Separate renal function studies in conscious dogs with renovascular hypertension

1978 ◽  
Vol 235 (4) ◽  
pp. F310-F316 ◽  
Author(s):  
J. M. DeForrest ◽  
J. O. Davis ◽  
R. H. Freeman ◽  
B. E. Watkins ◽  
G. A. Stephens
Keyword(s):  
Renal Artery ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Control Level ◽  
Plasma Renin ◽  
Filtration Fraction ◽  
Water Excretion ◽  
Contralateral Kidney ◽  
Reduce Blood Flow ◽  
Determining Factor

A new method was developed for separate kidney function studies by catheterizing the ureters and exteriorizing the catheters through the urethra into the vagina. Renal artery plication was performed to reduce blood flow to one kidney by 66 +/- 5%. Arterial pressure increased from 107 +/- 2 to 131 +/- 3 mmHg and remained elevated for 28 days. Plasma renin activity was increased for the first 7-10 days only. Sodium and water excretion were markedly reduced in the kidney with the stenosed renal artery and after the first 2 days Na and water excretion were incresed in the contralateral kidney. These changes in Na and water excretion were frequently associated with similar directional changes in glomerular filtration rate (GFR) and renal plasma flow. An exception was noted in that renal sodium and water excretion remained low throughout the 28 days in the kidney with the constricted renal artery, whereas GRF returned to near the control level by the end of 2 wk. Altered filtration fraction did not appear to be a determining factor in control of the rate of Na excretion. It is suggested that GFR, the renin-angiotensin-aldosterone system, and other as yet undefined factors are involved in salt and water homeostasis during unilateral renal artery stenosis with hypertension.

Renal blood flow changes in contralateral kidney of Goldblatt hypertensive dog

1981 ◽  
Vol 241 (2) ◽  
pp. H145-H148
Author(s):  
B. G. Zimmerman ◽  
C. Mommsen
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Control Level ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

Sequential changes in systemic arterial blood pressure (BP), renal blood flow (RBF) in the contralateral kidney, and plasma renin activity (PRA) were examined on conscious dogs with construction of a single renal artery (RAC). An increase of 24 mmHg in bP occurred within 2 days after RAC, and BP later plateaued at a lower level. RBF in the contralateral kidney transiently increased by 24% and then returned to the control level in 11-14 days. PRA also peaked early after RAC and then returned to control. The clamp was tightened and the renal artery was occluded (RAO) 3-20 days after RAC. BP, RBF, and PRA increased to an even greater degree than after RAC. BP peaked at 145 mmHg, and RBF increased 61.5% at 2-3 days after RAO. BP and RBF both decreased but remained above the control for the duration of the study, BP at 127 mmHg and RBF at 256 ml/min. RBF per gram for the hypertrophied contralateral kidney was calculated from the RBF before death and the weight at death. The final RBF per gram of the contralateral kidney (2.7 ml.min-1.g-1) decreased and renal vascular resistance increased compared with the estimated control RBF/g (3.7 ml.min-1.g-1) and renal vascular resistance. These results suggest that the final RBF of the contralateral kidney is not increased in proportion to its increase in weight and that it may be relatively hypoperfused in two-kidney one-clip Goldblatt hypertension.

Vasodilator capacity of contralateral kidney in Goldblatt hypertensive dog

1983 ◽  
Vol 245 (5) ◽  
pp. H790-H795
Author(s):  
B. G. Zimmerman ◽  
R. D. Largent
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Control Level ◽  
Plasma Renin ◽  
Artery Occlusion ◽  
Angiotensin I ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Artery Occlusion

Because of previous suggestions of impaired renal blood flow in the contralateral kidney of Goldblatt hypertensive animals, we examined the maximal vasodilator capacity of the contralateral kidney in 13 instrumented dogs during progression of Goldblatt hypertension. Constriction of a single renal artery (RAC) followed a week or more later by total renal artery occlusion (RAO) increased mean arterial blood pressure (BP) from a control level of 102 +/- 3 to 135 +/- 7 mmHg (P less than 0.001) and increased plasma renin activity (PRA) from 0.69 +/- 0.16 to 10.2 +/- 3.9 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at 2 wk after RAO. The hypertension was accompanied by an increase in basal renal blood flow (RBF) from 224 +/- 21 to 300 +/- 27 ml/min (P less than 0.01) and RBF at maximal vasodilatation from 505 +/- 24 to 673 +/- 52 ml/min (P less than 0.05). Hypertension and the increase in PRA waned, but BP remained higher than control at 4 wk after RAO (117 +/- 6 mmHg, P less than 0.005). Basal and maximal RBF were sustained at the higher levels throughout the 4-wk period after RAO. When RBF was expressed on a per gram basis, basal and maximal flow before (3.72 +/- 0.40 and 8.26 +/- 0.62 ml X min-1 X g-1, respectively) did not differ from that in the final experiment after RAO (3.85 +/- 0.34 and 8.19 +/- 0.78 ml X min-1 X g-1). The basal and minimal vascular resistances based on flow per gram were increased by 24 +/- 8 and 41 +/- 16% (P less than 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Sodium and Water Excretion in Nephrotic Patients: Effects of Changes in Renal Haemodynamics

