Angiotensin II Blockade in Normal Subjects and Essential Hypertensive Patients

1976 ◽  
Vol 51 (s3) ◽  
pp. 193s-196s
Author(s):  
G. A. MacGregor ◽  
P. M. Dawes
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Normal Subjects ◽  
Competitive Inhibitor ◽  
Hypertensive Patients ◽  
Sodium Diet ◽  
Incremental Rate ◽  
Standing Blood Pressure

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.

scholarly journals PENERAPAN ANJURAN DIET DASH DIBANDINGKAN DIET RENDAH GARAM BERDASARKAN KONSELING GIZI TERHADAP PENURUNAN TEKANAN DARAH PADA PASIEN HIPERTENSI DI PUSKESMAS LARANGAN UTARA

2021 ◽  
Vol 44 (1) ◽  
pp. 109-120
Author(s):  
Agustina Pungki Astuti ◽  
Didit Damayanti ◽  
Iskari Ngadiarti
Keyword(s):  
Blood Pressure ◽  
Nutritional Status ◽  
Diastolic Blood Pressure ◽  
Sodium Intake ◽  
Hypertensive Patients ◽  
Dash Diet ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Significant Difference

The low sodium and Diet Approaches to Stop Hypertension (DASH) are diets for reducing high blood pressure. This study aimed to analyze the effect of nutrition counseling on the DASH diet compared to low sodium diet on blood pressure in hypertensive patients. The study design was an experimental study that randomly allocated 34 respondents to DASH diet and 35 respondents to low sodium diet. The ages of respondents were 43 to 76 years and women were 74.3 percent. Nutrition counseling was conducted by researchers to respondents who visited health center or Posbindu Larangan Utara. Nutritional counseling was conducted for an average of 20 minutes using existing brochures. Low sodium diet emphasizes reducing sodium intake while DASH diet emphasis more on consuming lots of vegetables, fruit, nuts and low-fat products. Variables collected were the characteristics of respondent, disease, drugs taken and nutritional status, while blood pressure using a sphygmomanometer, food intake including sodium were measured before and 2 weeks after nutritional counseling. Results showed that there was a significant difference in diastolic blood pressure after patients were given DASH diet compared to low sodium diet (p 0.05) and there was a significant difference in delta of systolic and diastolic reduction in DASH diet compared to low sodium diet. Test also showed a significant reduction in systolic, diastolic blood pressure and sodium intake (p 0.001) in both diet groups after receiving counseling. It concluded that DASH diet can be recommended to decrease blood pressure in hypertensive patients with consider nutritional status. ABSTRAK  Diet Rendah Garam (RG) dan Diet Approaches to Stop Hypertension (DASH) adalah diet untuk menurunkan tekanan darah tinggi. Penelitian ini bertujuan untuk menganalisa pengaruh konseling gizi diet DASH dibandingkan diet RG terhadap tekanan darah pasien hipertensi. Rancangan penelitian adalah eksperimen yang secara acak mengalokasi diet DASH kepada 34 orang dan diet RG kepada 35 orang responden. Usia responden antara 43 hingga 76 tahun dan sebagian besar perempuan (74,3%). Konseling gizi dilakukan oleh tim peneliti kepada pasien hipertensi yang memeriksakan diri ke puskesmas atau posbindu Larangan Utara. Konseling gizi dilakukan rata-rata 20 menit menggunakan brosur yang sudah ada. Diet RG menekankan pengurangan asupan natrium sedangkan diet DASH lebih menekankan ke banyak konsumsi sayur, buah, kacang-kacangan dan produk rendah lemak. Variabel yang dikumpulkan adalah karakteristik responden, penyakit dan obat yang diminum serta status gizi sedangkan tekanan darah menggunakan sfigmomanometer, asupan makanan, zat gizi termasuk natrium diukur sebelum dan 2 minggu setelah konseling gizi dilakukan. Hasil menunjukkan adanya perbedaan yang bermakna pada tekanan darah diastolik setelah pasien diberi diet DASH dibandingkan dengan pasien yang diberi diet RG (p0,05) dan terdapat perbedaan delta penurunan sistolik dan diastolik bermakna pada diet DASH dibanding diet RG. Analisa juga menunjukkan adanya penurunan tekanan darah sistolik, diastolik dan asupan natrium  yang bermakna (p0.001) pada kedua kelompok diet setelah mendapat konseling diet DASH dan diet RG. Disimpulkan diet DASH dapat direkomendasikan untuk membantu menurunkan tekanan darah pada pasien hipertensi dengan memperhatikan status gizi. Kata kunci: hipertensi, tekanan darah, diet rendah garam, diet DASH

