Effect in the Conscious Dog of Constriction of the Renal Artery to a Sole Remaining Kidney on Haemodynamics, Sodium Balance, Body Fluid Volumes, Plasma Renin Concentration and Pressor Responsiveness to Angiotensin

1970 ◽  
Vol 38 (6) ◽  
pp. 741-766 ◽  
Author(s):  
G. Bianchi ◽  
L. Tilde Tenconi ◽  
R. Lucca

1. The renal artery to a lone remaining kidney was constricted in fourteen concious dogs. The following variables were measured in all animals: blood pressure (BP), cardiac rate (CR), plasma renin concentration (PRC), plasma volume (PV), extracellular fluid volume (ECFV) and plasma non-protein nitrogen (NPN). Sodium balance was estimated in eleven dogs. Cardiac output (CO), total peripheral resistence (TPR) and stroke volume (SV) were measured in nine dogs. Angiotensin responsiveness (AR) was measured in six animals. 2. Within 2 hr the following changes occurred: a sharp increment of BP, PRC and TPR, with initial reduction or no change in CO and CR; SV and PV were not changed. The linear regression of BP changes on PRC changes did not differ statistically from the one previously obtained during the infusion of exogenous renin in the conscious dog. AR was much depressed at 2 hr. 3. After 24 hr a slight but significant sodium retention developed, while PV and ECFV and SV increased, CO remained unchanged owing to a decrease of CR. PRC tended to return toward normal while BP remained high. Thus the linear regression between these two variables disappeared. At this stage AR increased toward normal and in two dogs exceeded normal. 4. On days 3–4 and 6–7 after constriction, CO increased owing to a rise of SV, while TPR decreased. PV and ECFV were expanded while sodium balance was maintained. AR varied very much in the individual dogs according mainly to changes of PRC, sodium balance and PV. 5. On days 12–14 sodium balance became positive again, PRC returned within normal levels in almost all the dogs. PV and ECFV also tended to decrease to normal. CO and AR were measured in only two dogs at this stage. 6. It is suggested that the early rise of blood pressure might be produced by the increase of PRC, while 3–6 days after the constriction the expansion of PV with the increase of CO contributed to the maintenance of the hypertension.

1972 ◽  
Vol 42 (6) ◽  
pp. 651-664 ◽  
Author(s):  
G. Bianchi ◽  
E. Baldoli ◽  
R. Lucca ◽  
P. Barbin

1. The renal artery was constricted leaving the opposite kidney intact in ten conscious and seven anaesthetized dogs. Intravenous infusion of exogenous renin was done in seven conscious dogs; in four of these the renal artery was constricted 15–17 days later. The following variables were measured in all animals before and after renal artery constriction: plasma renin concentration, blood pressure, cumulative sodium balance, plasma volume, extracellular fluid volume and plasma non-protein nitrogen. Before and after renal artery constriction in the conscious dogs cardiac output, stroke volume, total peripheral resistance and cardiac rate were also measured. In a few dogs angiotensin responsiveness and plasma concentration of renin substrate were also measured. 2. There was no significant difference between the regression of change in blood pressure on change in plasma renin concentration within 2 h from renal artery constriction in the conscious dogs and that observed during intravenous infusion of renin. Comparing the changes of these variables with the ones previously obtained with renal artery constriction to the lone remaining kidney, for a given increase of plasma renin concentration the rise of blood pressure was lower when the contralateral kidney was untouched. The changes of the other variables in the conscious dogs may be divided into three phases: a first phase lasting hours, in which, besides the changes described above, there was an increase of total peripheral resistance while the other variables remain unchanged: a second phase, 24 h after constriction, in which blood pressure, total peripheral resistance and plasma renin clearance decreased while plasma volume, cardiac output and extracellular fluid volume slightly increased; however, only the plasma volume change was statistically significant: and a third phase 6–7 days after constriction, when all the variables returned towards normal values, except that the blood pressure and total peripheral resistance remained significantly higher. Sodium balance remained at equilibrium throughout the study period. It is suggested that these results are compatible with the ‘autoregulation theory’ of renal hypertension. 3. Renal artery constriction in the anaesthetized animals caused a slight but significant sodium retention that very likely influenced the sequence of the events. On the second day after constriction, the plasma renin concentration was significantly increased, whereas the highest values of blood pressure, plasma volume and extracellular fluid volume occurred on the seventh day after constriction.


