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.

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.

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.

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.

Studies on the Mechanism of Hypernatriuresis in Essential Hypertension in Relation to Measurements of Plasma Renin Concentration, Body Fluid Compartments and Renal Function

1971 ◽  
Vol 41 (3) ◽  
pp. 219-231 ◽  
Author(s):  
M. A. D. H. Schalekamp ◽  
X. H. Krauss ◽  
M. P. A. Schalekamp-Kuyken ◽  
G. Kolsters ◽  
W. H. Birkenhäger
Keyword(s):  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Essential Hypertension ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Plasma Renin Concentration ◽  
Intrarenal Pressure

1. In twenty-two patients representing different stages of benign essential hypertension, hyperosmotic saline was administered intravenously. Determinations of intra-arterial pressure, renal plasma flow, glomerular filtration rate and plasma renin concentration were carried out before and, in the majority, also during and after saline infusion. Changes in cardiac output were followed in ten patients. Plasma volume and extracellular volume were determined in the control period only, although haemodilution was assessed by haematocrit readings. 2. Excess of sodium excretion showed a wide range and was related to the patient's age, as well as to a set of parameters reflecting intrarenal pressure patterns; hypernatriuresis consistently occurred in older patients, in whom renal vascular resistance and nitration fraction were elevated and plasma renin was suppressed. It could not be clarified whether hypernatriuresis together with renin suppression were determined by intrarenal pressure relationships or by an independent age-related factor in the hypertensive patient. 3. Excess of sodium excretion was not related to increments in arterial pressure, cardiac output, renal blood flow or glomerular filtration rate. 4. Plasma renin concentration failed to show consistent changes after hyperosmotic saline infusion. 5. It is concluded that natriuresis is not mediated by changes in the activity of the renin-angiotensin system. Hypernatriuresis appears to be a feature of progressive benign hypertension.

Prolonged Decrease in Blood Pressure after Atrial Natriuretic Peptide Infusion in Essential Hypertension: A New Anti-Pressor Mechanism?

1989 ◽  
Vol 77 (3) ◽  
pp. 253-258 ◽  
Author(s):  
D. R. J. Singer ◽  
N. D. Markandu ◽  
M. G. Buckley ◽  
M. A. Miller ◽  
A. L. Sugden ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Atrial Natriuretic Peptide ◽  
Cell Volume ◽  
Natriuretic Peptide ◽  
Packed Cell Volume ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Sodium Balance ◽  
High Sodium

1. To study the anti-hypertensive effects of atrial natriuretic peptide (ANP), eight patients with mild to moderate essential hypertension, on no treatment, were infused with α-human ANP (102–126) (37 pmol min−1 kg−1) or placebo for 60 min and observed for a further 4 h on the fifth day of low and high sodium diets in a randomized, cross-over study. 2. Plasma ANP levels increased over 30-fold into the high pathophysiological range during ANP infusion, but had returned to control values by 60 min after the end of infusion. With ANP infusion, there was a large decrease in supine blood pressure which was similar on both the low and high sodium intakes and was maximal 20–40 min after completion of the infusion. These reductions in blood pressure were sustained for a further 4 h after the end of ANP infusion and for 3 h after plasma ANP levels had returned to control values. 3. Maximal urinary sodium excretion increased 10-fold on the low sodium diet (negative sodium balance 20 mmol) and threefold on the high sodium diet (negative sodium balance 30 mmol) during ANP infusion; however, during the 4 h after infusion, urinary sodium excretion was below placebo values. During ANP infusion, packed cell volume increased significantly on both diets but returned to control values by 4 h after the end of infusion. 4. There were no significant changes in plasma renin activity compared with placebo during or after ANP infusion. However, plasma aldosterone was significantly greater than placebo values after the end of ANP infusion on both low and high sodium diets. 5. The sustained fall in blood pressure after ANP infusion appears to be unexplained by changes in sodium balance, packed cell volume and plasma ANP levels. These findings suggest that ANP may have a prolonged action on a pressor mechanism which remains to be defined.

Captopril Enhances Vascular and Adrenal Responsiveness to Angiotensin II in Essential Hypertension

1984 ◽  
Vol 66 (3) ◽  
pp. 299-305 ◽  
Author(s):  
Richard J. Koletsky ◽  
Murray B. Gordon ◽  
Meryl S. Leboff ◽  
Thomas J. Moore ◽  
Robert G. Dluhy ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Blood Pressure Response ◽  
Sodium Balance ◽  
Ang Ii ◽  
Before And After ◽  
Pah Clearance ◽  
Normotensive Subjects ◽  
Renal Vascular