1990 ◽  
Vol 79 (2) ◽  
pp. 123-129 ◽  
Author(s):  
Michael Allon ◽  
Charles B. Pasque ◽  
Mariano Rodriguez
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Sodium Reabsorption ◽  
Plasma Volume Expansion ◽  
Water Excretion ◽  
Significant Change

1. Eight nephrotic patients were studied in order to evaluate the effects of acute changes in renal plasma flow and glomerular filtration rate on renal solute and water handling, in the absence of plasma volume expansion. 2. The subjects were studied first after the administration of captopril, a manoeuvre that increased renal plasma flow without a significant change in glomerular filtration rate, and a second time after receiving combined therapy with captopril and ibuprofen, a manoeuvre that decreased glomerular filtration rate without a significant change in renal plasma flow. 3. After captopril therapy, despite the increase in renal plasma flow, there was no significant change in proximal sodium reabsorption (as estimated from fractional lithium reabsorption), urine volume or urine osmolality. 4. The decrease in glomerular filtration rate observed after the administration of captopril plus ibuprofen was associated with decreases in fractional excretion of sodium and urine volume, and an increase in urine osmolality. The changes in these parameters of tubular function were proportionate to the changes in glomerular filtration rate. Fractional proximal sodium reabsorption increased substantially. 5. These observations suggest that, in the absence of plasma volume expansion, an increase in renal plasma flow does not increase sodium or water excretion by the nephrotic kidney. Moreover, during acute decreases in glomerular filtration rate, glomerulotubular balance appears to be disrupted, resulting in disproportionately high rates of proximal tubule sodium reabsorption.

γ-l-Glutamyl-l-Dopa is a Dopamine Pro-Drug, Relatively Specific for the Kidney in Normal Subjects

1985 ◽  
Vol 69 (2) ◽  
pp. 207-214 ◽  
Author(s):  
D. P. Worth ◽  
J. N. Harvey ◽  
J. Brown ◽  
M. R. Lee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Urinary Sodium Excretion ◽  
Systemic Effects

1. γ-l-Glutamyl-l-dopa was given by intravenous infusion to eight normal subjects at doses of 12.5 and 100 μg min−1 kg−1. 2. Both doses of the dipeptide resulted in an increase in mean urinary sodium excretion. 3. Mean effective renal plasma flow rose at both doses, but mean glomerular filtration rate increased only at the lower dose. 4. There was a fall in mean plasma renin activity after the infusion of both 12.5 and 100 μg min−1kg−1. 5. Mean urine free dopamine excretion increased by 280- and 2500-fold at infusion rates of 12.5 and 100 μg min−1 kg−1 respectively. 6. Mean plasma free dopamine rose at both doses but the increase at 12.5 μg min−1 kg−1 was not to a level previously associated with systemic effects of the catecholamine. 7. On administration of the dipeptide at 12.5 μg min−1 kg−1 there were no changes in blood pressure or heart rate, but at the higher dose there was a fall in diastolic blood pressure. 8. At a dose of 12.5 μg min−1 kg−1 in man, there is kidney specific conversion of gludopa to dopamine.

Angiotensin II inhibition with captopril on plasma ADH, PG synthesis, and renal function in humans

1986 ◽  
Vol 250 (6) ◽  
pp. F986-F990 ◽  
Author(s):  
M. Usberti ◽  
G. Di Minno ◽  
B. Ungaro ◽  
B. Cianciaruso ◽  
S. Federico ◽  
...  
Keyword(s):  
Urine Output ◽  
Filtration Rate ◽  
Enzyme Inhibitor ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Ang Ii ◽  
Urinary Osmolality ◽  
Endogenous Prostaglandins ◽  
The Relationship ◽  
Control Study

