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.

Plasma Renin Levels and Systemic Haemodynamics in Essential Hypertension

1977 ◽  
Vol 52 (6) ◽  
pp. 591-597 ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
T. Reybrouck ◽  
P. Lijnen ◽  
L. Billiet ◽  
...  
Keyword(s):  
Renal Function ◽  
Cardiac Output ◽  
Essential Hypertension ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Inverse Relation ◽  
Plasma Renin Concentration ◽  
Low Renin Hypertension

1. Plasma renin concentration, intra-arterial pressure, cardiac output and total peripheral resistance have been studied in 50 patients with essential hypertension and normal renal function. 2. Total peripheral resistance and plasma renin were negatively correlated (r = −0·45), indicating that ‘high-renin’ essential hypertension is not necessarily associated with arteriolar vasoconstriction. 3. The inverse relation between mean arterial pressure and plasma renin (r = −0·46) suggests a role for the renal baroreceptor mechanism in the suppression of renin in ‘low-renin’ hypertension. 4. Cardiac output was positively related to plasma renin concentration (r = +0·42). 5. Multiple regression analysis indicates that the described relationships were independent of age.

Effect of Intravenous Frusemide on Plasma Renin Concentration: Suppression of Response in Hypertension

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 ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
High Blood Pressure ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Hyperaldosteronism ◽  
Plasma Renin Concentration ◽  
Low Renin Hypertension ◽  
Renal Adaptation

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.

Relationships between Plasma Renin Activity and Urinary and Plasma Catecholamines

1974 ◽  
Vol 48 (s2) ◽  
pp. 287s-290s ◽  
Author(s):  
U. Werner ◽  
H. Günnewig ◽  
K. D. Bock
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Renovascular Hypertension ◽  
Significant Positive Correlation ◽  
Plasma Renin ◽  
Primary Hypertension ◽  
Renin Activity ◽  
Positive Correlation ◽  
Noradrenaline Concentration

1. The relations between the changes in plasma renin activity (PRA) and urinary catecholamine excretion (UCA) or plasma noradrenaline concentration have been investigated (a) in patients with benign primary hypertension, with renovascular hypertension and with idiopathic asympatheticotonic hypotension (ASH), and (b) during orthostasis and after administration of frusemide, of the β-blocking agent tenormin, of clonidine and of dihydralazine. 2. In primary hypertension noradrenaline and mean arterial pressure (Pm) showed a close positive correlation. 3. The mean values of both PRA and UCA were higher in renovascular hypertension than in primary hypertension and extremely low in ASH. The overlap of individual values between the patient groups was markedly reduced by using the quotient PRA/UCA. There was a statistically significant positive correlation between PRA and UCA in primary hypertension and in renovascular hypertension, with a different slope of the regression lines. 4. The increase of PRA and of noradrenaline during orthostasis was closely correlated. Frusemide and β-receptor blockade changed the slope of the regression line by additional stimulation or inhibition respectively of PRA. 5. Clonidine decreased, and dihydralazine increased both PRA and noradrenaline concentration. These changes again showed a significant positive correlation. The fall of mean arterial pressure produced by clonidine was correlated with the decrease of PRA and of noradrenaline concentration.

Renin–Angiotensin System in Mild Essential Hypertension. the Functional Significance of Angiotensin II in Untreated and Thiazide-Treated Hypertensive Patients

1978 ◽  
Vol 55 (s4) ◽  
pp. 319s-321s ◽  
Author(s):  
H. Ibsen ◽  
A. Leth ◽  
H. Hollnagel ◽  
A. M. Kappelgaard ◽  
M. Damkjaer Nielsen ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Functional Significance ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. 2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole. 3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure. 4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.

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.