1. The converting-enzyme inhibitor captopril (25–50 mg orally every 6 h for 66 h) was used to dissociate the circulating levels of angiotensin II (ANG II) from changes in sodium balance in 11 patients with normal renin essential hypertension on 10 mmol of sodium/day intake. Pressor, renal vascular and adrenal responses to graded infusions of ANG II (0.3, 1 and 3 pmol kg−1 min−1) were measured before and after captopril administration. Systemic vascular responses were assessed by measuring diastolic blood presusre (DBP), renovascular responses by measuring p-aminohippurate (PAH) clearance and adrenal responses by measuring plasma aldosterone. 2. After receiving captopril for 66 h the hypertensive subjects showed a significantly (P<0.004) enhanced blood pressure response to the infused ANG II but not to noradrenaline when compared with the response before captopril. ANG II (3 pmol kg−1 min−1) also produced a significantly (P<0.03) greater reduction in PAH clearance after (−194 ± 40 ml/min) compared with before (−104 ± 15 ml/min) captopril. These results suggest that the responsiveness to ANG II in these two target tissues is determined by the circulating ANG II level. 3. In the adrenal gland the aldosterone responses to ANG II also were significantly greater after (P < 0.01) than before captopril (increment at 3 pmol kg−1 min−1: 660 ± 88 vs 381 ± 94 pmol/l). These results are in distinct contrast with the responses previously reported for normotensive subjects and support the hypothesis that the regulation of aldosterone secretion is altered in subjects with essential hypertension.

An Inherited Sodium Ion-Potassium Ion Cotransport Defect in Essential Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 191s-193s ◽  
Author(s):  
R. P. Garay ◽  
G. Dagher ◽  
P. Meyer
Keyword(s):  
Essential Hypertension ◽  
Secondary Hypertension ◽  
Sodium Balance ◽  
Sodium Permeability ◽  
Sodium Potassium ◽  
A Cell ◽  
Cotransport System ◽  
Normotensive Subjects ◽  
Sodium Potassium Pump ◽  
Sodium Extrusion

1. In erythrocytes, the extrusion of a cell sodium load is accomplished by the ouabain-sensitive sodium-potassium pump and by the frusemide-sensitive sodium-potassium cotransport, which operate against the passive sodium permeability. All these three components of the cell sodium balance were studied in essential hypertension (410 subjects were investigated). 2. An abnormally low rate of net sodium extrusion by the sodium-potassium cotransport system was observed in essential hypertensive patients and in a high proportion of their young normotensive offspring. A normal cotransport system found in secondary hypertensive subjects devoid of familial history of hypertension confirmed that the abnormal cotransport system is not the consequence of high blood pressure per se. 3. A 20–40% increase in the rate of net sodium extrusion by the sodium-potassium pump seems to compensate for the abnormal cotransport in erythrocytes from some young normotensive subjects born of essential hypertensive parents and from some benign essential hypertensive subjects. 4. No difference could be detected between the passive sodium permeability of erythrocytes from hypertensive subjects and in those from normotensive controls. 5. In conclusion, essential hypertension seems to be associated with an inherited defect in the sodium-potassium cotransport system. We propose therefore the laboratory study of this system for: (i) the distinction between essential and secondary hypertension and (ii) the preventive investigation of young normotensive subjects in hypertensive families.

Sodium and left ventricular mass in untreated hypertensive and normotensive subjects

1992 ◽  
Vol 263 (1) ◽  
pp. H177-H181 ◽  
Author(s):  
G. Du Cailar ◽  
J. Ribstein ◽  
J. P. Daures ◽  
A. Mimran
Keyword(s):  
Essential Hypertension ◽  
Arterial Pressure ◽  
Left Ventricular Mass ◽  
Sodium Excretion ◽  
Systolic Arterial Pressure ◽  
Urinary Sodium Excretion ◽  
Left Ventricular ◽  
Urinary Sodium ◽  
Ventricular Mass ◽  
Normotensive Subjects

To determine whether urinary sodium excretion (a rather rough estimate of sodium intake) can influence left ventricular mass independently of arterial pressure, 91 untreated subjects with essential hypertension and 50 normotensive subjects of similar age were studied. Left ventricular mass index (M-mode echocardiography) was positively correlated with urinary sodium excretion in hypertensive (r = 0.22, P less than 0.01) as well as normotensive subjects (r = 0.22, P less than 0.05), and systolic arterial pressure was correlated only in hypertensive subjects (r = 0.23, P less than 0.01). When hypertensive subjects were divided into groups with appropriate or inappropriate left ventricular mass by reference to a theoretical optimal left ventricular mass for each subject's level of systolic arterial pressure, left ventricular mass was appropriate in 68% and inappropriate in 32% of subjects. Urinary sodium excretion was higher in subjects with inappropriate left ventricular mass compared with those with appropriate left ventricular mass. In conclusion, sodium excretion may be an important modulator of the influence of arterial pressure on the left ventricle in normotensive subjects and subjects with essential hypertension.

Aging and Endothelial Function in Normotensive Subjects and Patients With Essential Hypertension

Circulation ◽  
1995 ◽  
Vol 91 (7) ◽  
pp. 1981-1987 ◽  
Author(s):  
Stefano Taddei ◽  
Agostino Virdis ◽  
Paola Mattei ◽  
Lorenzo Ghiadoni ◽  
Alessandra Gennari ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Endothelial Function ◽  
Normotensive Subjects
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