Development of Hypertension in Renal Disease

1983 ◽  
Vol 64 (2) ◽  
pp. 141-152 ◽  
Author(s):  
J. Brod ◽  
J. Bahlmann ◽  
M. Cachovan ◽  
P. Pretschner
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Stage I ◽  
Renin Activity ◽  
Circulating Blood Volume ◽  
Venous Distensibility

1. Central and peripheral haemodynamics, circulating blood volume and plasma renin activity (PRA) were investigated under resting conditions in 97 patients with chronic nonuraemic renal parenchymatous disease and without anaemia. For comparison a group of 17 healthy subjects was used. 2. An initial abnormality appeared in 12 out of 32 normotensive renal patients. It consisted of a markedly increased circulating blood volume, raised cardiac output, low total peripheral and forearm vascular resistance, hyperfusion of the forearm and increased venous distensibility. PRA was slightly (but insignificantly) higher in these hyperkinetic subjects with relaxed peripheral vessels than in the other 20 normotensive renal patients who did not differ haemodynamically from the control subjects. 3. Fifteen out of 47 renal patients with a mild or moderate hypertension (stage I–II WHO) were hyperkinetic. However, in these there was no compensatory vasodilatation in response to the high cardiac output: forearm blood flow was normal and venous distensibility below that of the control subjects. Blood volume was normal. Plasma renin activity (PRA) was the same as in the normotensive renal patients. 4. The difference between stage I–II and stage III was due entirely to a rise in total peripheral vascular resistance. 5. A re-examination of these patients 2-8 years after they had been first studied revealed that 11 out of the 12 originally hyperkinetic normotensive renal patients were now hypertensive compared with only one-half of the originally normokinetic normotensive renal subjects. 6. It is concluded that an inability of the diseased kidney to control volume homoeostasis leads to hypervolaemia, which raises cardiac output in the renal patients whilst still normotensive. As long as the arterioles adjust to the high output and the capacitance system to the high volume, blood pressure remains normal. When this adaptation of the periphery ceases, blood pressure rises, normalizing (possibly through a pressure diuresis) blood volume. PRA does not correlate with any of these changes and only in advanced renal hypertension may its rise partly contribute to the maintenance of high blood pressure without being its cause.

Blood volume restitution after hemorrhage in the newborn lamb

1989 ◽  
Vol 257 (3) ◽  
pp. R647-R652 ◽  
Author(s):  
S. M. Block ◽  
J. E. Pixley ◽  
A. H. Wray ◽  
D. Ray ◽  
K. D. Barnes ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Protein ◽  
Plasma Glucose ◽  
Initial Phase ◽  
Plasma Renin ◽  
Renin Activity ◽  
Newborn Lamb ◽  
Lying Down

Blood volume restitution after hemorrhage was investigated in lambs in the first week of life. Two groups of nonsplenectomized lambs were bled 10 and 20% of their blood volume at 2%/min while being suspended horizontally in a sling with their legs dependent, and a third group was bled 20% while lying down. Blood pressure fell 8% in the lambs bled both 10 and 20% while lying down and 44% in those bled 20% while being suspended. Blood volume was completely restored in all three groups by 5 h after the hemorrhage, the rate of restitution being equal among the groups. The initial phase of restitution was slower when the lambs were bled while lying down. Vasopressin levels were increased only in the lambs bled 20% of their blood volume while being suspended. Plasma renin activity increased similarly in all groups. Hemorrhage increased plasma glucose but did not change plasma protein and serum osmolality. We conclude that lambs bled up to 20% of blood volume restitute relatively quickly at a rate independent of the volume shed. The position of the animal affects the degree of hypotension, the levels of vasopressin, and the rate of the initial phase of volume restoration.

Blood Pressure Control in End-Stage Renal Disease in Man: Indirect Evidence of a Complex Pathogenic Mechanism besides Renin or Blood Volume

1977 ◽  
Vol 52 (1) ◽  
pp. 19-21
Author(s):  
G. Cannella ◽  
A. Castellani ◽  
G. Mioni ◽  
M. Usberti ◽  
U. Guerra ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Indirect Evidence ◽  
Plasma Renin ◽  
Pressure Control ◽  
High Plasma ◽  
Renin Activity ◽  
Before And After ◽  
Stage Renal Disease

1. In twenty-three uraemic patients on regular dialysis, plasma renin activity and blood volume were measured before and after a single dialysis. Three groups were identified; the first had a low or normal plasma renin activity and a high or normal blood volume, the second had a high plasma renin activity and a low blood volume and the third had both variables above normal. 2. In spite of these differences, diastolic blood pressure before and after dialysis was the same in the three groups and multiple regression analyses failed to demonstrate any dependence of blood pressure on plasma renin activity, blood volume or body weight taken separately or together. 3. We conclude that other factors besides plasma renin activity and blood volume are important in maintaining arterial hypertension in terminal renal failure.