Acute Effects of Captopril on Blood Pressure and Circulating Hormone Levels in Salt-Replete and Depleted Normal Subjects and Essential Hypertensive Patients

1981 ◽  
Vol 61 (1) ◽  
pp. 75-83 ◽  
Author(s):  
J. A. Millar ◽  
B. P. McGrath ◽  
P. G. Matthews ◽  
C. I. Johnston
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Primary Role ◽  
Ang Ii ◽  
Acute Effects ◽  
Mean Values ◽  
Plasma Renin Concentration

1. The acute effects of a single oral dose of captopril on blood pressure, pulse rate and circulating levels of angiotensin I (ANG I), angiotensin II (ANG II), renin, bradykinin and catecholamines were studied in three groups: eight normal subjects, six salt-depleted normal subjects and 16 patients with essential hypertension. 2. Captopril treatment did not cause any significant fall in supine blood pressure in salt-replete normal subjects or patients with untreated essential hypertension but was associated with a fall in mean blood pressure from 85 ± 2 to 75 ± 2 mmHg in salt-depleted normal subjects and from 131 ± 7 to 117 ± 5 mmHg in patients with essential hypertension treated with diuretics. There was no change in pulse rate in any group. 3. Hormonal responses to captopril were qualitatively similar in the three groups and consisted of significant falls in ANG II with corresponding increases in ANG I and plasma renin concentration. The changes in plasma renin concentration and ANG I were greater in salt-depleted normal subjects (mean values at 90 min were 1140% and 990% of basal levels respectively) than in salt-replete normal subjects (410%, 190%) and were blunted in patients with essential hypertension (140%, 120%). Blood bradykinin, noradrenaline and adrenaline concentrations did not change after captopril in any group. 4. The parallel fall in blood pressure and ANG II levels in salt-depleted normal subjects is consistent with maintenance of blood pressure by increased levels of ANG II in sodium depletion. 5. The failure of captopril to reduce acutely blood pressure in patients with essential hypertension despite suppression of plasma ANG II and without change in circulating bradykinin confirms that the renin-angiotensin system does not play a primary role in essential hypertension.

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.

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.

Cardiovascular effects of AVP and ANG in experimental pulmonic stenosis in rats

1988 ◽  
Vol 254 (3) ◽  
pp. H438-H442
Author(s):  
G. A. Riegger ◽  
M. Albert ◽  
K. Kochsiek
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Tone ◽  
Plasma Renin ◽  
Normal Diet ◽  
Peripheral Vascular ◽  
Hemodynamic Changes ◽  
Pulmonic Stenosis ◽  
Plasma Renin Concentration ◽  
Peripheral Vascular Tone

Our objectives were to examine the role of vasopressin and renin in the regulation of peripheral vascular tone in an animal model of right ventricular failure due to chronic (10 wk) pulmonic stenosis. We tested in chronically instrumented conscious control rats and in rats with pulmonic stenosis on a normal and a high-sodium diet both vasoconstrictor systems by applying specific inhibitors. The rats with pulmonic stenosis showed significant hemodynamic changes, a hypertrophy of the right ventricle, increased levels of plasma renin concentration, and inappropriately elevated plasma levels of vasopressin in comparison to control animals. Plasma renin concentration was suppressed in the sodium-loaded controls. After the administration of a specific inhibitor of the vascular receptors of arginine vasopressin [30 micrograms, d(CH2)5Tyr(Me)AVP], we found no hemodynamic changes in control rats on the normal diet, a reduction of mean arterial pressure in the sodium-loaded controls (4 +/- 4 mmHg; P less than 0.005), and in the animals with pulmonic stenosis and normal sodium intake (5 +/- 5 mmHg; P less than 0.001) and high-salt diet (6 +/- 7 mmHg; P less than 0.02). Intravenous bolus injection of teprotide (1 mg/kg) resulted in a decrease of mean arterial pressure in the control group (normal diet) of 9 +/- 8 mmHg (P less than 0.005). The fall of blood pressure (22 +/- 10 mmHg; P less than 0.001) in the rats with pulmonic stenosis was significantly greater (P less than 0.01) and was strongly related to plasma renin concentration. Therefore, vasopressin and the renin-angiotensin system contribute to an increase of peripheral vascular tone in chronic pulmonic stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

The Value of Plasma Renin Concentration Per Se, and in Relation to Plasma and Extracellular Fluid Volume in Diagnosis and Prognosis of Human Renovascular Hypertension

1970 ◽  
Vol 39 (5) ◽  
pp. 559-576 ◽  
Author(s):  
G. Bianchi ◽  
L. Campolo ◽  
A. Vegeto ◽  
V. Pietra ◽  
U. Piazza
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Renal Disease ◽  
Renovascular Hypertension ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Plasma Renin Concentration ◽  
Diagnosis And Prognosis

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.

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