Abnormal Renal Haemodynamics and Renin Suppression in Hypertensive Patients

1970 ◽  
Vol 38 (1) ◽  
pp. 101-110 ◽  
Author(s):  
M. A. D. H. Schalekamp ◽  
M. P. A. Schalekamp-Kuyken ◽  
W. H. Birkenhäger
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Hypertensive Disease ◽  
Filtration Fraction ◽  
Plasma Renin Concentration ◽  
Renal Vascular ◽  
Intravascular Pressure

1. Intra-arterial pressure, renal plasma flow and glomerular filtration rate were estimated in thirty-two patients with benign essential hypertension. In twenty cases plasma renin concentrations were also determined. Variability of blood pressure was estimated by automatic indirect pressure recording. 2. There was an even distribution between high and low values of renal vascular resistance and filtration fraction. Variability of blood pressure was inversely related to renal vascular resistance. 3. In five patients plasma renin concentration was found to be abnormally low both in the recumbent and in the 45° tilt position. 4. Plasma renin concentration was related to renal blood flow, renal vascular resistance, filtration fraction and variability of blood pressure. 5. The results suggest that in hypertension renin release is suppressed by an increase in intravascular pressure at the level of the juxtaglomerularcells. The extent of renin suppression seems to be related to the stage of hypertensive disease.

Long-Term versus Short-Term Effects of Hydrochlorothiazide on Renal Haemodynamics in Essential Hypertension

1979 ◽  
Vol 56 (5) ◽  
pp. 463-469 ◽  
Author(s):  
P. Van Brummelen ◽  
M. Woerlee ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Blood Flow ◽  
Essential Hypertension ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Vanillylmandelic Acid ◽  
Plasma Renin Concentration ◽  
Renal Vascular

1. Renal blood flow, glomerular filtration rate, renal vascular resistance and filtration fraction were studied in ten patients with essential hypertension, during placebo, and after 1 week, 3, 6 and 9 months of hydrochlorothiazide. Plasma renin concentration and urinary excretion of vanillylmandelic acid were also measured. 2. Mean arterial pressure was lowered significantly during hydrochlorothiazide, the long-term effect being slightly more pronounced than the short-term effect. 3. The decrease in renal blood flow during the first week (P < 0·01) was followed by a progressive rise. After 9 months renal blood flow was above placebo level in eight of the ten patients. After an initial decrease, glomerular filtration rate returned gradually to its original value. Renal vascular resistance and filtration fraction increased during the first week and declined thereafter. After 3, 6 and 9 months renal vascular resistance was significantly lower compared with placebo values. 4. Plasma renin concentration and urinary excretion of vanillylmandelic acid increased significantly during the first week of hydrochlorothiazide. Subsequently, vanillylmandelic acid fell to below pretreatment amounts (P < 0·05), whereas plasma renin concentration remained elevated. 5. Long-term treatment of essential hypertension with hydrochlorothiazide has a favourable effect on abnormal renal haemodynamics. Besides the influence of blood pressure reduction per se, humoral and neural factors may be involved.

Renal Haemodynamics and Plasma Renin in Patients with Essential Hypertension

1976 ◽  
Vol 50 (5) ◽  
pp. 409-414 ◽  
Author(s):  
E. B. Pedersen ◽  
H. J. Kornerup
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Control Group ◽  
Hypertensive Patients ◽  
Control Subjects ◽  
Hypertensive Group ◽  
Renal Vascular

1. Blood pressure, glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured in twenty-three patients with essential hypertension and in twenty-one control subjects. Plasma renin concentration was measured in all the hypertensive patients and in fifteen control subjects. 2. GFR and RPF were similar in the hypertensive group and in the control group, whereas the renal vascular resistance was significantly higher in the hypertensive patients. GFR and RPF decreased with increasing blood pressure in both groups. Increasing age induced a further reduction in GFR and RPF in the control subjects but not in the hypertensive patients. 3. Plasma renin concentration in the hypertensive group did not differ from that in the control subjects. The concentration was not correlated to age in either the hypertensive or normal group. 4. Plasma renin index was positively correlated to GFR and RPF and inversely correlated to filtration fraction and renal vascular resistance. 5. It is concluded that GFR and RPF depend on blood pressure in both hypertensive patients and normotensive control subjects. In contrast to the control group, the age effect was negligible in the hypertensive group. It is suggested that renin release depends on changes in renal vascular resistance in the arterioles at the glomerulus and the results support the baroreceptor theory of renin release.

