Effect of Captopril on the Blood Pressure and Renal Responses to Acute Saline Loading in Normal and Essential Hypertensive Subjects

1982 ◽  
Vol 63 (s8) ◽  
pp. 223s-225s ◽  
Author(s):  
A. Mimran ◽  
J. Ribstein
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Normal Subjects ◽  
Sodium Balance ◽  
Saline Loading ◽  
Diuretic Response ◽  
Normotensive Subjects ◽  
Renal Responses

1. Systemic, humoral and renal responses to isotonic volume expansion (1800 ml in 3 h) were assessed in normal subjects and patients with normal renin essential hypertension before and during captopril administration. 2. Essential hypertensive subjects had a greater natriuretic and diuretic response to volume expansion than had normotensive subjects. 3. Captopril induced a fall in pre-saline mean arterial pressure more marked in hypertensive (20 ± 3 mmHg) than in normotensive subjects (9 ± 2 mmHg) and did not produce any change in sodium balance. 4. Captopril exaggerated the response of arterial pressure to volume expansion since mean arterial pressure increased more markedly after than before captopril in both normotensive (18.7 ± 3.8%) and hypertensive subjects (16.9 ± 3.7%). 5. Captopril blunted the exaggerated natriuretic response to volume expansion observed in patients with essential hypertension, whereas the renal response was unchanged in normotensive subjects.

Effect of Converting Enzyme Inhibition on the Systemic and Renal Responses to Acute Isotonic Volume Expansion in Normal Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 285s-287s ◽  
Author(s):  
A. Mimran ◽  
J. Ribstein
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Volume Expansion ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Converting Enzyme ◽  
Volume Dependence ◽  
Converting Enzyme Inhibition ◽  
Normal Man ◽  
Renal Responses

1. Systemic, humoral and renal responses to isotonic volume expansion (1800 ml in 3 h) were assessed in normal subjects before and during captopril administration. 2. Captopril, which otherwise induced a decrease in pre-saline mean arterial pressure (MAP), unmasked the volume-dependence of MAP, which increased linearly during volume expansion (+ 18.7 ± 3.8% at the end of volume expansion). 3. Captopril prevented the fall in plasma aldosterone produced by volume expansion but did not modify the natriuretic response to saline. 4. These results suggest that intrarenal rather than circulating angiotensin II may be one of the determinants of the natriuretic response to volume expansion in normal man.

Intrarenal Pressure and Exaggerated Natriuresis in Essential Hypertension

1970 ◽  
Vol 38 (3) ◽  
pp. 359-374 ◽  
Author(s):  
J. Lowenstein ◽  
E. R. Beranbaum ◽  
H. Chasis ◽  
D. S. Baldwin
Keyword(s):  
Essential Hypertension ◽  
Hypertonic Saline ◽  
Sodium Excretion ◽  
Renal Vein ◽  
Sodium Balance ◽  
Prolonged Infusion ◽  
Saline Loading ◽  
Arteriolar Resistance ◽  
Normotensive Subjects ◽  
Intrarenal Pressure

1. Intrarenal pressure, estimated by measurement of wedged renal vein pressure, was elevated in patients with essential hypertension. Despite increased afferent arteriolar resistance, glomerular pressure was elevated indicating that the higher systemic pressure in essential hypertension is transmitted beyond the arterioles and accounts for elevation of intrarenal pressure. 2. During hypertonic saline loading in hypertensives, renal arteriolar resistance falls, resulting in further increase in intrarenal pressure. Increments in intrarenal pressure paralleled increases in sodium excretion in patients with essential hypertension during the exaggerated natriuresis and in normotensive subjects after the prolonged infusion of hypertonic saline. 3. The marked increase in intrarenal pressure which appears to be responsible for exaggerated natriuresis in essential hypertension is attributable to an altered (exaggerated) response of the renal arterioles. The data suggest that elevated intrarenal pressure may play a role in the regulation of sodium balance in patients with essential hypertension.

scholarly journals Renin Inhibition Improves Pressure Natriuresis in Essential Hypertension

2000 ◽  
Vol 11 (10) ◽  
pp. 1813-1818
Author(s):  
PIETER VAN PAASSEN ◽  
DICK DE ZEEUW ◽  
PAUL E. DE JONG ◽  
GERJAN NAVIS
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
Raas Blockade ◽  
Renin Inhibition ◽  
Pressure Natriuresis

