Mechanisms of leucocyte sodium influx in essential hypertension

1988 ◽  
Vol 75 (5) ◽  
pp. 521-526 ◽  
Author(s):  
L. L. Ng ◽  
M. Harker ◽  
E. D. Abel

1. Leucocyte Na+ influx in media containing 10 mmol/l Na+ was studied directly using a triple-isotope method for measuring initial 22Na uptake rates in 20 normal and 18 untreated hypertensive subjects. The effects of 1 mmol/l amiloride (a Na+-H+-antiport inhibitor) and 0.1 mmol/l bumetanide (a Na+, K+, Cl−-symport inhibitor) were also examined. 2. The total, amiloride-sensitive and bumetanide-sensitive influx rates were raised in hypertensive compared with normotensive subjects [median (range): total 0.63 (0.25–1.82) vs 0.40 (0.09–0.65) mmol min−1 l−1, P < 0.002; amiloride-sensitive 0.43 (0.18–1.56) vs 0.26 (0.04–0.48) mmol min−1 l−1, P < 0.002; bumetanide-sensitive 0.12 (−0.03 to 0.83) vs 0.02 (−0.25 to 0.21) mmol min−1 l−1, P < 0.005]. 3. We conclude that hypertensive patients have a raised leucocyte total Na+ influx when measured in media containing 10 mmol/l Na+ and that this is contributed mainly by amiloride-sensitive and bumetanide-sensitive Na+ influx mechanisms.

1988 ◽  
Vol 75 (2) ◽  
pp. 179-184 ◽  
Author(s):  
L. L. Ng ◽  
M. Harker

1. A triple-isotope method for measuring initial 22Na uptake rates in unactivated human leucocytes in the presence of serum, using 3H2O, [14C]sucrose and 22Na, is described. 2. This 22Na influx is inhibited by amiloride, with half-maximal inhibition at a concentration of 10−5 mol/l. 3. About 70% of the 22Na influx in normal human leucocytes is inhibited by 1 mmol/l amiloride, with an external Na+ concentration of 10 mmol/l. 4. External Na+ antagonizes this inhibition by amiloride. The Km for external Na+ is 9 mmol/l. 5. Intracellular acidification from either external Na+ depletion or ammonium chloride incubation leads to an activation of amiloride-sensitive Na+ influx. 6. The amiloride-sensitive Na+–H+ antiport provides the major influx pathway for Na+ in unactivated human leucocytes in the presence of serum.


1982 ◽  
Vol 63 (s8) ◽  
pp. 41s-43s ◽  
Author(s):  
W. Zidek ◽  
H. Vetter ◽  
K.-G. Dorst ◽  
H. Zumkley ◽  
H. Losse

1. The intracellular Na+ and Ca2+ activity and Na+ concentration were measured in erythrocytes of normotensive subjects, with and without a familial disposition to hypertension, in essential hypertensive patients with and without a family history of hypertension, and in patients with secondary hypertension. 2. In normotensive subjects without a genetic trait of hypertension intracellular Na+ activity and concentration were 7.00 ± 1.38 mmol/l and 5.67 ± 0.95 mmol/l respectively. The intracellular Ca2+ activity was 4.82 ± 4.49 μmol/l. In normotensive subjects with a familial hypertensive disposition intracellular Na+ activity and concentration were 9.74 ± 1.43 mmol/l (P < 0.01) and 6.63 ± 0.88 mmol/l (P < 0.05). Intracellular Ca2+ was 9.59 ± 9.71 μmol/l (P < 0.05). 3. Essential hypertensive patients without a familial genetic trait had an elevated intracellular Na+ activity (8.35 ± 2.08 mmol/l, P < 0.05). Intracellular Na+ concentration was 6.64 ± 0.79 mmol/l (P < 0.05). The intracellular Ca2+ activity was markedly elevated to 25.33 ± 19.03 μmol/l (P < 0.01). The essential hypertensive patients with a familial disposition had an elevated intracellular Na+ activity (17.19 ± 4.37 mmol/l, P < 0.001) and Ca2+ activity (32.8 ± 32.51 μmol/l, P < 0.01). The intracellular Na+ concentration was 6.25 ± 1.23 mmol/l. 4. The results indicate that in essential hypertension intracellular Na+ activity is increased, particularly in patients with a familial disposition for hypertension. Intracellular Ca2+ is increased in essential hypertension whether or not there was a family disposition to hypertension.