Haemodynamic Characteristics of Low-Renin Hypertension

1977 ◽  
Vol 52 (4) ◽  
pp. 405-412 ◽  
Author(s):  
M. A. D. H. Schalekamp ◽  
W. H. Birkenhäger ◽  
G. A. Zaal ◽  
G. Kolsters
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Plasma Renin Concentration ◽  
Low Renin Hypertension ◽  
Renal Vascular ◽  
The Relationship

1. Intra-arterial pressure, cardiac output, renal blood flow and glomerular filtration rate were measured in 19 patients with low-renin hypertension and in 30 patients with normal-renin hypertension. 2. Cardiac output and renal blood flow were significantly lower in low-renin hypertension. Total peripheral and renal vascular resistance were markedly higher in this group. 3. Plasma renin concentration correlated inversely with both total peripheral and renal vascular resistance as well as with age. Multiple regression analysis indicated that part of the relationship between renin and haemodynamic variables did not depend on age. Furthermore, plasma renin concentration did not decrease with age in a group of 40 normotensive control subjects of similar age to the hypertensive patients. 4. The results provide further confirmation that renin decreases as hypertension progresses.

scholarly journals Association of Noise Annoyance with Measured Renal Hemodynamic Changes

2021 ◽  
pp. 1-8
Author(s):  
Dennis Kannenkeril ◽  
Susanne Jung ◽  
Christian Ott ◽  
Kristina Striepe ◽  
Julie Kolwelter ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Plasma Flow ◽  
Renal Plasma Flow ◽  
Renal Vascular Resistance ◽  
Hemodynamic Parameters ◽  
Filtration Fraction ◽  
Noise Annoyance ◽  
Renal Hemodynamic ◽  
Renal Vascular

<b><i>Background:</i></b> Chronic mental stress is recognized as a modifiable risk factor for cardiovascular disease. The aim of this study was to demonstrate that noise annoyance-induced stress is associated with changes in renal hemodynamics. <b><i>Methods:</i></b> Renal hemodynamic parameters were measured using steady-state input clearance with infusion of para-aminohippuric acid and inulin in individuals with normal, high normal, and elevated blood pressure. All individuals ranked subjective annoyance due to noise in everyday life on a 7-grade Likert scale. The median of all rankings was used as a cutoff point to divide the group into noise-annoyed and non-noise-annoyed individuals. Different renal hemodynamic parameters were calculated based on the Gomez equation. <b><i>Results:</i></b> Noise-annoyed individuals (<i>n</i> = 58) showed lower renal plasma flow (599 ± 106 vs. 663 ± 124 mL/min, <i>p</i> = 0.009), lower renal blood flow (1,068 ± 203 vs. 1,172 ± 225 mL/min, <i>p</i> = 0.047), higher filtration fraction (22.7 ± 3.3 vs. 21.3 ± 3.0, <i>p</i> = 0.012), higher renal vascular resistance (88.9 ± 25.6 vs. 75.8 ± 22.9 mm Hg/[mL/min], <i>p</i> = 0.002), and higher resistance of afferent arteriole (2,439.5 ± 1,253.4 vs. 1,849.9 ± 1,242.0 dyn s<sup>−1</sup> cm<sup>−5</sup>, <i>p</i> = 0.001) compared to non-noise-annoyed individuals (<i>n</i> = 55). There was no difference in measured glomerular filtration rate (133 ± 11.8 vs. 138 ± 15 mL/min, <i>p</i> = 0.181), resistance of efferent arteriole (2,419.4 ± 472.2 vs. 2,245.8 ± 370.3 dyn s<sup>−1</sup> cm<sup>−5</sup>, <i>p</i> = 0.060), and intraglomerular pressure (64.0 ± 3.1 vs. 64.6 ± 3.5 mm Hg, <i>p</i> = 0.298) between the groups. After adjusting for age, renal plasma flow, renal blood flow, and renal vascular resistance remained significantly different between the groups, with a trend in increased afferent arteriolar resistance and filtration fraction. <b><i>Conclusion:</i></b> In this study, noise annoyance was associated with reduced renal perfusion attributed to increased renal vascular resistance predominantly at the afferent site. Long-term consequences of this renal hemodynamic pattern due to noise annoyance need to be investigated.

Glycerol-Induced Acute Renal Failure in Brattleboro Rats with Hypothalamic Diabetes Insipidus

1979 ◽  
Vol 56 (2) ◽  
pp. 133-138 ◽  
Author(s):  
A. Konrads ◽  
K. G. Hofbauer ◽  
K. Bauereiss ◽  
J. Möhring ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Diabetes Insipidus ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Renal Vascular

1. During the development of glycerol-induced acute renal failure in Sprague-Dawley rats, plasma concentrations of vasopressin rise and probably induce an increase in blood pressure. 2. In the present studies the role of vasopressin in acute renal failure was further analysed by experiments in Brattleboro rats homozygous for hereditary hypothalamic diabetes insipidus which were injected intramuscularly with 10 ml of glycerol/kg (61 mmol/l). 3. After the injection of glycerol plasma osmolality increased transiently and packed cell volume was elevated. The rats became anuric and plasma urea concentrations rose progressively. Plasma renin concentration increased significantly within 2 h. Plasma renin substrate concentration rose progressively and had almost doubled by 8 h. 4. In contrast with previous observations in Sprague-Dawley rats, blood pressure did not rise in rats with diabetes insipidus after the injection of glycerol. 5. When 2 h after the injection of glycerol kidneys were taken from rats with diabetes insipidus and perfused with an electrolyte solution in a single-pass system for 1 h, renal vascular resistance was 30% higher than in control kidneys 10 min after the start of the perfusion and remained elevated thereafter. In similar experiments with kidneys from Sprague-Dawley rats with acute renal failure, renal vascular resistance was increased fivefold immediately after the start of the perfusion, but decreased subsequently. 6. These data support the idea that in glycerol-induced acute renal failure of Sprague-Dawley rats an increased release of vasopressin is responsible for the elevation of blood pressure and suggest that this hormone also participates in renal vasoconstriction. However, a rise of plasma vasopressin concentrations alone cannot fully explain the increase in renal vascular resistance and the development of acute renal failure.