Using captopril (C), an angiotensin (ANG) I converting-enzyme inhibitor, to increase endogenous prostaglandins (PGs) and to decrease endogenous ANG II synthesis, we studied the relationship between endogenous ANG II, PG, and antidiuretic hormone (ADH) release in seven normal volunteers before (control study) and after inhibition of PG synthesis by a single dose of aspirin (ASA study). In the control study, following the administration of 100 mg of C, there was a significant increase of plasma PGE2, plasma-renin activity (PRA), and urinary PGE2 and 6-keto-PGF1 alpha and a decrease of plasma ADH. Glomerular filtration rate (GFR) and renal plasma flow (RPF) were unaffected by C; urine output, fractional sodium excretion (FENa), and osmolal clearance (Cosmol) increased; and urinary osmolality (Uosmol) decreased significantly after C. In the ASA study PG were undetectable in plasma and significantly reduced in urine 1 h after aspirin and did not increase when C was added. Plasma ADH decreased and PRA increased, as in the control study, after C, whereas GFR, RPF, urine output, FENa, Cosmol, and Uosmol were unchanged. These results suggest that the effect of C on ADH release may be mediated, to a large extent, by a fall in endogenous circulating ANG II, since ADH decreased in the presence of both high or undetectable levels of PGE2. The results also suggest that the increase in PGE2 induced by C may precipitate the diuretic and natriuretic effects of acute C administration.

Haemodynamic and Endocrine Responses of the Kidney to Frusemide in Mild Essential Hypertension

1985 ◽  
Vol 68 (2) ◽  
pp. 159-164 ◽  
Author(s):  
I. G. Mackay ◽  
K. Nath ◽  
A. D. Cumming ◽  
A. L. Muir ◽  
M. L. Watson
Keyword(s):  
Glomerular Filtration Rate ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Underlying Factor ◽  
Induced Changes

1. Prostaglandin-dependent, frusemide-induced changes in renal plasma flow, glomerular filtration rate and plasma renin activity were measured in 14 patients with mild essential hypertension. 2. The renal haemodynamic responses to frusemide were the same as in 10 normal subjects. 3. Frusemide-induced changes in urinary PGE and kallikrein excretion were also the same as in normal subjects. 4. Impaired renal release of vasodilator prostaglandins in essential hypertension is likely to be secondary to the hypertension rather than an underlying factor in its development.

Renal actions of angiotensin II in renovascular hypertension

1987 ◽  
Vol 65 (8) ◽  
pp. 1559-1565 ◽  
Author(s):  
W. P. Anderson ◽  
R. L. Woods ◽  
K. M. Denton ◽  
D. Alcorn
Keyword(s):  
Angiotensin Ii ◽  
Renal Artery ◽  
Glomerular Filtration ◽  
Renal Artery Stenosis ◽  
Renovascular Hypertension ◽  
Plasma Renin ◽  
Artery Stenosis ◽  
Filtration Fraction ◽  
Severe Stenosis ◽  
Glomerular Ultrafiltration

In renal artery stenosis severe enough to cause hypertension, angiotensin II maintains glomerular filtration rate (GFR) both in the initial high renin phase of hypertension and later when plasma levels are normal. Angiotensin II also maintains GFR in less severe stenosis, which does not cause hypertension. This homeostatic action of angiotensin II to maintain GFR has minimal effects on blood flow. In renal-wrap hypertension, plasma renin levels are elevated for longer than after renal artery stenosis, but in other respects this initial phase of the hypertension is similar to that after renal artery stenosis. GFR is reduced, the rate of development of hypertension is accelerated by angiotensin II, and angiotensin II maintains the glomerular filtration fraction. Renal resistance is markedly increased owing to both compression of the kidney by the hypertrophying renal capsule and to angiotensin II. Thus angiotensin II apparently plays a primarily homeostatic role in renovascular hypertension to maintain glomerular ultrafiltration. It is suggested that the angiotensin II may be formed intrarenally and may act on sites other than resistance blood vessels.

Renal hydrogen ion secretion after release of unilateral ureteral obstruction

1976 ◽  
Vol 231 (4) ◽  
pp. 1233-1239 ◽  
Author(s):  
K Thirakomen ◽  
N Kozlov ◽  
JA Arruda ◽  
NA Kurtzman
Keyword(s):  
Ureteral Obstruction ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Unilateral Ureteral Obstruction ◽  
Outer Cortex ◽  
Urinary Ph ◽  
Contralateral Kidney ◽  
Saline Loading ◽  
K Secretion ◽  
Inner Cortex

