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

The authors studied a population of 4.023 subjects from several rural and urban communities selected on the basis of age, work tasks and social class. Genetic predisposition to essential hypertension was evaluated by determining intraerythrocyte sodium levels in all subjects with essential hypertension and their families. The authors also verified the behaviour of some biohumoral factors (PRA, aldosterone, ANP, intraerythrocyte, Na) as possible markers of essential hypertension and the role of some acquired risk factors in the development of the disease and its cerebrocardiovascular complications. The hypertense subjects were divided into groups and treated with diet alone or diet associated with drugs depending on the prevalence of pathogenetic factors. The results were evaluated after 1, 3, 6 and 12 months.
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PMID:[Evaluation of genetic predisposition and acquired risk factors in development of essential hypertension and its acute complications]. 208 9

We have studied the hemodynamic and humoral effects of ketanserin, an S2 antagonist, and whether PG synthesis blockade, induced by indomethacin, might modify its effects. Eight patients with uncomplicated essential hypertension were submitted to a treatment for three days with indomethacin (50 mg/b.i.d.) and for 3 days with placebo. At the end of each period, saline and ketanserin (10 mg i.v.) were given. The effects of placebo and of ketanserin were assessed for one hour by measuring the following parameters: blood pressure (BP), heart rate (HR), renal plasma flow (RPF), glomerular filtration rate (GFR), renal vascular resistance (RVR), PRA, aldosterone, noradrenaline (NA) serum and urinary thromboxane, urinary 6-keto-PGF1 alpha. Under placebo and as compared in saline, ketanserin significantly reduced BP aldosterone and RVR and increased HR, GFR, PRA, NA, serum and urinary thromboxane and urinary 6-keto-PGF1 alpha without modifying RPF. Pretreatment with indomethacin which significantly reduced serum thromboxane and urinary thromboxane and 6-keto-PGF 1 alpha prevented the renin stimulating effect and the increase in GFR induced by ketanserin without changing the other actions of this drug. Taken together, these findings indicate that PG do not play a relevant role in the antihypertensive effect of ketanserin, but mediate the GFR increase induced by this drug.
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PMID:[Humoral and hemodynamic (systemic and renal) effects of ketanserin in patients with essential hypertension: what is the role of prostaglandins?]. 210 33

In order to investigate the behaviour of atrial natriuretic peptide (ANP) in untreated mild to moderate essential hypertension and the influence of blood pressure normalisation by a beta 1-receptor blocker a study was conducted in groups of normotensive and hypertensive middle aged subjects. 10 normal subjects and 10 patients with essential hypertension (WHO I-II) without any medication and on betaxolol monotherapy were studied at rest and during graded exercise. In addition the response of ANP, cyclic guanosine monophosphate (cGMP) and the renin-aldosterone-system was investigated. Normal subjects and hypertensive patients did not differ in ANP levels at rest and also responded with a comparable exercise dependent increase at all workload levels. A steady decrease of ANP was noticed during the recovery period in both groups. After beta-blocker treatment in the hypertensive patients ANP concentrations significantly rose, both at rest and more pronounced during exercise. cGMP reacted in a similar way but showed a more inert response. A counter-regulatory behaviour between ANP and PRA or aldosterone, as seen under volume shifts, could not be detected. These findings demonstrate that plasma ANP is not altered in untreated essential hypertension. Increased ANP levels in beta 1-blocker treatment may contribute to its blood lowering effect.
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PMID:[Effect of a beta 1-receptor blocker on the plasma level of atrial natriuretic peptide in patients with essential hypertension in the exercise test]. 216 49

The effects of 1-year antihypertensive treatment with the diuretic fenquizone were evaluated in 16 patients with mild essential hypertension. During treatment with placebo, after 2, 4, 24, and 52 weeks of treatment we measured blood pressure, heart rate, forearm blood flow (FBF) and vascular resistance (FVR) at rest and after 10 minutes ischemia, and forearm venous distensibility. Subjects whose diastolic blood pressure after fenquizone was reduced at least 10% were classified as responders. On this basis, 56% of patients after 1 month and 68% after 1 year responded to fenquizone. Responders, in comparison to nonresponders, were characterized by a greater increase in FBF and a greater decrease in FVR. The reduction in diastolic blood pressure was significantly related to the fall in FVR whereas no correlation was found between blood pressure and venous compliance changes. Nonresponders had a PRA increase similar to that observed in responders but they showed a much greater increase in aldosterone, whose changes were inversely related to modifications of both FVR and blood pressure. Our results demonstrate that chronic therapy with fenquizone causes a reduction of FVR, and that nonresponders have an exaggerated rise in aldosterone. This observation further reinforces the hypothesis that factors influencing the secretion of aldosterone are important determinants of the antihypertensive mechanism of diuretics.
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PMID:Hemodynamic and humoral effects of chronic antihypertensive treatment with fenquizone: importance of aldosterone response. 217 89

