateral intrarenal arterial KCl infusion in dogs (12 mueq/kg per min) on bilateral renal function, renin secretory rates, and aldosterone excretion were studied. During KCl infusion, infused-side renal arterial plasma [K+] increased by 2.2 +/- 0.6 meq/liter. Systemic plasma [K+] simultaneously rose by 0.6 +/- 0.1 meq/liter. Plasma renin activity decreased 29 +/- 9%, and the decrease correlated with the increases in plasma [K+]. Renin secretory rate decreased bilaterally, the decrease being greater in each experiment on the infused side. Aldosterone excretion increased during KCl infusion by 72 +/- 17%, despite a decrease in plasma renin activity. With KCl infusion there was a bilateral increase in K+ excretion, and a positive correlation was observed between the net alterations in K+ and Na+ excretion. No significant alterations in systemic blood pressure, glomerular filtration rate, total renal blood flow, or intracortical renal blood flow distribution were observed. These studies suggest that K+ inhibits the release of renin by an intrarenal mechanism, which may be related to a K+-induced alteration in Na+ absorption.

Renal response to captopril in conscious dogs pretreated with indomethacin

1982 ◽  
Vol 243 (6) ◽  
pp. F543-F548
Author(s):  
Jack M. DeForrest ◽  
Thomas L. Waldron ◽  
Michael J. Antonaccio
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Effective Renal Plasma Flow ◽  
Potassium Excretion ◽  
Captopril Treatment

This study was designed to determine whether the prostaglandins mediate the renal effects of captopril in the conscious sodium-replete dog. In a group of control animals (n = 8), effective renal plasma flow (ERPF) increased from 185 ± 15 to 230 ± 12 ml/min and plasma renin activity (PRA) increased from 0.64 ± 0.15 to 12.9 ± 1.1 ng ANG I·ml-1·h-1 after captopril (10 mg/kg bolus plus 10 μg·kg-1·min-1i.v.) administration. Glomerular filtration rate (GFR) and sodium excretion (UKV) were also increased significantly following captopril treatment, whereas urine volume (V), potassium excretion (UKV), mean arterial pressure (MAP), and heart rate (HR) remained unchanged throughout the experiment. When the same dose of captopril was given to indomethacin-pretreated dogs (5 mg/kg bolus plus 2 μg·kg-1·min-1i.v.), ERPF increased from 170 ± 8 to 265 ± 18 ml/min and PRA increased from 1.2 ± 0.4 to 14.6 ± 3.0 ng ANG I·ml-1·h-11 after the captopril administration. GFR was also increased significantly after captopril, while UNaV, UKV, and V remained unchanged. These data demonstrate that the prostaglandins do not mediate the ability of captopril to increase PRA or effective renal plasma flow in this experimental model. prostaglandins; effective renal blood flow; plasma renin activity; angiotensin II; arachidonic acid Submitted on September 25, 1981 Accepted on June 25, 1982

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