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.

Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

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.

CNS-induced natriuresis and renal hemodynamics in conscious rats

1983 ◽  
Vol 245 (6) ◽  
pp. F763-F771 ◽  
Author(s):  
D. Beasley ◽  
R. L. Malvin ◽  
D. R. Mouw
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Antidiuretic Hormone ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Renal Nerve ◽  
Natriuretic Hormone ◽  
Renal Nerve Activity

Sodium excretion was studied following experimental elevation of cerebrospinal fluid (CSF) sodium in heterozygous and homozygous (DI) Brattleboro rats given exogeneous antidiuretic hormone. Sodium excretion increased 4.5-fold in heterozygous and 3.5-fold in DI rats. The natriuresis in both groups was rapid in onset and occurred with a simultaneous kaliuresis. Blood pressure increased approximately 10 mmHg in the heterozygous but not in the DI rats. Accordingly, increased blood pressure may contribute to the natriuresis but is not the sole mechanism. Plasma renin concentration did not change in the DI rats during high Na CSF infusion, and chronic bilateral renal denervation did not abolish the natriuresis. Glomerular filtration rate increased during the high Na period in both the intact and renally denervated rats. These data provide evidence that a natriuretic mechanism exists that is not mediated by changes in antidiuretic hormone, renal nerve activity, mean arterial pressure, aldosterone, or angiotensin II, and thus may be due to another circulating substance or natriuretic hormone. This hormone may act totally or in part by increasing glomerular filtration rate.

Fluid volumes and hemodynamics in hypertension produced by chemical renal medullectomy

1985 ◽  
Vol 249 (2) ◽  
pp. H415-H420 ◽  
Author(s):  
D. Taverner ◽  
R. F. Bing ◽  
J. D. Swales ◽  
H. Thurston
Keyword(s):  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Plasma Volume ◽  
Filtration Rate ◽  
Exchangeable Sodium ◽  
Efferent Activity ◽  
Sympathetic Efferent Activity

We have investigated the mechanisms by which chemical renal medullectomy with 2-bromoethylamine hydrobromide (200 mg/kg body wt) produces hypertension in rats. Groups of chemically medullectomized rats were compared with normal rats and rats that had been partially nephrectomized to produce an equivalent fall in glomerular filtration rate. Mean arterial pressure was elevated in the medullectomized (142 +/- 6 mmHg) compared with normal rats (124 +/- 3). In the medullectomized animals this was associated with significant tachycardia (483 +/- 15 vs. 450 +/- 6 beats/min) and an increase in cardiac output (61.1 +/- 5.0 vs. 49.9 +/- 2.2 ml X min-1 X 100 g body wt-1). Plasma volume was significantly reduced in medullectomized rats (2.16 +/- 0.15 vs 3.29 +/- 0.20 ml/100 g body wt), whereas exchangeable sodium was unchanged (39.9 +/- 0.5 vs. 39.7 +/- 0.5 meq/kg body wt). By contrast, both plasma volume and exchangeable sodium were increased in partially nephrectomized rats. These results are consistent with the hypothesis that chemical medullectomy produces hypertension by increased selective sympathetic efferent activity, raising cardiac output and postcapillary venular resistance. This may be the consequence of reducing the secretion of a renomedullary humoral substance that normally inhibits such activity.

Studies on the Mechanism of Sodium Excretion in Uraemia

1972 ◽  
Vol 42 (6) ◽  
pp. 711-723 ◽  
Author(s):  
R. Wilkinson ◽  
J. A. Luetscher ◽  
A. J. Dowdy ◽  
C. Gonzales ◽  
G. W. Nokes
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Creatinine Clearance ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Sodium Depletion ◽  
Sodium Loading ◽  
Arteriolar Tone

1. A group of eight patients with advanced renal failure, and a creatinine clearance of 3·8–24 ml/min, were subjected to sodium loading and sodium depletion. 2. With sodium loading there was a consistent increase in blood pressure (0·01 < P <0·02), an increase in creatinine clearance that was significantly related to changes in mean arterial pressure (r = +0·3, 001 < P < 0·02); an increase in urinary sodium excretion that was closely correlated with changes in creatinine clearance (r = +0·82, P < 0·001); a decrease in fractional reabsorption of filtered sodium that was inversely proportional to creatinine clearance (r = −0·63, 0·05< P < 0·1). 3. Fractional reabsorption of filtered sodium was proportional to creatinine clearance both in the sodium-loaded (r = +0·86, 0·001 < P < 0·01) and sodium-depleted states (r = +0·92, 0·001 < P < 0·01). 4. Urinary aldosterone excretion and plasma renin activity consistently increased with sodium depletion, the percentage increases of the two being significantly related (r = +0·95, P < 0·001). 5. The results suggest that excretion of a sodium load in uraemia may be effected in part as the result of a raised blood pressure that elevates the glomerular filtration rate; by increasing the peritubular capillary pressure this may be responsible for the observed decrease in reabsorption of filtered sodium. The responsiveness of glomerular filtration rate to blood pressure changes suggests a decrease in afferent arteriolar tone that may account for the increased sodium excretion per nephron which occurs even in uraemic patients without hypertension. 6. It is suggested that aldosterone may continue to play an important regulatory role in sodium homeostasis in uraemia and that renin concentrations are the major determinants of aldosterone production in uraemia.

Hypertension and renal dysfunction in primary hyperparathyroidism: effect of parathyroidectomy

1989 ◽  
Vol 76 (3) ◽  
pp. 289-296 ◽  
Author(s):  
A. K. Salahudeen ◽  
T. H. Thomas ◽  
L. Sellars ◽  
S. Tapster ◽  
P. Keavey ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Essential Hypertension ◽  
Primary Hyperparathyroidism ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Whole Body ◽  
Before And After ◽  
51Cr Edta ◽  
Normotensive Control

1. Twenty-four patients with primary hyperparathyroidism were studied before and 18 restudied 6.5 months (mean) after parathyroidectomy, to investigate the pathogenesis of the hypertension which may accompany this condition. Comparison was made with age-matched patients with essential hypertension and with normotensive control subjects. 2. There was a significant inverse relationship between mean arterial pressure and 51Cr-labelled ethylenediaminetetra-acetate (51Cr-EDTA) clearance in patients with hyperparathyroidism both before and after parathyroidectomy, but not in patients with essential hypertension. 3. Creatinine clearance appeared to overestimate glomerular filtration rate in some patients with hyperparathyroidism, falling significantly after surgery while 51Cr-EDTA clearance was unchanged. This observation may explain the failure of some previous studies to relate hypertension to impairment of renal function. 4. Plasma renin activity, plasma aldosterone and whole-body exchangeable sodium did not differ between normotensive and hypertensive patients with primary hyperparathyroidism and were unchanged after surgery. 5. Parathyroidectomy did not result in any change in blood pressure or in glomerular filtration rate measured by 51Cr-EDTA clearance.

Effect of Proportional Reduction of Sodium Intake on the Adaptive Increase in Glomerular Filtration Rate/Nephron and Potassium and Phosphate Excretion in Chronic Renal Failure in the Rat

1975 ◽  
Vol 49 (3) ◽  
pp. 193-200 ◽  
Author(s):  
C. H. Espinel
Keyword(s):  
Renal Failure ◽  
Glomerular Filtration Rate ◽  
Chronic Renal Failure ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Control Group ◽  
Phosphate Excretion

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of ‘autonomous adaptation’ in chronic renal failure is presented.

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