1984 ◽  
Vol 67 (5) ◽  
pp. 521-528 ◽  
Author(s):  
D. Taverner ◽  
R. F. Bing ◽  
A. Fletcher ◽  
G. Russell ◽  
J. D. Swales ◽  
...  

1. The rat renal papilla was selectively destroyed by 2-bromoethylamine hydrobromide; increasing doses produced a graded severity of histological damage, polyuria and a reduction in urinary prostaglandin E2 excretion. 2. Destruction of at least half of the papilla caused significant hypertension, but plasma renin concentration and plasma creatinine did not change. 3. After graded medullary damage Goldblatt two-kidney, one-clip hypertension was induced. Four weeks later the severity of hypertension was similar in medulla-damaged and medulla-intact groups. 4. When Goldblatt two-kidney, one-clip hypertension was reversed by removal of the renal artery clip, the blood pressure fall was less when the inner renal papilla was ablated than when it was intact, although plasma renin concentration and sodium balance were similar. The final blood pressure was similar to that observed in normal rats treated with 2-bromoethylamine compared with their respective controls. 5. These findings are consistent with the hypothesis that the inner renal medulla produces a vasodepressor that influences blood pressure in normal rats, and also lowers blood pressure when two-kidney, one-clip hypertension is reversed surgically.


1981 ◽  
Vol 61 (s7) ◽  
pp. 335s-338s ◽  
Author(s):  
R. F. Bing ◽  
G. I. Russell ◽  
J. D. Swales ◽  
H. Thurston ◽  
A. Fletcher

1. Chemical renal medullectomy was produced in rats by injection of 2-bromoethylamine hydrobromide. Plasma creatinine and blood pressure were unchanged although urine volume was increased fourfold. 2. Left renal artery constriction resulted in similar degrees of hypertension in both intact and medullectomized rats. This was associated with a significantly smaller rise in plasma renin concentration in the latter. 3. Blood pressure in conscious intact hypertensive rats became normal within 24 h of unclipping whereas blood pressure of medullectomized rats remained significantly elevated. 4. The presence of an intact renal medulla is essential to the complete reversal of two-kidney, one-clip hypertension in the rat. This may reflect the loss of a medullary vasodepressor system.


1972 ◽  
Vol 42 (1) ◽  
pp. 47-55 ◽  
Author(s):  
G. Bianchi ◽  
C. Ponticelli ◽  
U. Bardi ◽  
B. Redaelli ◽  
L. Campolo ◽  
...  

1. Blood pressure, plasma renin concentration, exchangeable body sodium, plasma volume and extracellular fluid volume were measured in five patients on maintenance haemodialysis for end-stage renal disease in whom hypertension was relatively easy to control by the combination of dialysis and restriction of salt intake. Measurements were made on three occasions: on a free salt intake the day before dialysis; on a low salt intake the day after dialysis; on a free salt intake the day before dialysis after nephrectomy. 2. The fall of blood pressure after haemodialysis and salt intake restriction was accompanied by a decrease of exchangeable body sodium and body fluids while plasma renin concentration increased. The fall of blood pressure after bilateral nephrectomy was accompanied by a fourfold decrease of plasma renin without any change of the other variables. 3. The hypertension of these patients might thus be considered ‘salt and water dependent’ or ‘renin dependent’ according to the means used to decrease blood pressure.


1974 ◽  
Vol 48 (s2) ◽  
pp. 69s-71s
Author(s):  
G. G. Geyskes ◽  
P. Boer ◽  
F. H. H. Leenen ◽  
E. J. Dorhout Mees

1. In nineteen patients, five with unilateral renal artery stenosis and fourteen with essential hypertension (WHO grades I–II), blood pressure, plasma and extracellular fluid volumes and plasma renin activity were studied at the end of three sequential periods: (a) after at least 3 days on a 60 mmol Na+ diet; (b) after 3 days of salt depletion induced with a diuretic and sustained on a 20 mmol Na+ diet; (c) after 3 days during which the 20 mmol Na+ diet was continued and beta-receptor blockade was induced by increasing dosages of propranolol up to 320 mg daily. 2. After sodium depletion extracellular fluid volume and plasma volume decreased and plasma renin activity increased; blood pressure did not change significantly. 3. After adding propranolol, plasma volume and extracellular fluid volume remained low, and there was a significant decrease in plasma renin activity and blood pressure. 4. No correlation could be demonstrated between changes of blood pressure and plasma renin activity. 5. When the responses of the five patients with renal artery stenosis were compared with those of the fourteen patients with essential hypertension, no significant differences were found. 6. Propranolol has a strong anti-hypertensive effect after Na+ depletion, irrespective of the absolute activities of plasma renin.


