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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hypotensive and hormonal effects of the angiotensin converting enzyme (ACE) inhibitor enalapril (10 mg twice daily) were compared with those of hydrochlorothiazide (25 mg twice daily), with the two drugs in combination and with placebo in 21 patients with essential hypertension. For each patient there were four randomised double-blind treatment phases, each of four weeks' duration, which comprised a 2 X 2 factorial experiment. All blood pressure parameters were reduced in the three active treatment phases compared to placebo (p less than 0.001). Supine mean blood pressures were 119 mmHg (placebo), 113 mmHg (hydrochlorothiazide), 108 mmHg (enalapril), and 98 mmHg (hydrochlorothiazide plus enalapril) (SEM 3 mmHg, ANOVA). Enalapril and hydrochlorothiazide were equally effective and well tolerated and their hypotensive effects were additive. Enalapril increased plasma renin activity (PRA), reduced plasma angiotensin II (AII) and aldosterone concentrations, and reduced ACE activity, whereas hydrochlorothiazide increased PRA, plasma AII, and aldosterone concentrations without altering ACE activity. With combination treatment the effects of enalapril on PRA and plasma AII concentrations were potentiated whereas those on plasma aldosterone concentration and ACE activity were additive. Atrial natriuretic factor plasma concentration in the placebo phase was 92 pg/ml and increased to 145 pg/ml in the hydrochlorothiazide phase (p less than 0.001, SEM 13 pg/ml), but there was no significant change in either the enalapril or combination phases.
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PMID:Effects of enalapril and hydrochlorothiazide on blood pressure, renin-angiotensin system, and atrial natriuretic factor in essential hypertension: a double blind factorial cross-over study. 302 94

In this review, we first summarized the evidence from animals and man for and against a role for dietary sodium in the genesis and treatment of hypertension. The evidence for a role for dietary sodium in the genesis of hypertension is strongest in those subjects with impaired ability to excrete sodium due to organic renal disease or mineralocorticoid excess. Here restriction of dietary sodium promptly lowers arterial pressure. Its role in the genesis of essential hypertension is still controversial. Nevertheless, it appears that some patients with mild to moderate essential hypertension respond to moderate sodium restriction with a modest fall in blood pressure. This restriction also seems to reduce the amount of antihypertensive medication needed to keep blood pressure under control. We next considered the mechanism of the pressure response to dietary sodium chloride, concentrating upon the increase in extracellular fluid volume, potassium depletion, and increased plasma levels of prohypertensive sodium pump inhibitor and antihypertensive atrial natriuretic factor. We next summarized the evidence for a primary role for dietary potassium in the genesis of hypertension and pointed out that certain subsets of subjects with a high incidence of hypertension also have a lower dietary potassium intake. Some investigators find that dietary potassium supplementation lowers blood pressure in established hypertension. This may result from natriuresis and from vasodilation subsequent to stimulation of Na+, K+-ATPase in vascular smooth muscle and adrenergic nerve terminals. We then considered practical aspects of dietary sodium restriction and dietary potassium supplementation in the therapy for established hypertension. The review concludes with comments on their possible roles in the prevention of hypertension.
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PMID:Dietary sodium and potassium in the genesis, therapy, and prevention of hypertension. 329 78

Atrial cardiocytes contain specific atrial granules ( SAGs ) which are the storage site of atrial natriuretic factor (ANF). The purpose of the present study was to determine whether ANF produces natriuresis by inhibiting Na+-K+ pump activity and whether this factor is similar to the humoral sodium transport inhibiting factor ( HSTIF ) previously demonstrated in acutely volume expanded animals and humans as well as in experimental and human essential hypertension. Our results indicate that, in contrast to the HSTIF , ANF does not inhibit membrane Na+,K+-ATPase, vascular smooth muscle cell Na+-K+ pump activity, or sodium transport in the toad bladder. Intravenous infusion of ANF in the bilaterally nephrectomized, hexamethonium-treated rat produces only a small transient pressor response, probably due to potentiation of endogenous norepinephrine. These findings strongly suggest that the ANF is not the same as the HSTIF detected on acute volume expansion and in some forms of hypertension. They also suggest that the diuretic and natriuretic effects of ANF are due to mechanism(s) other than blood pressure elevation and inhibition of Na+-K+ pump activity.
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PMID:Effects of rat atrial extract on sodium transport and blood pressure in the rat. 632 56