Abstract. Pressure natriuresis (PN), i.e., a rise in renal sodium excretion in response to a higher BP, is involved in long-term BP regulation. PN is blunted in essential hypertension, but the mechanism is unknown. This study assessed the role of the renin-angiotensin-aldosterone system (RAAS) in PN in eight essential hypertensive men from the individual correlations between spontaneous fluctuations in BP and time corresponding changes in sodium excretion (collected at 2- and 4-h intervals for 48 h), during strict sodium balance, without treatment, and during renin inhibition (remikiren, 600 mg oral compound). Without treatment, daily values for mean arterial pressure were 109.5 ± 1.9 and 107 ± 1.9 mmHg, for urinary sodium excretion were 37.2 ± 2.8 and 42.0 ± 2.8 mmol/24 h, and for plasma renin activity were 2.34 ± 0.48 and 2.23 ± 0.44 nmol/L per h, respectively, for two consecutive days. During remikiren treatment, mean arterial pressure was 101.9 ± 1.7 and 100.8 ± 1.7 mmHg (P < 0.05, versus baseline). Urinary sodium excretion was 39.3 ± 3.7 and 45.2 ± 5.3 mmol/24 h (not significant versus baseline), and plasma renin activity was 0.79 ± 0.11 and 0.82 ± 0.13 nmol/L per h (P < 0.05 versus baseline). During remikiren treatment, BP correlated positively with sodium excretion in all patients but in only three of eight patients without treatment. The slope of the regression equation was steeper during remikiren treatment in seven of eight patients. Thus, the relationship between BP and natriuresis was more readily apparent during RAAS blockade, suggesting that RAAS activity blunts PN in hypertensive patients. Improved PN may contribute to the hypotensive effect of RAAS blockade and to maintenance of sodium balance at a lower BP level without volume expansion.

Orthostatic Changes of Haemodynamics, Renal Function, Plasma Catecholamines and Plasma Renin Concentration in Normal and Hypertensive Man

1972 ◽  
Vol 42 (2) ◽  
pp. 209-222 ◽  
Author(s):  
M. Molzahn ◽  
TH. Dissmann ◽  
S. Halim ◽  
F. W. Lohmann ◽  
W. Oelkers
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Renovascular Hypertension ◽  
Negative Correlation ◽  
Positive Relationship ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Filtration Fraction ◽  
Plasma Renin Concentration

1. In eight normal subjects, ten patients with labile hypertension, six with advanced essential hypertension and six with renovascular hypertension, plasma renin concentration, cardiac output, mean arterial pressure, clearances of creatinine and p-aminohippurate (PAH), and sodium excretion were measured before and after 30 min of 45° upright tilting. Changes in plasma adrenaline and noradrenaline concentration were measured in addition in the normal subjects, and in plasma volume in normal subjects and patients with labile essential hypertension. 2. In patients with advanced essential hypertension, heart rate and calculated peripheral resistance increased significantly less than in normal subjects, and plasma renin increased by 15% in this group, in comparison to 37% in normal subjects, 48% in labile essential hypertension, and 57% in renovascular hypertension. There was a positive relationship between changes in renin and noradrenaline concentrations in normal subjects. 3. Apart from a negative correlation between the increases in plasma renin concentration and mean arterial pressure in patients with renovascular hypertension, there were no significant relationships between changes in plasma renin and haemodynamics. 4. A negative correlation between changes in plasma renin and filtration fraction and a positive relationship between changes in renin and sodium excretion were found in normal subjects and patients with labile hypertension. Plasma renin increase was directly related to changes in the tubular rejection fraction of sodium in patients with labile hypertension. In the same group there was a negative correlation between changes of sodium rejection fraction and filtration fraction. 5. The results suggest a role of the adrenergic system in orthostatic renin release, but the functional connection between renal haemodynamics, tubular sodium handling and renin release across orthostasis cannot fully be explained on the basis of our present knowledge of renin releasing mechanisms.

Response of atrial natriuretic peptide to acute saline loading in essential hypertension

1988 ◽  
Vol 255 (6) ◽  
pp. F1085-F1090 ◽  
Author(s):  
A. Mimran ◽  
J. Nussberger ◽  
J. Ribstein ◽  
B. Waeber ◽  
H. R. Brunner
Keyword(s):  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Normal Subjects ◽  
Saline Loading ◽  
Fractional Excretion Of Sodium ◽  
Atrial Natriuretic

To further investigate the mechanism(s) of the exaggerated natriuretic response of hypertensives to volume expansion (VE; 1,800 ml iv isotonic saline over 3 h), the plasma levels of immunoreactive atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (HT). NT and HT groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in HT, mean +/- SE). In response to VE, ANP increased to the same extent in both groups (a change of 19.3 +/- 5.2 in NT and of 22.2 +/- 7.1 pg/ml in HT) despite the finding of an exaggerated natriuretic response to VE in essential hypertension (36 +/- 3.5 in NT and 54.9 +/- 6.3 nmol/3 h in HT, P less than 0.02). In addition, the fall in hematocrit and serum protein associated with saline infusion was less marked in HT than NT. The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. These observations suggest that ANPs may participate in the control of the renal response to isotonic VE; however they do not support an unequivocal influence of ANP in the exaggerated natriuretic response to VE of patients with essential hypertension.

