An Increase in a Circulating Inhibitor of Na+,K+-Dependent ATPase: A Possible Link between Salt Intake and the Development of Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 17s-20s ◽  
Author(s):  
G. A. MacGregor ◽  
S. Fenton ◽  
J. Alaghband-Zadeh ◽  
N. D. Markandu ◽  
J. E. Roulston ◽  
...  

1. The plasma's ability to stimulate guinea-pig renal glucose 6-phosphate dehydrogenase (G6PD) in vitro was measured by a cytochemical technique in 23 normotensive subjects and 19 patients with hypertension, all of whom were studied on their normal sodium intake. The ability of plasma to stimulate renal G6PD was significantly (P < 0.001) increased in the hypertensive patients (mean 195 ± 52 units/ml) compared with the normotensive subjects (mean 22.2 ± 5.8 units/ml). In all 42 individuals, there was a significant correlation between diastolic pressure and the ability of plasma to stimulate G6PD (r = 0.69 P < 0.001). 2. The ability of plasma to stimulate G6PD was greatest in the hypertensive patients with values of plasma renin activity below the normal range. In the normotensive subjects the ability of plasma to stimulate G6PD was significantly greater in the older subjects. 3. As the ability of plasma to stimulate G6PD reflects its ability to inhibit Na+,K+-dependent ATPase, these results suggest that patients with essential hypertension have an increase in a circulating inhibitor of Na+,K+-ATPase. The results support the hypothesis that a rise in a circulating sodium transport inhibitor may, in part, be responsible for the rise in blood pressure in essential hypertension, and may form the link between salt intake, abnormalities of sodium transport and a rise in blood pressure.

1981 ◽  
Vol 60 (5) ◽  
pp. 483-489 ◽  
Author(s):  
W. Kiowski ◽  
F. R. Bühler ◽  
P. Vanbrummelen ◽  
F. W. Amann

1. Plasma noradrenaline concentrations and blood pressure were measured in 45 patients with essential hypertension and 34 matched normotensive subjects. Plasma noradrenaline was similar in both groups, but in the hypertensive patients plasma noradrenaline correlated with blood pressure. 2. The increase in forearm flow in response to an intra-arterial infusion of phentolamine was determined in 12 of the hypertensive and 14 of the normotensive subjects to assess the α-adrenoceptor-mediated component of vascular resistance. Although the dilator response to phentolamine was similar in both groups, in the hypertensive patients it was correlated with the control plasma noradrenaline (r = 0.83, P<0.01) as well as the height of mean blood pressure (r = 0.73, P<0.01). 3. These results suggest that in hypertensive patients plasma noradrenaline can be a marker for both sympathetic activity and the α-adrenoceptor-mediated component of vascular resistance.


1977 ◽  
Vol 52 (3) ◽  
pp. 319-323 ◽  
Author(s):  
R. F. Bing ◽  
J. Harlow ◽  
A. J. Smith ◽  
M. M. Townshend

1. The 24 h urinary excretion of adrenaline, noradrenaline, normetadrenaline, metadrenaline and vanilloylmandelic acid has been compared in 17 male normotensive subjects and 25 age-matched male hypertensive patients studied under similar in-patient conditions. 2. 24 h urinary metadrenaline was significantly lower in the hypertensive patients. With this exception, no significant differences were found between the two groups when the total 24 h excretion of free catecholamines and their metabolites was analysed. 3. Diurnal variation in free catecholamine excretion was found in both normotensive and hypertensive subjects. There was no corresponding variation in metabolite excretion. 4. No correlation could be established between systolic or diastolic blood pressure and the amounts of the catecholamines or their metabolites in the urine of either group. 5. The results are considered in the light of recent work demonstrating high plasma catecholamine concentrations in hypertension. They lend no support to the concept that excessive circulating catecholamines are responsible for the elevated blood pressure in essential hypertension.


1976 ◽  
Vol 51 (s3) ◽  
pp. 211s-213s
Author(s):  
M. Ulrych ◽  
Z. Ulrych

1. Relationships between labelled albumin disappearance rate (LADR), plasma volume, blood volume, plasma renin activity (PRA) and blood pressure (BP) were studied in normotensive control subjects and patients with hypertension of different aetiology and severity. In essential hypertensive patients without complications an inverse linear relationship was found between blood pressure and plasma or blood volume. 2. Very close inverse correlations were found between LADR and PRA in both normotensive subjects and patients with uncomplicated essential hypertension. LADR appears to be an excellent reference standard for PRA. 3. It is postulated that LADR mainly reflects the relation between circulating fluid and vascular capacitance tone. LADR is increased in hypertension and blood volume may still be inappropriately high.