Around half of all humans with essential hypertension are resistant to salt (blood pressure does not change by more than 5 mm Hg when salt intake is high), and although various inbred strains of rats display salt-insensitive elevated blood pressure, a gene defect to account for the phenotype has not been described. Atrial natriuretic peptide (ANP) is released from the heart in response to atrial stretch and is thought to mediate its natriuretic and vaso-relaxant effects through the guanylyl cyclase-A receptor (GC-A). Here we report that disruption of the GC-A gene results in chronic elevations of blood pressure in mice on a normal salt diet. Unexpectedly, the blood pressure remains elevated and unchanged in response to either minimal or high salt diets. Aldosterone and ANP concentrations are not affected by the genotype. Therefore, mutations in the GC-A gene could explain some salt-resistant forms of essential hypertension and, coupled with previous work, further suggest that the GC-A signaling pathway dominates at the level of peripheral resistance, where it can operate independently of ANP.
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PMID:Salt-resistant hypertension in mice lacking the guanylyl cyclase-A receptor for atrial natriuretic peptide. 747 88

To appreciate the role of some neuropeptides in the antihypertensive mechanism of clonidine, 17 patients with essential hypertension were given po clonidine 150 micrograms tid for 3 d. Plasma atrial natriuretic factor (ANF), vasopressin (Vas), and dynorphin A (Dyn A) were measured by radioimmunoassay. After the treatment, mean blood pressure (MBP), heart rate and 24 h urine norepinephrine, epinephrine were decreased, but no change was found in plasma Dyn A. The magnitudes of increased ANF and decreased Vas were correlated with the decreased MBP (r = -0.57 and 0.53, respectively, P < 0.05). These results suggest that both ANF and Vas are involved in the antihypertensive mechanism of clonidine.
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PMID:[Possible involvement of atrial natriuretic factor and vasopressin in antihypertensive mechanism of clonidine in humans]. 790 63

Atrial natriuretic peptide (ANP) response during acute saline loading and its relationship to changes in blood pressure (BP) and sodium excretion were studied in 21 patients with essential hypertension (EH) and nine normotensive volunteers. Following 2 liters of isotonic saline infusion at a rate of 500 mL/hour, plasma ANP concentrations in patients with EH increased significantly from 69.9 +/- 6.0 (mean +/- SEM) to 103.6 +/- 17.1 pg/mL (p < 0.05) in the first hour and peaked at the second hour. In normal subjects, the increase in plasma ANP was not significant until the third hour of infusion (64.6 +/- 6.2 to 82.0 +/- 7.5 pg/mL, p < 0.05). Mean BP (MBP) remained stable and the natriuretic responses were similar in the two groups. However, hypertensive patients with a prompt rise in ANP during the initial two hours of infusion (fast responders) maintained a BP balance more efficiently than those with a delayed rise in ANP (slow responders), as the latter displayed a significant increase in MBP two hours after saline loading (126 +/- 5 to 133 +/- 5 mmHg, p < 0.05). Fast responders also had a greater percent of suppression of plasma aldosterone (-49.7 +/- 9.2 vs 15.9 +/- 42.0%, p = 0.05) one hour after saline loading, and a higher increment of natriuresis (263.9 +/- 43.8 vs 97.5 +/- 27.4%, p < 0.025) in the second hour of infusion than slow responders. Our results indicate that during acute saline loading, patients with EH have a faster and greater rise in plasma ANP than normotensives.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic peptide and blood pressure responses during acute sodium loading in patients with essential hypertension. 790 59

We examined plasma renin activity (PRA), plasma aldosterone (PA), atrial natriuretic factor (ANF) and endogenous digitalis-like factor (DLF) in 15 healthy subjects and 15 patients with essential hypertension (EH) to obtain basal values and values after extracellular fluid volume (ECFV) expansion caused by infusion of isotonic saline solution over a period of 2 hours (20 mg/kg). A significant increase in diuresis and natriuresis accompanied by a decrease in PRA and PA and an increase in ANF was observed in both groups. No significant differences were observed in ANF levels between normotensive subjects and hypertensive patients. Hypertensive patients showed significantly higher basal values of DLF than normotensive subjects. However, an increase in plasma DLF following ECFV expansion was observed only in the group of healthy subjects. There was a positive correlation between ANF and natriuresis and a negative correlation between ANF and systolic and diastolic blood pressure (BP). Changes in DLF correlated positively with changes in diastolic BP in both groups, while in healthy subjects a negative correlation was recorded between PRA and DLF. We conclude that the increased diuresis and natriuresis in ECFV expansion is presumably accounted for not only by suppression of PRA and PA, but also by stimulated ANF secretion, while in healthy subjects stimulation of DLF may be involved as well. The insufficient DLF response to saline infusion may indicate an exhausted DLF reserve in hypertensive patients. As a vasoactive substance, DLF can participate in the regulation of blood pressure and play a role in the pathogenesis of arterial hypertension.
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PMID:The role of endogenous digitalis-like factor in blood pressure regulation in essential hypertension. 797 61