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.


1982 ◽  
Vol 63 (s8) ◽  
pp. 219s-221s ◽  
Author(s):  
N.-H. Holstein-Rathlou ◽  
U. G. Svendsen ◽  
P. P. Leyssac

1. Ten patients with essential hypertension and ten normotensive control subjects were investigated before and after an isotonic volume load. 2. The increases in the clearances of lithium and of sodium were greater in the hypertensive than in the normotensive subjects (P < 0.05). The fractional increases showed a positive correlation (rs = 0.68, P < 0.05) in the hypertensive patients. 3. An increase in glomerular filtration rate in the hypertensive patients correlated positively with the increase in proximal output (rs = 0.70, P < 0.05), but did not correlate with the change in sodium excretion. 4. The exaggerated natriuresis was accompanied by a significant rise in the absolute rate of sodium reabsorption in the distal segments, but distal fractional reabsorption decreased. 5. It is concluded that the exaggerated natriuresis can be accounted for by an increase in the proximal output of sodium and water.


2005 ◽  
Vol 33 (2) ◽  
pp. 170-177 ◽  
Author(s):  
H Sumino ◽  
M Nara ◽  
K Seki ◽  
T Takahashi ◽  
T Kanda ◽  
...  

Hypertension is an important risk factor for cardiovascular disease, and antihypertensive drugs can decrease the occurrence of such events in hypertensive patients. This study compared the rheological properties of blood in 22 untreated hypertensive patients, 42 patients taking antihypertensive drugs and 74 normotensive subjects. Using a microchannel method, the whole blood passage time was measured and blood movement was observed with a microscope connected to an image display unit. The blood passage time in untreated hypertensive patients was significantly higher than in treated hypertensive patients or normotensive subjects, but was similar in the latter two groups. Microscopic observations showed that platelet aggregation and leucocyte adhesion were increased in untreated hypertensive patients, resulting in poor flow, while blood samples from treated hypertensive patients and normotensive subjects passed smoothly through the microchannels. These rheological differences could contribute to the decrease in cardiovascular disease seen when hypertensive patients are treated effectively.


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.


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 &lt; 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 &lt; 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.


1970 ◽  
Vol 5 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Rehnuma Tabassum ◽  
Noorzahan Begum ◽  
Sultana Ferdousi ◽  
Shelina Begum ◽  
Taskina Ali

Background: Essential hypertension may be associated with altered cardiovascular autonomic nervefunction. Heart Rate Variability (HRV) analysis is an important tool for quantitative measurement ofautonomic nerve activity. Objective: To assess the cardiac autonomic nerve function status in essentialhypertension by analyzing time domain measures of heart rate variability. Methods: This cross sectional study was carried out in the Department of Physiology, Bangabandhu Sheikh Mujib MedicalUniversity from 1st July 2008 to 30th June 2009.For this purpose, 60 hypertensive male patients withage ranged between 40-60 years (group B) were enrolled from the Out Patient Department of Cardiology,BSMMU, Dhaka. Based on treatment received, hypertensive patients were subdivided into group B1i.e.untreated patients on their 1st day of diagnosis and group B2 i.e.patients with antihypertensivetherapy. For comparison, 30 age & sex matched apparently healthy normotensive subjects (group A)were also studied as control group. Time domain measures of Heart Rate Variability (HRV) such asMean RR intervals, Mean HR, SDNN & RMSSD were assessed by a Polygraph machine to observeboth sympathetic and parasympathetic nerve function status. For statistical analysis of data,Independent sample t-test, One-way ANOVA test, were used as applicable. Results: Mean R-R interval SDNN and RMSSD were significantly (P<0.01) lower but mean heart rate was significantly (P<0.01)higher in untreated hypertensive patients than those of normotensive subjects. But differences in allthese 4 parameters when compared between control and treated hypertensive patients were foundstatistically non significant. Conclusion: Impaired cardiac autonomic nerve function characterized bysympathetic overactivity may occur in hypertensive patients.Key words: Mean RR; SDNN; RMSSD; hypertensionDOI: 10.3329/jbsp.v5i1.5411J Bangladesh Soc Physiol. 2010 June; 5(1): 1-7


Sign in / Sign up

Export Citation Format

Share Document