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 ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Sodium Transport ◽  
Salt Intake ◽  
Diastolic Pressure ◽  
Sodium Intake ◽  
Hypertensive Patients ◽  
Dependent Atpase ◽  
Normotensive Subjects

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.

scholarly journals Active kallikrein response to changes in sodium-chloride intake in essential hypertensive patients.

1996 ◽  
Vol 7 (3) ◽  
pp. 443-453 ◽  
Author(s):  
C Ferri ◽  
C Bellini ◽  
A Carlomagno ◽  
G Desideri ◽  
A Santucci
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Intake ◽  
Hypertensive Patients ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Sodium Load ◽  
Atrial Natriuretic

To evaluate the behavior of active kallikrein excretion in salt-sensitive and salt-resistant hypertensive patients during changes in sodium-chloride (NaCl) intake, 61 male, nonobese, nondiabetic outpatients affected by uncomplicated essential hypertension were given a diet that contained 140 mmol NaCl per day for 2 wk. Patients then received either a low- (20 mmol NaCl/day) or a high- (320 mmol NaCl/day) sodium diet for 2 wk, according to a randomized, double-blind, cross-over protocol. Hypertensive patients were classified as salt sensitive when their diastolic blood pressure rose by at least 10 mm Hg after the high-sodium diet, and decreased by at least 10 mm Hg after the low-sodium diet, considering as baseline blood pressure values those that were taken at the end of the 140 mmol NaCl/day intake period. The remaining patients were classified as salt resistant or, when diastolic blood pressure increased by 10 mm Hg or more after low-sodium intake, as counter-regulating. Twenty-three patients were therefore classified as salt sensitive, 28 as salt resistant, and 10 as counter-regulating. The baseline active kallikrein excretion was significantly lower (P < 0.0001) in salt-sensitive (0.62 +/- 0.31 U/24 h) patients than in salt-resistant (1.39 +/- 0.44 U/24 h) and counter-regulating patients (1.27 +/- 0.38 U/24 h). Surprisingly, the kallikrein response to changes in sodium intake was similar in all subgroups, although enzyme excretion was always at the lowest level in salt-sensitive hypertensive patients. This latter group also showed the highest plasma atrial natriuretic peptide levels (28.2 +/- 8.5 fmol/mL, P < 0.0001 versus salt-resistant and counter-regulating patients), and the greatest peptide increment with sodium load (P < 0.0001 versus salt-resistant and counter-regulating patients). Counter-regulating patients showed the steepest increase in plasma renin activity (from 0.24 +/- 0.18 to 0.83 +/- 0.21 ng/L per s, P < 0.001) and decrease of plasma atrial natriuretic peptide (from 26.1 +/- 6.3 to 6.8 +/- 3.1 fmol/mL, P < 0.001) when switched from a high to a low-sodium intake. In conclusion, salt-sensitive hypertensive patients excrete less active kallikrein than do salt-resistant and counter-regulating patients, but maintain a normal enzyme response to changes in dietary sodium intake. The exaggerated response of atrial natriuretic peptide to high-sodium intake that was observed in the same patients could be compensating for an impaired renal capability to excrete a sodium load.