Interrelations among blood pressure, blood volume, plasma renin activity and urinary catecholamines in benign essential hypertension

1977 ◽  
Vol 62 (2) ◽  
pp. 209-218 ◽  
Author(s):  
Peter Weidmann ◽  
David Hirsch ◽  
Carlo Beretta-Piccoli ◽  
Francois C. Reubi ◽  
Walter H. Ziegler
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Urinary Catecholamines

Renin, Blood Volume and Response to Saralasin in Patients on Chronic Haemodialysis: Evidence against Volume- and Renin-‘Dependent’ Hypertension

1978 ◽  
Vol 54 (3) ◽  
pp. 305-312
Author(s):  
B. P. McGrath ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Blood Volume ◽  
Plasma Renin ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Dietary Sodium ◽  
Chronic Haemodialysis ◽  
Plasma Angiotensin

1. No significant relationship was found between blood pressure and blood volume, sulphate space or plasma angiotensin II concentration in 59 non-nephrectomized haemodialysis patients, of whom 42 were hypertensive. Supine mean blood pressure was only weakly correlated with plasma renin activity and the correlation was not improved when blood pressure was related to expressions combining renin and volume. 2. Changes in supine mean blood pressure during saralasin infusion were related to pre-infusion plasma renin activity (P < 0·001) or plasma angiotensin II (P < 0·02) but also to blood volume (P < 0·001) or sulphate space (P < 0·001). A fall of more than 10% in mean blood pressure during saralasin infusion was observed in only 12 patients (one normotensive), in five of whom there was evidence of volume depletion. 3. Thirteen patients (nine hypertensive) were studied at two levels of dietary sodium: 100 mmol/day and < 20 mmol/day. Supine mean blood pressure in hypertensive patients was lower during the period of higher salt intake despite increased volumes. 4. Hypertension in haemodialysis patients cannot be adequately explained by abnormalities either in volume homeostasis and/or in the renin—angiotensin system.

Mechanism of the Haemodynamic Interaction between Atenolol, a Cardioselective β-Adrenoreceptor-Blocking Agent, and Chlorthalidone in Hypertensive Patients

1979 ◽  
Vol 57 (s5) ◽  
pp. 363s-365s
Author(s):  
M. Velasco ◽  
J. Guevara ◽  
J. Morillo ◽  
A. Ramírez ◽  
A. Urbina-Quintana ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Blood Flow ◽  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renin Activity ◽  
Mean Blood Pressure ◽  
Time Interval ◽  
Calf Blood Flow

1. The effect of the cardioselective β-adrenoreceptor antagonist atenolol on blood pressure, heart rate, systolic time interval, limb blood flow and limb vascular resistance was studied, both when the drug was used by itself, and also when combined with chlorthalidone. Plasma renin activity and plasma atenolol concentration were also measured. 2. After the administration of atenolol alone, there was a decrease in mean blood pressure from 131·8 ± sem 2·88 mmHg to 119·0 ± 4·05 mmHg (P &lt; 0·001), in heart rate from 76·4 ± 3·58 beats/min to 57·0 ± 2·55 beats/min (P &lt; 0·001), in calf blood flow from 9·23 ± 1·39 ml min−1100 g−1 to 5·05 ± 0·89 ml min−1 100 g−1 (P &lt; 0·001), and an increase in calf vascular resistance from 16·54 ± 1·90 (mmHg min−1100 g−1)/ml to 28·53 ± 3·40 (mmHg min−1 100 g−1)/ml) (P &lt; 0·005). Atenolol did not alter the pre-ejection period index significantly (P &gt; 0·1). In atenolol-treated patients, upon addition of chlorthalidone there was a further decrease in mean blood pressure from 119·0 ± 4·05 mmHg to 105·9 ± 4·12 mmHg (P &lt; 0·001). There was no further significant alteration in heart rate, pre-ejection period index, calf blood flow or calf vascular resistance. 3. Atenolol decreased plasma renin activity from 4·69 ± 0·87 to 2·85 ± 0·68 ng h−1 ml−1 (P &lt; 0·05), and the addition of chlorthalidone increased it from 2·85 ± 0·68 to 3·81 ± 0·98 ng h−1 ml−1 (P &lt; 0·05). 4. There was a 7·8 fold-interindividual variability in the relationship between plasma atenolol concentration and the dose of atenolol after a single oral dose of 100 mg of the drug.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

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