1989 ◽  
Vol 77 (2) ◽  
pp. 217-222 ◽  
Author(s):  
Sergio Castellani ◽  
Luca Scarti ◽  
Ji Lin Chen ◽  
Attilio Del Rosso ◽  
Marino Carnovali ◽  
...  

1. In a double-blind, randomized, cross-over study the effects of potassium canrenoate administration (100 mg twice daily for 10 days orally) on renal prostaglandin synthesis (prostaglandin E2 and prostaglandin F2α) were evaluated in 10 normotensive females and in 10 females with essential hypertension. 2. When compared with normotensive subjects, hypertensive patients in baseline conditions showed a reduced excretion of urinary prostaglandin E2 associated with an excessive prostaglandin F2α production. 3. Potassium canrenoate significantly reduced mean blood pressure in hypertensive patients [from 118.9 ± 8.7 mmHg (1.62 ± 0.12 kPa) to a peak minimum value of 104.7 ± 9.8 mmHg (1.42 ± 0.13 kPa) on the seventh day of treatment; P < 0.01 for the whole period] but not in control subjects [from 88 ± 9.4 mmHg (1.20 ± 0.13 kPa) to 84.3 ± 8.3 mmHg (1.15 ± 0.11 kPa) on the eighth day, NS] even though potassium canrenoate significantly increased sodium excretion in both groups. Renal prostaglandin excretion was affected differently in the two groups: in control subjects excretion of both prostaglandin E2 and prostaglandin F2α was increased after drug administration, whereas in hypertensive patients only prostaglandin E2 excretion was enhanced.


1976 ◽  
Vol 51 (s3) ◽  
pp. 193s-196s
Author(s):  
G. A. MacGregor ◽  
P. M. Dawes

1. Saralasin (Sar1-Ala8-angiotensin II), a competitive inhibitor of angiotensin II (AII), has been infused into normal subjects and patients with essential hypertension when deprived of sodium by 5 days of a 10 mmol/day sodium diet. 2. When saralasin was given by an incremental rate of infusion starting at 0·25 μg min—1 kg—1, sodium-deprived normal subjects showed a fall in standing blood pressure with no change in lying blood pressure, sodium-deprived normal-renin hypertensive patients showed no change in lying or standing blood pressure and sodium-deprived low-renin patients showed a significant sustained rise in lying and standing blood pressure. 3. These findings suggest that: (a) standing blood pressure in sodium-deprived normal subjects is angiotensin II dependent; (b) normal-renin hypertensive patients when sodium deprived by diet alone do not appear to be angiotensin II dependent (angiotensin II is unlikely therefore to be directly maintaining their blood pressure on their normal sodium intake); (c) the rise in blood pressure seen in low-renin hypertensive patients with saralasin may be a further way of distinguishing this group of patients.


1981 ◽  
Vol 60 (3) ◽  
pp. 7P-7P
Author(s):  
P. S. Parfrey ◽  
N. D. Markandu ◽  
J. E. Roulston ◽  
B. E. Jones ◽  
G. A. MacGregor

1990 ◽  
Vol 1 (1) ◽  
pp. 43-52
Author(s):  
G G Krishna

Epidemiologic, experimental, and clinical studies suggest that potassium is an important regulator of blood pressure. Surveys conducted in widely divergent geographic locations indicate higher prevalence of hypertension in populations ingesting diets low in potassium. Amelioration of hypokalemia lowers blood pressure in mineralocorticoid-induced hypertension in rats and in essential hypertensive patients receiving thiazide diuretics. We observed that in normotensive subjects ingesting normal amounts of sodium, short-term potassium depletion increases the mean arterial pressure from 90.9 +/- 2.2 mm Hg to 95.0 +/- 2.2 mm Hg (P less than 0.01). Furthermore, acute sodium loading increases blood pressure in potassium-depleted subjects but it had no effect in subjects ingesting normal amounts of potassium. Preliminary studies indicate that short-term potassium depletion also elevates blood pressure in hypertensive patients. Potassium supplementation lowers blood pressure in hypertensive patients ingesting normal amounts of sodium. Blacks appear to be more sensitive to the hypotensive effects of potassium. The mechanism of potassium-induced changes in blood pressure is not well understood. Potassium depletion consistently induces sodium retention. The hypertensive effects of potassium depletion and hypotensive effects of potassium supplementation are not observed when sodium intake is kept low. Direct vasoconstrictive effects of hypokalemia may contribute to the pressor effect of potassium depletion. The role of altered vascular sensitivity to vasoactive hormones and alterations in divalent cation metabolism in mediating the potassium-induced changes in blood pressure require further study.