Plasma Catecholamines and the Pressor Response to Sar1-Ala8-Angiotensin II in Man

1977 ◽  
Vol 53 (4) ◽  
pp. 341-348
Author(s):  
B. P. McGrath ◽  
J. G. G. Ledingham ◽  
C. R. Benedict
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Angiotensin Ii ◽  
Pressor Response ◽  
Plasma Catecholamines ◽  
Normal Subjects ◽  
Plasma Noradrenaline ◽  
Dialysis Patients ◽  
Anephric Patients ◽  
Change In Mean

1. The initial blood pressure response to saralasin (Sar1-Ala8-angiotensin II) infusion was examined in 15 normal subjects, eight patients with untreated essential hypertension and 65 patients established on chronic haemodialysis (including six anephric patients), and related to measurements of plasma renin activity (PRA), angiotensin II, plasma catecholamines (noradrenaline and adrenaline), blood volume and extracellular fluid volume ([35S]sulphate space or exchangeable sodium). 2. A transient rise in arterial pressure, maximum after 5–6 min, occurred in all normal subjects, patients with essential hypertension and anephric patients, and in 41 of the 59 dialysis patients with kidneys. 3. In the normal subjects, saralasin infusion resulted in a significant rise in plasma noradrenaline (mean increase 360%, P < 0·02) without change in plasma adrenaline concentration. The change in noradrenaline was significantly related to the change in mean blood pressure (P < 0·05) and was similar to the response to 5 min of a 40° head-up tilt. 4. An increase in plasma noradrenaline also occurred in dialysis patients (P < 0·005) but the change in mean blood pressure with saralasin in this group was inversely related to PRA (P < 0·001) and angiotensin II (P < 0·001), directly related to blood volume (P < 0·001), but unrelated to the change in plasma noradrenaline. 5. The pressor response to saralasin may be mediated not only by angiotensin-like action on vascular receptors but also by an action on the central or peripheral autonomic nervous system.

The effectiveness of differentiated treatment of patients with essential hypertension

1982 ◽  
Vol 63 (2) ◽  
pp. 19-21
Author(s):  
Yu. A. Panfilov ◽  
N. N. Kryukov ◽  
E. D. Baibursyan
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Beta Blocker ◽  
Hypotensive Effect ◽  
Blood System ◽  
Differential Treatment ◽  
Hypertensive Patients ◽  
Bed Days

Abstract. Depending on the hemodynamic type and state of the kallikreinkinin 'blood system, differential treatment of 246 hypertensive patients was carried out using the beta-blocker anaprilin and the peripheral arteriolar vasodilator apressin. A pronounced hypotensive effect was observed in 82.5% of patients. In patients who underwent differential treatment, a decrease in blood pressure was observed 3.2 days earlier than in patients who were treated empirically; hospitalization terms were reduced by an average of 2.5 bed-days.

Change in Blood Pressure during Altered Sodium Intake is not Associated with Calciotropic Hormone Level

1997 ◽  
Vol 93 (2) ◽  
pp. 153-157 ◽  
Author(s):  
Ryoji Ozono ◽  
Tetsuya Oshima ◽  
Hideo Matsuura ◽  
Katsuhiko Ishibashi ◽  
Mitsuaki Watanabe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Calcium Metabolism ◽  
Sodium Intake ◽  
Urinary Calcium ◽  
Urinary Calcium Excretion ◽  
Mean Blood Pressure ◽  
Calcium Excretion ◽  
Sodium Restriction ◽  
Sodium Diet ◽  
Change In Mean

1. We evaluated the effects of the dietary restriction of sodium chloride on blood pressure and systemic calcium metabolism in 19 in-patients with essential hypertension (11 men and 8 women, mean age 49.9 ± 12.1 years). 2. All patients received a high-sodium diet (250 mmol/day) for 1 week, followed by a low-sodium diet (10 mmol/day) for another week. Intake of potassium (100 mmol/day) and of calcium (15 mmol/day) were kept constant throughout the study. 3. Sodium restriction significantly reduced the mean blood pressure (from 114.0 ± 1.9 to 105.0 ± 13.7 mmHg, P < 0.01). Urinary calcium excretion was significantly reduced (from 5.1 ± 2.4 to 2.2 ± 1.0 mmol/day, P < 0.01). 4. The change in mean blood pressure after sodium restriction was not correlated with a change in any parameter of calcium metabolism [whole blood ionized calcium, plasma intact parathyroid hormone, or 1,25-(OH)2 vitamin D3]. 5. Plasma renin activity during a regular sodium diet, an index of renin status, was significantly and inversely correlated with the change in blood pressure during sodium restriction, but not with any change in the parameters of calcium metabolism. 6. We conclude that sodium restriction reduces blood pressure and decreases urinary calcium excretion. However, we observed no significant role of extracellular calcium concentration or of calciotropic hormone concentration in the mechanism of sodium sensitivity.

