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.

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.

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.

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.

Abstract P1119: Serum Gdf-15 is a Determinant Factor of Renal Vascular Resistance in Patients With Essential Hypertension

Hypertension ◽  
2019 ◽  
Vol 74 (Suppl_1) ◽  
Author(s):  
Satoru Shichijo ◽  
Takafumi Okura ◽  
Tomoaki Nagao ◽  
Fumikazu Kondo ◽  
Ayu Makita ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Vascular ◽  
Determinant Factor

Intrarenal Formation of Angiotensin II in the Rat: Interference by Saralasin and SQ 20881

1974 ◽  
Vol 48 (s2) ◽  
pp. 37s-40s
Author(s):  
H. Zschiedrich ◽  
K. G. Hofbauer ◽  
E. Hackenthal ◽  
G. D. Baron ◽  
F. Gross
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Renal Vascular Resistance ◽  
Angiotensin I ◽  
Renin Substrate ◽  
Vasoconstrictor Effect ◽  
Renal Vascular ◽  
Dose Dependent

1. Isolated rat kidneys were perfused with a medium free of components of the renin-angiotensin system. 2. Angiotensin II, angiotensin I, tetradecapeptide renin substrate or rat plasma renin substrate added to the medium caused a dose-dependent increase of renal vascular resistance. 3. The vasoconstrictor effect of angiotensin II was inhibited by 1-Sar-8-Ala-angiotensin II (Saralasin). The inhibition was dose-dependent, being complete at the highest doses applied. In this dose range, Saralasin increased renal vascular resistance. Saralasin also inhibited vasoconstriction induced by tetradecapeptide renin substrate. 4. The vasoconstrictor effect of angiotensin I was suppressed by SQ 20881, up to a maximum of 87% depending on the dose. Similarly the increase in renal vascular resistance induced by a purified preparation of rat plasma renin substrate was inhibited by 55%; no effect on the action of tetradecapeptide renin substrate was observed. 5. The data suggest that, within the kidney, angiotensin I is converted into angiotensin II to the extent of about 1.25%. Since no angiotensin I is formed from synthetic renin substrate, the vasoconstrictor effect of the tetradecapeptide may be either due to a direct interaction with the angiotensin II receptor or the consequence of the intrarenal formation of angiotensin II. In contrast, the results with rat plasma renin substrate suggest that angiotensin I is formed from ‘natural’ substrate and is subsequently converted into angiotensin II.

Natriuretic Response to Head-Out Immersion in Humans with Recent Kidney Transplants

1993 ◽  
Vol 85 (4) ◽  
pp. 471-477 ◽  
Author(s):  
Ton J. Rabelink ◽  
Karin A. van Tilborg ◽  
Ronald J. Hené ◽  
Hein A. Koomans
Keyword(s):  
Plasma Renin Activity ◽  
Vascular Resistance ◽  
Sodium Excretion ◽  
Water Immersion ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Renin Activity ◽  
Control Group ◽  
Control Subjects ◽  
Renal Vascular

1. Recently implanted kidneys may have decreased flexibility to adjust sodium excretion to volume challenges, since modulation by renal sympathetic nerve activity is absent. To examine this hypothesis, we studied the natriuretic response to head-out water immersion in eight patients with well-functioning renal allografts of 37 days (range 24–56 days), at a time when renal re-innervation has probably not occurred. 2. By the third hour of head-out water immersion, sodium excretion had increased equally in the patients (from 120 +21 to 204 +37 μmol/min) and in eight healthy control subjects (from 105 +9 to 191+19 μmol/min). 3. Glomerular filtration rate was 60 + 6 ml/min in the patients and 113 +6 ml/min in the control subjects, and did not change upon head-out water immersion. Estimated renal plasma flow increased upon head-out water immersion in the control group but not in the patients. Blood pressure decreased similarly in both groups. The renal vascular resistance, calculated from these data, decreased in response to head-out water immersion in the control subjects but not in the renal transplant patients. 4. Head-out water immersion suppressed plasma renin activity only in the normal group, whereas the plasma aldosterone level was suppressed in both groups. The natriuretic response in patients was associated with about 3-fold elevated plasma levels of atrial natriuretic peptide. 5. Since renal re-innervation at 37 days after transplantation is very unlikely, these data suggest that inact renal innervation is not mandatory for a normal natriuretic response to head-out water immersion in humans. However, sympathetic modulation might be involved in the decrease in renal vascular resistance and plasma renin activity normally observed during immersion.

Uranyl Nitrate Acute Renal Failure in the Dog: Early Changes in Renal Function and Haemodynamics

1975 ◽  
Vol 48 (1) ◽  
pp. 9-16 ◽  
Author(s):  
J. G. Kleinman ◽  
J. S. McNeil ◽  
W. Flamenbaum
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Uranyl Nitrate ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renal Vascular Resistance ◽  
Inulin Clearance ◽  
Renal Vascular

1. Sodium excretion, plasma renin activity (PRA), inulin clearance, total renal blood flow (RBF), renal cortical radiomicrosphere distribution and systemic haemodynamics were examined during the first 3 h after intravenous administration of uranyl nitrate (19.9 μmol/kg body wt.; 10 mg/kg) in the dog. 2. During the 3 h of study after uranyl nitrate, urine flow remained stable or increased, sodium excretion increased approximately fivefold, renal vascular resistance increased threefold, and concordant decreases in RBF and inulin clearance to 40–50% of control values occurred. At 3 h total cortical RBF decreased to 35% of control values and the ratio of blood flow in outer to inner cortical zones also decreased, reflecting outer cortical ischaemia. PRA increased in the first hour after uranyl nitrate and slowly declined thereafter, though not to control values. 3. Respiratory rate, heart rate, mean systemic blood pressure and cardiac output were unchanged after uranyl nitrate, demonstrating that the changes in renal vascular resistance occurred without a change in peripheral vascular resistance. 4. It is postulated that increased renin-angiotensin system activity mediates the change in renal haemodynamics and the consequent fall in glomerular filtration.

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