1970 ◽  
Vol 39 (5) ◽  
pp. 559-576 ◽  
Author(s):  
G. Bianchi ◽  
L. Campolo ◽  
A. Vegeto ◽  
V. Pietra ◽  
U. Piazza

1. Plasma renin concentration (PRC) has been measured in 212 hypertensive patients. In fourteen patients with essential hypertension and in seventeen patients with renovascular hypertension, plasma volume (PV) and extracellular fluid volume (ECFV) were measured. 2. The results obtained have been discussed in three ways: (a) PRC in relation to the aetiology of hypertension; (b) PRC in relation to the effect on blood pressure of surgery for unilateral renal diseases; (c) PRC, PV and ECFV in ‘essential’ and renovascular hypertension. 3. Excluding patients with ophthalmoscopic signs of malignant hypertension, PRC is significantly higher in renovascular hypertension than in normal subjects and patients suffering from ‘essential’ hypertension and hypertension associated with bilateral renal disease; but the overlapping of the single values of the patients with these diseases is marked. Thus a normal PRC has no diagnostic value, while a high PRC without sodium deficiency or retinopathy might favour a diagnosis of renovascular disease. 4. In twenty-seven out of thirty-three patients submitted to surgery for unilateral renal disease and followed up for 12 months or longer, blood pressure has been significantly reduced. This group includes twelve patients with a normal preoperative PRC and fifteen patients with a high PRC. These results clearly demonstrate that unilateral renal disease may maintain a high blood pressure without increasing PRC and that PRC has no prognostic value. 5. Concurrent estimations of PRC, PV and ECFV in patients with renovascular or essential hypertension revealed the following differences. In cases of renovascular hypertension with normal PRC, PV and ECFV were significantly increased while in those with raised PRC, PV did not differ and ECFV was barely raised with respect to values obtained in patients with essential hypertension. PV of renovascular patients with normal renin was significantly higher than that of renovascular patients with high renin. The analysis of these results with quadratic discriminant functions demonstrated that an integrated evaluation of blood pressure, PV, ECFV and PRC allows a separation between the two types of hypertension. In other words these factors, taken together, in some way seem to reflect a difference between the two diseases. These results may indicate a new type of approach to the diagnosis and prognosis of renovascular hypertension.


1984 ◽  
Vol 66 (4) ◽  
pp. 473-480 ◽  
Author(s):  
Robert F. Bing ◽  
John D. Swales ◽  
David Taverner ◽  
Herbert Thurston

1. Pressor responses to angiotensin II and noradrenaline have been examined in two models of renovascular hypertension (two-kidney one-clip and one-kidney one-clip) before and 24 h after removal of the renal artery clip to examine the possible role of pressor hyper-responsiveness in the maintenance of hypertension. Early and chronic hypertension was studied to assess the part played by progressive structural hypertrophy. 2. Plasma renin concentration was elevated in early two-kidney hypertensive rats, whereas it was similar to that in age-matched normal rats in early one-kidney and chronic two-kidney hypertensive rats. Twenty-four hours after unclipping plasma renin concentration was the same in all groups. Unclipping restored blood pressure to normal levels by 24 h, whereas sham-operated animals remained hypertensive. 3. Angiotensin II responses in both early and chronic two-kidney one-clip hypertensive rats were lower than in age-matched normal rats. In unclipped rats responses were similar to those in normals. One-kidney hypertensive rats had similar angiotensin II responses to normal rats and there was no change with unclipping. Blockade of endogenous angiotensin II production by converting enzyme inhibition resulted in similar angiotensin II responses in hypertensive and unclipped groups. 4. In normal rats, angiotensin II responses were inversely related to plasma renin concentration (r = −0.47, P<0.001). Angiotensin II responses in hypertensive and unclipped rats were found to show a similar relationship to plasma renin concentration as normal rats. 5. Noradrenaline responses in hypertensive rats were similar to those in age-matched normals and there was no significant change with unclipping. In normal rats there was no relationship between noradrenaline responses and plasma renin concentration (r = −0.11, P<0.5). 6. These results emphasize the importance of the activity of endogenous renin-angiotensin in determining angiotensin II responses in vivo. It is concluded that neither the maintenance of hypertension nor the fall in blood pressure produced by removal of the renal artery clip in renovascular hypertension is due to changes in responsiveness to angiotensin II.