Secretion rate of dehydroepiandrosterone and dehydroepiandrosterone sulfate in benign essential hypertension as compared to normal subjects

1970 ◽  
Vol 48 (12) ◽  
pp. 1308-1313 ◽  
Author(s):  
A. Shao ◽  
W. Nowaczynski ◽  
O. Kuchel ◽  
J. Genest
Keyword(s):  
Essential Hypertension ◽  
Isotope Dilution ◽  
Normal Subjects ◽  
Dehydroepiandrosterone Sulfate ◽  
Secretion Rate ◽  
Isotope Dilution Method ◽  
Dilution Method ◽  
Hypertensive Patients ◽  
Double Isotope ◽  
Column Chromatographic

A study of the secretion rate of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEA-S) in normal subjects and patients with benign essential hypertension by a double isotope dilution method showed a fivefold increase in the secretion rate of dehydroepiandrosterone (from 9.8 mg/day ± 3.1 mg/day S.D. to 52.0 mg/day ± 15.5 mg/day S.D.), and a sixfold increase of dehydroepiandrosterone sulfate in hypertensive patients (from 10.7 mg/day ± 2.9 mg/day S.D. to 60.7 mg/day ± 18.6 mg/day S.D.). This study was carried out following the administration of 14C-labelled DHEA and 3H-labelled DHEA-S and involved an initial column chromatographic separation of urinary DHEA-glucuronide and sulfate.

Intrarenal renin inhibition increases renal function by an angiotensin II-dependent mechanism

1988 ◽  
Vol 255 (4) ◽  
pp. F749-F754 ◽  
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Plasma Renin ◽  
Competitive Inhibitor ◽  
Urinary Flow ◽  
Renin Substrate ◽  
Plasma Aldosterone Concentration ◽  
Renin Inhibition

ACRIP is a competitive inhibitor of renin in which an analogue of statine, (3R,4S)-4-amino-3-hydroxy-6-methylheptanoic acid, is incorporated into analogues of porcine renin substrate. ACRIP inhibits the enzymatic activity of renin, thus blocking the initiation of the angiotensin cascade. We studied the intrarenal action of ACRIP in small quantities without measurable systemic effects on renal function. In the first experiment, ACRIP was administered intrarenally at 0.02, 0.2, and 2 micrograms.kg-1.min-1 to uninephrectomized conscious dogs (n = 6) in metabolic balance at sodium intake of 10 meq/day. ACRIP, in doses of 0.02 and 0.2 micrograms.kg-1.min-1, markedly increased urine sodium excretion (UNaV) from 5.8 +/- 1.4 to 15.1 +/- 5.1 and 19.9 +/- 3.2 mu eq/min, respectively. Urinary flow rate (UV) underwent a similar increase and glomerular filtration rate (GFR) increased from 25.7 +/- 2.5 to 35.6 +/- 2.5 at 0.02 micrograms.kg-1.min-1 of ACRIP. Renal plasma flow (RPF), plasma renin activity (PRA), and plasma aldosterone concentration (PAC) were not affected. At 2 micrograms.kg-1.min-1, ACRIP traversed the kidney in quantities large enough to produce a reduction in systemic PRA and mean arterial pressure and caused natriuresis, diuresis, and increased GFR. In a second experiment, ACRIP was administered intrarenally at 0.2 micrograms.kg-1.min-1 in a separate group (n = 4) under identical conditions. ACRIP-induced increases in UV and UNaV were completely blocked by concurrent intrarenal administration of angiotensin II. The results indicate that intrarenal angiotensin II acts as a physiological regulator of renal sodium and fluid homeostasis.

Sign in / Sign up

Export Citation Format

Share Document