The effect of 24 h of unilateral ureteral obstruction on HCO3 reabsroption and urinary acidification was studied in dogs. The postobstructed kidney (EK) had a significantly lower glomerular filtration rate and renal plasma flow than the contralateral kidney (CK). Urinary pH prior to HCO3 loading was significantly higher in the EK as was maximal HCO3 reabsorption. Saline loading depressed HCO3 reabsorption to the same degree in both kidneys. Urinary PCO2, during HCO3 loading, and during phosphate infusion, was significantly lower in the EK than the CK. Fractional Na excretion was significantly higher in the EK than the CK after deoxycorticosterone acetate administration. Na2SO4 administration enhanced acid excretion only in the CK. K excretion was significantly lower in the EK than the CK both during HCO3 loading and Na2SO4 administration. There was redistribution of cortical blood flow from the outer cortex toward the inner cortex in the EK as compared to the CK. There was no difference in plasma renin activity from both renal veins. These data demonstrate enhanced proximal H+ secretion (which is abolished by volume expansion) and impaired distal H+ secretion by the postobstructed kidney. The distal defect is likely an effect of a generalized disorder of distal transport in that both K secretion and steroid-responsive Na reabsorption were impaired in the postobstructed kidney.

Influence of the Adrenal Cortex on Renal Hemodynamics in the Dog

1956 ◽  
Vol 185 (1) ◽  
pp. 159-166 ◽  
Author(s):  
J. Maxwell Little ◽  
Weston M. Kelsey ◽  
Ernest H. Yount
Keyword(s):  
Renal Function ◽  
Adrenal Cortex ◽  
Considerable Increase ◽  
Renal Plasma Flow ◽  
Control Level ◽  
Renal Hemodynamics ◽  
Depressing Effect ◽  
Filtration Fraction ◽  
Renal Functions ◽  
Before And After

The effect of ACTH administration on glomerular filtration rate (GFR), effective renal plasma flow (ERPF), effective renal blood flow (ERBF) and on filtration fraction (FF) was studied in unanesthetized female dogs before and after the production of atrophic changes in the zonae reticularis and fasciculata of the adrenal cortex. The atrophic changes were produced by Rhothane (DDD) which has been shown to produce changes in the two inner zones of the adrenal cortex. The administration of ACTH to normal dogs caused a considerable increase in GFR, ERPF, ERBF, and a significant decrease in FF. The administration of DDD resulted in varying degrees of necrosis and atrophy of the zonae fasciculata and reticularis of the adrenal cortex with minimal histological evidence of glomerulosa damage. There was a concomitant decrease below control values for the renal function studied in three of five dogs. The subsequent administration of ACTH restored the renal functions to the control level in all five dogs, with the exception of FF. The simultaneous administration of ACTH and Rhothane resulted in a progressive decrease to or below control values from elevated levels in three of five dogs studied. In one dog there was no appreciable elevation of renal function with ACTH under these conditions. In the other dog ACTH administration was continued uninterrupted, and the addition of Rhothane abolished the renal stimulating effect of ACTH within five days. It is concluded that the two inner zones of the adrenal gland influence renal hemodynamics, as manifested by the stimulating effect of ACTH and the depressing effect of Rhothane.

Urodilatin, a natriuretic factor from kidneys, can modify renal and cardiovascular function in men

1990 ◽  
Vol 259 (5) ◽  
pp. F832-F838 ◽  
Author(s):  
H. Saxenhofer ◽  
A. Raselli ◽  
P. Weidmann ◽  
W. G. Forssmann ◽  
A. Bub ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Factor ◽  
Healthy Subjects ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Cardiovascular Function ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Amino Acid Residues ◽  
Natriuretic Factor

Urodilatin is a newly identified analogue of human atrial natriuretic factor-(99-126) [ANF-(99-126)], which has recently been isolated from human urine and has 32 amino acid residues [ANF-(95-126)]. To investigate renal and cardiovascular effects in men, eight healthy subjects received injections of 25, 50, and 100 micrograms urodilatin iv compared with 50 micrograms ANF-(99-126) and placebo. Blood pressure decreased (P less than 0.05) after 50 micrograms ANF-(99-126), whereas urodilatin lowered diastolic blood pressure only at the highest dose (P less than 0.01). Heart rate increased (P less than 0.05-0.01) dose dependently after urodilatin injections. Glomerular filtration rate rose after 100 micrograms (from 120 +/- 3 to 156 +/- 7 ml.min-1.1.73 m-2, P less than 0.001) and 50 micrograms urodilatin (from 116 +/- 7 to 149 +/- 13 ml.min-1.1.73 m-2, P less than 0.01) but not after 25 micrograms urodilatin, ANF-(99-126), or placebo. Effective renal plasma flow was not significantly modified. Diuresis and excretion of sodium, chloride, and guanosine 3',5'-cyclic monophosphate increased (P less than 0.001) dose dependently; effects of 25 micrograms urodilatin equaled those of 50 micrograms ANF-(99-126). Plasma renin, aldosterone, and catecholamines were unchanged. We conclude that urodilatin can acutely modify renal and cardiovascular function in men and seems to exert more potent renal effects than ANF-(99-126).

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