Development of chronic perinephritic hypertension in dogs without volume expansion

1977 ◽  
Vol 233 (4) ◽  
pp. F278-F281 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
B. E. Watkins
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Volume Expansion ◽  
Left Kidney ◽  
Renal Hypertension ◽  
Control Level ◽  
Whole Body ◽  
Sodium Balance ◽  
Contralateral Kidney ◽  
Experimental Renal Hypertension

The theory of whole body autoregulation to explain the pathogenesis of experimental renal hypertension states that hypertension is initiated in response to an early increase in salt and water retention and a subsequent elevation of the cardiac output. This hypothesis was evaluated in the present study. Dogs (n,5) were made hypertensive by wrapping the left kidney in cellophane and removing the contralateral kidney 3 wk later. One week prior to right nephrectomy, the dogs were volume depleted by placing them on a low sodium intake (less than 3 meq of sodium/day) and giving them a mercurial diuretic for the first 3 days of the diet. This superimposed sodium depletion (negative sodium balance of 137 +/- 17 meq) increased plasma renin activity 3-5 times but did not change arterial pressure or heart rate. Within 2 days after nephrectomy, the mean arterial pressure increased from the control level of 105 +/- 1 to 135 +/- 6 mmHg (P less than 0.005) and pressure remained elevated throughout an additional 4-wk period in which volume depletion was enforced. The present study suggests, therefore, that initial blood volume expansion with such possible consequences as elevated cardiac output are not essential to the pathogenesis of experimental renal hypertension.

Home Monitoring Service Improves Mean Arterial Pressure in Patients with Essential Hypertension

2001 ◽  
Vol 134 (11) ◽  
pp. 1024 ◽  
Author(s):  
Mary A.M. Rogers ◽  
David Small ◽  
Debra A. Buchan ◽  
Carl A. Butch ◽  
Christine M. Stewart ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Home Monitoring ◽  
Monitoring Service

Relation of Plasma Noradrenaline to Blood Pressure, Age, Sex and Sodium Balance in Patients with Stable Essential Hypertension and in Normotensive Subjects

1978 ◽  
Vol 55 (s4) ◽  
pp. 81s-83s ◽  
Author(s):  
H. M. Brecht ◽  
W. Schoeppe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Essential Hypertension ◽  
Diastolic Blood Pressure ◽  
Plasma Noradrenaline ◽  
Sodium Balance ◽  
Creatinine Ratio ◽  
Control Subjects ◽  
Normotensive Subjects ◽  
Normotensive Control

1. Plasma noradrenaline was measured in 125 patients with stable essential hypertension (WHO I—II) and in 107 normotensive control subjects lying and standing. 2. In normotensive subjects and in patients with essential hypertension no sex-related differences of plasma noradrenaline were found between age-matched groups. 3. Plasma noradrenaline was not related to sodium balance indexed by urinary sodium/creatinine ratio. 4. In patients with essential hypertension plasma noradrenaline increases with age. 5. Mean plasma noradrenaline concentrations are significantly higher in patients with essential hypertension compared with age-matched normotensive subjects both lying and standing. 6. In patients with essential hypertension diastolic blood pressure and heart rate correlated significantly with supine plasma noradrenaline concentrations.

Plasma Noradrenaline Concentrations and Haemodynamics in the Early Stage of Essential Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 69s-71s ◽  
Author(s):  
Y. Miura ◽  
K. Kobayashi ◽  
H. Sakuma ◽  
H. Tomioka ◽  
M. Adachi ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Cardiac Index ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Young Patients ◽  
Plasma Noradrenaline ◽  
Age Related ◽  
Wide Range

1. Plasma noradrenaline concentrations and haemodynamic status were simultaneously studied in young patients with uncomplicated essential hypertension and in age-matched normal controls. 2. Resting plasma noradrenaline in the controls tended to increase slightly, but progressively, with age. The hypertensive subjects had significantly higher plasma noradrenaline concentrations than those in the controls, but these values did not show any age-related variation. The response of plasma noradrenaline to the standing position tended to increase with age in the controls, whereas plasma noradrenaline in the hypertensive subjects showed a wide range of responses without any fixed relationship with age. 3. The cardiac index was significantly greater in the labile hypertensive subjects than in the controls, whereas total peripheral resistance was significantly greater in the sustained hypertensive subjects than in the labile patients and in the controls. Mean arterial pressure in these patients was closely related with the values of total peripheral resistance rather than with the cardiac index. 4. Of the patients with raised plasma noradrenaline 80% showed significantly increased values of either total peripheral resistance or cardiac index. Plasma noradrenaline was correlated significantly to total peripheral resistance, and marginally to mean arterial pressure. 5. These findings support the view that sympathetic nervous overactivity is an important factor underlying the haemodynamic findings in these patients.

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