A total of 42 patients with malignant arterial hypertension (MAH) were examined. Of these, 32 patients had essential hypertension (26 with normal renal function and 6 with renal failure treated by programmed hemodialysis) and 10 suffered from chronic glomerulonephritis. The patients were examined for central hemodynamics, hormonal background (plasma renin activity) (PRA), plasma aldosterone and cortisol concentration. 14 patients underwent closed puncture biopsy of the kidneys. All the patients manifested high PRA associated activation of gluco- and mineralocorticoid adrenal function along with the hyperkinetic syndrome. MAH was characterized by dramatic discrepancy between the stroke and cardiac indices and specific peripheral resistance. Nephrosclerosis whose extent varied, attaining maximum in patients with associated essential hypertension and renal failure and in autopsy material, in addition to severe lesions of the renal vessels appeared to be the common feature of all morphological alterations. Plasmic impregnation and fibrinoid necrosis of the arterioles were not detectable in all the patients, being of focal character. The same alterations were identified in the patients during exacerbation of glomerulonephritis and in the absence of MAH. The data obtained point to the nonuniformity of MAH. Four clinicomorphological variants of MAH are suggested.
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PMID:[The malignant hypertension syndrome: incontrovertible and questionable truths]. 221 9

The part played by calcium in genesis of essential hypertension may be suspected. Yet, the whole of epidemiological research as well in the animal as in man is still not very convincing. The objective of such a research has been to appreciate the calcium intestinal absorption before and after nicardipine treatment in 11 subjects (5 M/6 F) aged between 32 and 82. The group is made up of 7 hypertensive patients (2 M/5 F) and 4 normotensive ones (3 M/1 F). Subjects showing bone disease, kidney insufficiency and stone in kidneys or under such a treatment as to interfere with calcium metabolism had been excluded. Dosage of calcium and phosphate, Na, K, aldosterone, in blood and urine and PTH and PRA in blood had been effectuated. Estimation of true calcium absorption has been made by double isotope deconvolution method. Blood pressure has been measured by semi-ambulatory monitoring method. Similar evaluation has been made after four weeks treatment (60 mg of nicardipine a day). Without any treatment, normotensive subjects have a lower intestinal absorption coefficient than the hypertensive ones, which is normal (non significative statistical results: NS). Under nicardipine, hypertensive patients seem to get lower intestinal absorption (NS); other clinical, biological parameters show no change, except a rise of apoprotein A after nicardipine treatment (P less than or equal to 0.05). So, the intestinal absorption of calcium would become higher in hypertensive subjects and diminished by calcium antagonist treatment.
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PMID:[Calcium intestinal absorption in normotensive and essential hypertensive subjects before and after nicardipine]. 251 Jun 63

To assess the hemodynamic characteristics in malignant hypertension, echocardiography was performed in 18 patients with malignant essential hypertension (MH-I, n = 9) and secondary hypertension (MH-II, n = 9). Patients with benign hypertension with or without left ventricular hypertrophy (n = 8 and 7, respectively), patients with hypertensive heart failure (n = 7) and normotensive volunteers (n = 10) were subjected to controls. Plasma noradrenaline (NA) and renin activity (PRA) were also measured prior to the antihypertensive therapy. There were no significant differences in the durations of hypertension before the malignant phase, and the mean arterial pressure between MH-I and MH-II. Although posterior wall thickness (PWTd) in MH-II was similar to that in MH-I, interventricular septal thickness (IVSTd) was less marked in MH-II. The plasma NA and PRA were markedly increased in both MH-I and MH-II. End-diastolic dimension (Dd) of the left ventricle was within normal range, but end-systolic dimension (Ds) was significantly increased in MH-I, MH-II and hypertensive heart failure. The moderate decreases in ejection fraction (EF) and mean velocity of circumferential fiber shortening (mVcf) were observed in both MH-I and MH-II. Marked decreases in EF and mVcf were also observed in patients with hypertensive heart failure. The relationship between systolic blood pressure and Dd/PWTd was shifted toward the right and upper portion of the normal relation in MH-I and MH-II. The present study demonstrated that the hemodynamic characteristics in malignant hypertension are an inappropriate left ventricular hypertrophy due to a marked increase in systolic stress; dilatation of the left ventricle in systole; and a moderate decrease in ventricular systolic function. It is suggested that a decrease in left ventricular systolic function in malignant hypertension might be due in part to a marked increase in the influence of neurohumoral factors on hemodynamics.
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PMID:[Echocardiographic features of left ventricular hypertrophy and contractility in malignant hypertension]. 253 Mar 33