1985 ◽  
Vol 249 (6) ◽  
pp. F941-F947 ◽  
Author(s):  
J. C. Roos ◽  
H. A. Koomans ◽  
E. J. Dorhout Mees ◽  
I. M. Delawi

We studied renal sodium handling, extracellular fluid volume (ECFV), plasma renin activity, aldosterone and norepinephrine, and blood pressure in eight healthy volunteers after equilibration on intakes of 20, 200, and 1,128 +/- 141 meq sodium, respectively. Renal sodium handling was assessed by means of clearance studies during maximal water diuresis and lithium clearance. Urinary sodium excretions were 22 +/- 4, 202 +/- 19, and 1,052 +/- 86 meq/day. From the lower to the upper sodium intake level, 24-h creatinine clearance rose from 111 +/- 7 to 136 +/- 11 ml/min and inulin clearance from 103 +/- 9 to 129 +/- 9 ml/min, whereas proximal and distal fractional sodium reabsorption (FSRprox and FSRdist, respectively) fell from 86.8 +/- 1.3 to 79.0 +/- 2.7% and from 96.5 +/- 0.5 to 76.0 +/- 1.9%, respectively. During the normal sodium intake (200 meq), intermediate values were recorded. The changes in fractional lithium clearance were less consistent but correlated with FSRprox (r = 0.78, P less than 0.001) and not with FSRdist. Major changes in plasma renin activity, aldosterone, and, to a lesser extent, norepinephrine accompanied these changes in kidney function, displaying inverse and exponential correlations with daily sodium excretion and ECFV. No consistent rise in blood pressure was detected. These observations indicate that in healthy humans renal adaptation to vast variations in sodium intake includes resetting of glomerular filtration rate, FSRprox, and, in particular, FSRdist. Alterations in neurohumoral factors may play a dominant role in this adaptation.


1981 ◽  
Vol 61 (6) ◽  
pp. 663-670 ◽  
Author(s):  
W. P. Anderson ◽  
P. I. Korner ◽  
J. A. Angus ◽  
C. I. Johnston

1. Mild, moderate and severe renal artery stenosis was induced in uninephrectomized conscious dogs by inflating a renal artery cuff to lower distal pressure to 60, 40 or 20 mmHg respectively. The renal artery was narrowed progressively over the next 3 days by further inflation of the cuff to relower the distal renal artery pressure to the initial values. 2. Graded progressive stenosis produced graded progressive rises in blood pressure, plasma renin activity and total renal resistance to flow over the 3 day period, followed by a return to control values 24 h after cuff deflation. 3. The rise in total renal resistance to flow was almost entirely due to the stenosis, with only small changes occurring in renal vascular resistance. 4. in moderate and severe stenosis cardiac output did not alter significantly and thus increases in blood pressure were due to increases in total peripheral resistance. in these groups the resistance to blood flow of the stenosis accounted respectively for about 36 and 26% of the rises in total peripheral resistance. Vasoconstriction of the other non-renal vascular beds accounted for the remainder of the increase in total peripheral resistance. 5. in mild stenosis the changes in both cardiac output and total peripheral resistance were variable and not statistically significant. in this group the rise in stenosis resistance was compensated by vasodilatation of the non-renal vascular beds. 6. in all groups rises in plasma renin activity and blood pressure correlated with the haemodynamic severity of the stenosis. 7. Thus the resistance to blood flow of the moderate and severe renal artery stenoses accounted for one-quarter to one-third of the increases in total peripheral resistance. The remainder of the increase in total peripheral resistance was due to vasoconstriction of nonrenal beds.


1975 ◽  
Vol 49 (4) ◽  
pp. 353-358 ◽  
Author(s):  
P. L. Padfield ◽  
M. E. M. Allison ◽  
J. J. Brown ◽  
A. F. Lever ◽  
R. G. Luke ◽  
...  

1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium. 2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism. 3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed. 4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension. 5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity. 6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.


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