Plasma concentration of two main cardiovascular substances - atrial natriuretic factor (ANF) and endothelin - were studied in control subjects (n = 21) under basal conditions and 90 minutes after oral administration of glucose. In hypertensive patients (n = 21) these determinations were repeated after 12 weeks treatment with an angiotensin I-converting enzyme inhibitor lisinopril (Prinivil, Merck Sharp and Dohme). While basal and post-glucose ANF concentrations did not differ in controls and hypertensive patients, a tendency to the higher endothelin levels was found in our group of essential hypertension when compared to normotensive subjects. Glucose loading did not change significantly ANF concentrations in any studied group but significantly lowered plasma endothelin in both controls (from 13 +/- 0.95 to 9.50 +/- 0.95 fmol/ml) and hypertensive patients (from 15.05 +/- 1.23 to 12.15 +/- 1.03 fmol/min). Treatment of hypertensive patients with lisinopril paradoxically increased concentrations of ANF (from 6.43 +/- 2.53 to 11.47 +/- 4.90 fmol/ml) and lowered that of endothelin (from 15.05 +/- 1.23 to 12.17 +/- 1.58 fmol/ml). From our findings we may suggest that the relative predominance of the vasoconstrictor (endothelin) over the vasodilator (ANF) humoral substances might participate in pathogenesis of EH and that the reversal of this disadvantageous ratio after lisinopril (increase of ANF and decrease of endothelin) might contribute to the blood pressure reducing effect of ACEI. The drop in plasma endothelin after glucose remains so far unexplained consequence of glucose loading in both control and hypertensive subjects.
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PMID:Plasma concentrations of some cardiovascular humoral factors in essential hypertension and their changes during the treatment with converting enzyme inhibitor lisinopril. 799 8

In patients with essential hypertension, left ventricular hypertrophy (LVH) increases the risk for cardiovascular morbidity and mortality. Thus its reversal represents one of the principal end-points of antihypertensive treatment. We assessed the cardiovascular effects of 1-year antihypertensive treatment with rilmenidine (1 or 2 mg/day orally), a new oxazoline with a potent antihypertensive action that acts selectively through imidazoline-preferring receptors. In 11 hypertensive patients (mean age, 49 +/- 2 years) with LVH, we measured systemic hemodynamics, large artery compliance, cardiac anatomy, and endocrine function. Patients underwent M-mode and 2-dimensional echocardiography as well as Doppler and peripheral pulsed Doppler flowmetry, determination of plasma atrial natriuretic factor (ANF) levels and renin activity (PRA), and of 24-hour urinary electrolyte and creatinine excretion in control conditions (systolic/diastolic blood pressure, 148 +/- 3/102 +/- 1 mm Hg), 4 weeks after blood pressure normalization (131 +/- 2/84 +/- 2 mm Hg; p < 0.01), after 1 year of satisfactory antihypertensive treatment (142 +/- 3/90 +/- 1 mm Hg; p < 0.01) and, finally, 1 month after therapy withdrawal (155 +/- 3/106 +/- 2 mm Hg; difference not significant [NS]). One-year of rilmenidine treatment induced an improvement in brachial artery compliance (from 0.92 +/- 0.06 to 1.16 +/- 0.08 cm4/dyne; p < 0.05), which persisted after withdrawal of treatment (1.17 +/- 0.06 cm4/dyne; p < 0.05). LVH was reversed after 1 year of rilmenidine treatment (from 152 +/- 5 to 131 +/- 4 g/m2 body surface area; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of one-year treatment with rilmenidine on systemic hypertension-induced left ventricular hypertrophy in hypertensive patients. 799 84

Some metabolic and humoral deviations found in normotensive offspring from hypertensive families can be modified in the course of years either as a result of ageing or of the clinical manifestation of essential hypertension (EH). The authors compared therefore some metabolic indicators (blood sugar level, IRI, C-peptide and plasma lipids) and humoral factors (plasma catecholamines, renin activity, atrial natriuretic factor and endothelin) in four groups of subjects: 27 young normotensive sons from normotensive families (SNF) and 30 from hypertensive families (SHF) with the findings of normotonics (NT) (n = 21) and patients with EH (n = 21) by 15 years older. Despite a tendency towards higher blood sugar levels in SHF and EH, the basal as well as oGTT stimulated blood sugar values were within the normal range. They were, however, associated with higher IRI and C-peptide concentrations in SHF with a further increase in NT and a much higher increase in EH. This indicates that normal blood sugar homeostasis in these groups is achieved only by an increased insulin secretion. The reduction of the blood sugar/IRI ratio in older NT accentuated in EH, suggests an increasing insulin resistance. In the lipid spectrum the authors found an increase of total cholesterol with advancing age, this being most marked in EH where also a decline of HDL cholesterol was recorded. As to humoral factors, higher catecholamine concentrations were found in SHF. Their increase with advancing age was more marked in EH. The plasma renin activity declined with age in NT as well as in EH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Metabolic and humoral variations during the development of essential hypertension]. 802 66


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