1986 ◽  
Vol 70 (6) ◽  
pp. 583-586 ◽  
Author(s):  
H. H. Gray ◽  
P. J. Hilton ◽  
P. J. Richardson

1. This study has confirmed that serum from patients with essential hypertension inhibits sodium transport and elevates intracellular sodium in normal human leucocytes in vitro when compared with that of well matched normotensive controls. 2. The magnitude of this effect was positively correlated with the diastolic blood pressure of the hypertensive patient. 3. The degree of sodium transport inhibition conferred by the hypertensive's serum was correlated with the abnormal sodium transport in the hypertensive's own leucocytes. 4. These results confirm the presence of a serum inhibitor of sodium transport in essential hypertension. The relationship between the inhibitory effect and severity of hypertension argues that it may be of mechanistic importance.


1973 ◽  
Vol 44 (3) ◽  
pp. 213-226 ◽  
Author(s):  
M. D. Esler ◽  
P. J. Nestel

1. The effect of 25° head-up tilt on blood pressure, urinary catecholamines, and creatinine clearance has been studied in untreated essential hypertensive patients and normotensive subjects. 2. The mean rise in diastolic pressure for all subjects with hypertension was 4.9 mmHg which did not differ significantly from the mean rise of 5.4 mmHg in the normal subjects. Ten of forty-one hypertensives had a diastolic pressure response greater than the response in any of eleven normal subjects, with a rise of greater than 10 mmHg. 3. The increase in urinary noradrenaline excretion with tilt was greater in these orthostatic hypertensive patients (1.74 μg/h) than in either the remaining hypertensive (0.34 μg/h) or the normotensive subjects (0.56 μg/h). Overall there was a significant correlation between changes in diastolic blood pressure and urinary noradrenaline. 4. Creatinine clearance was reduced by tilting. The mean reduction was similar for normally reacting hypertensive and normotensive subjects (6.0% and 7.2% respectively). The ten orthostatic hypertensive patients, however, had a greater reduction in creatinine clearance (23.4%), and in the hypertensive group as a whole changes in diastolic blood pressure and creatinine clearance were negatively correlated. 5. Those patients with excessive response to tilt tended to be young, not obese, and with recent onset of hypertension when documentation of this was adequate.


2016 ◽  
Vol 12 (1) ◽  
pp. 38-43
Author(s):  
Rehnuma Tabassum ◽  
Sangita Mithun ◽  
SM Nurul Irfan

Introduction: Hypertension is independent and the most powerful predictor of cardiovascular morbidity and mortality. Sympathetic overdrive may be related to essential hypertension. Heart Rate Variability (HRV) analysis is one of the most quantitative markers of autonomic activity in hypertensive patients. Objective: To assess the cardiac autonomic nerve function status by heart rate variability in essential hypertension. Materials and Methods: This cross sectional study was carried out to observe the HRV in 60 hypertensive male patients with age ranging from 40-60 years (group B) in the Department of Physiology, Bangabandhu Sheikh Mujib Medical University (BSMMU) from 1st July 2008 to 30th June 2009. Based on treatment, hypertensive patients were divided into B1 (untreated patients on their 1st day of diagnosis) and B2 (patients with antihypertensive therapy for less than 5 years). For comparison, 30 apparently healthy normotensive subjects (group A) matched by age sex were also studied. The study group was selected from the Out Patient Department of Cardiology, BSMMU, Dhaka and the control group was selected by personal contact. Heart Rate Variability parameters were assessed by Polygraph (RMS Polyrite D, version2.2) and for statistical analysis Independent sample t-test, One-way ANOVA test, Chi-square test and Pearson’s correlation coefficient tests were done as applicable. Results: LF/HF(Low Frequency/High Frequency) ratio and LF norm (normalized unit) were significantly (p<0.001) higher and HF norm was significantly (p<0.001) lower in untreated hypertensive patients in comparison to those of healthy normotensive subjects. parameters were observed between treated hypertensive and healthy control subjects. The LF/HF ratio and LF norm showed positive correlations and HF norm showed negative correlations with SBP (systolic blood pressure) and DBP (diastolic blood pressure) in both the hypertensive groups. However, all these findings were more marked in untreated hypertensive patients than those of treated group. Conclusion: Hypertensive patients may have sympathovagal imbalance and is usually characterized by higher sympathetic as well as lower vagal modulation of the heart rate. Journal of Armed Forces Medical College Bangladesh Vol.12(1) 2016: 38-43


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