Follow-up of Renin in Essential Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 173s-175s
Author(s):  
W. H. Birkenhäger ◽  
T. L. Kho ◽  
M. A. Schalekamp ◽  
G. A. Zaal ◽  
A. Wester ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Essential Hypertension ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Gradual Rise ◽  
Plasma Renin Concentration ◽  
Renal Vascular

1. Twenty-three subjects with essential hypertension were followed for a period of up to 7 years. They were untreated during the investigations. 2. Plasma renin concentration was found to decrease temporarily in some subjects. The ultimate change was a gradual rise. In those subjects who suffered myocardial infarction renin tended to rise more sharply. 3. A relationship was established with the rise in renal vascular resistance, which almost invariably occurred over the years.

Limb tourniquet and intramuscular clostridial toxin effects on renal function

1962 ◽  
Vol 17 (1) ◽  
pp. 83-86 ◽  
Author(s):  
James F. Nickel ◽  
John A. Gagnon ◽  
Leonard Levine
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Renal Vascular Resistance ◽  
Arterial Blood ◽  
Hind Limbs ◽  
Renal Changes ◽  
Anesthetized Dogs ◽  
Peripheral Trauma ◽  
Renal Vascular

Eight anesthetized dogs, given Clostridium perfringens type A toxic filtrate into the hind-limb muscles, showed severe spreading edema, hemoconcentration, marked reduction in para-aminohippurate (PAH) and creatinine clearances, and a rise in the renal vascular resistance. In the first 4 hr sodium excretion fell sharply, and mean arterial blood pressure, slightly. In eight similar dogs venous-occlusive pneumatic tourniquets were applied high on both hind limbs for 90 min. Edema was localized and minimal. Hematocrit was unchanged. PAH and creatinine clearances were extremely low in the second 30-min period of the occlusion but had risen somewhat in the last 30-min period. Sodium excretion was greatly reduced. Arterial pressure and vascular resistance rose very significantly. Upon removal of the tourniquets, PAH and creatinine clearances, blood pressure, and renal vascular resistance returned toward normal. Sodium excretion continued to fall. In many respects the renal changes resulting from two different forms of peripheral trauma are similar. Submitted on August 14, 1959

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

Inhibition of ROMK blocks macula densa tubuloglomerular feedback yet causes renal vasoconstriction in anesthetized rats

2017 ◽  
Vol 312 (6) ◽  
pp. F1120-F1127 ◽  
Author(s):  
Magali Araujo ◽  
William J. Welch ◽  
Xiaoyan Zhou ◽  
Kathleen Sullivan ◽  
Shawn Walsh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Volume Depletion ◽  
Renal Vasoconstriction ◽  
Compound C ◽  
Altered Blood ◽  
Renal Vascular ◽  
Dose Dependent

The Na+-K+-2Cl− cotransporter (NKCC2) on the loop of Henle is the site of action of furosemide. Because outer medullary potassium channel (ROMK) inhibitors prevent reabsorption by NKCC2, we tested the hypothesis that ROMK inhibition with a novel selective ROMK inhibitor (compound C) blocks tubuloglomerular feedback (TGF) and reduces vascular resistance. Loop perfusion of either ROMK inhibitor or furosemide caused dose-dependent blunting of TGF, but the response to furosemide was 10-fold more sensitive (IC50 = 10−6 M for furosemide and IC50 = 10−5 M for compound C). During systemic infusion, both diuretics inhibited TGF, but ROMK inhibitor was 10-fold more sensitive (compound C: 63% inhibition; furosemide: 32% inhibition). Despite blockade of TGF, 1 h of constant systemic infusion of both diuretics reduced the glomerular filtration rate (GFR) and renal blood flow (RBF) by 40–60% and increased renal vascular resistance (RVR) by 100–200%. Neither diuretic altered blood pressure or hematocrit. Proximal tubule hydrostatic pressures (PPT) increased transiently with both diuretics (compound C: 56% increase; furosemide: 70% increase) but returned to baseline. ROMK inhibitor caused more natriuresis (3,400 vs. 1,600% increase) and calciuresis (1,200 vs. 800% increase) but less kaliuresis (33 vs. 167% increase) than furosemide. In conclusion, blockade of ROMK or Na+-K+-2Cl− transport inhibits TGF yet increases renal vascular resistance. The renal vasoconstriction was independent of volume depletion, blood pressure, TGF, or PPT.

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