Plasma from 37 essential hypertensive patients, from 11 subjects with primary aldosteronism and from 23 normotensive subjects was tested for ouabain-like activity. Despite a very substantial overlap, hypertensive patients (both essential and secondary) showed significantly higher levels of a ouabain-like plasma factor compared to normotensive controls. No substantial differences could be detected, however, between the two forms of hypertension; in particular, no significant changes were observed in the low-PRA subgroup. Our results are hardly compatible with the hypothesis that this substance may be of crucial importance in the development either of essential hypertension or of primary aldosteronism.
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PMID:Plasma ouabain-like activity in essential hypertensive patients and in subjects with primary aldosteronism. 255 4

The known physiological adaptation of cardiovascular sensitivity to variations in angiotensin II (Ang II) levels would predict that the blood pressure (BP)-lowering effect of Ang II inhibition might be at least partly counterbalanced by enhanced Ang II reactivity. Therefore, factors other than Ang II inhibition per se may contribute to the antihypertensive mechanisms of angiotensin converting enzyme (ACE) inhibitors. In order to further investigate this, the body sodium-blood volume state as well as the pressor reactivity to infused Ang II or norepinephrine (NE) were assessed in 12 normal subjects and 16 patients with essential hypertension given a placebo, and after 6 weeks of intervention with enalapril (20-40 mg/day). Enalapril produced in both groups similar falls in plasma ACE activity (P less than 0.0001) and upright plasma aldosterone (P less than 0.01), and a rise in plasma renin activity (PRA; P less than 0.05). BP decreased from 156/107 +/- 3/2 (mean +/- s.e.m.) to 142/94 +/- 5/3 mmHg (P less than 0.001) in the hypertensives and from 118/84 +/- 4/2 to 111/73 +/- 4/3 mmHg (P less than 0.01) in the normal subjects. In the hypertensive patients only, the Ang II pressor reactivity relative to Ang II plasma levels during Ang II infusion was increased (P less than 0.01), while the NE pressor reactivity relative to NE plasma levels during NE infusion (P less than 0.01) as well as the exchangeable body sodium (-5%, P less than 0.001) were reduced significantly. Blood and plasma volume, levels of plasma atrial natriuretic factor and catecholamines, and the heart rate and its response to isoproterenol were unchanged in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antihypertensive contribution of sodium depletion and the sympathetic axis during chronic angiotensin II converting enzyme inhibition. 255 35

The physiological role of inactive renin, especially the question of whether and how a conversion to active renin takes place in vivo, remains controversial. In order to show the dynamic alterations from inactive to active renin following acute ACE-inhibition, both forms of renin were investigated in both renal veins and the peripheral circulation of 20 patients with essential hypertension and 20 patients with renovascular hypertension before and 1 h after 25 mg of captopril. Active and inactive renin were determined indirectly as plasma renin activity (PRA, unit: ng/ml x h). In vitro activation of inactive renin was achieved with trypsin (1 mg/ml plasma), followed by a further determination of PRA (= total renin). Subtraction of the active renin from the total renin yields the amount of inactive renin. In patients with essential hypertension, the mean values of active renin increase equally in both renal veins (1.4 and 1.3 before, 1.9 and 1.8 after captopril) and the peripheral circulation (0.9 and 1.3) (p less than 0.002), whereas the inactive renin decreases correspondingly. Renal veins: 7.6 and 8.2 before, 7.2 and 7.6 after captopril; peripheral circulation: 7.7 before and 7.0 after captopril (p less than 0.05). In all patients with renovascular hypertension, there is basally a marked lateralization of active renin (6.4 vs 3.5; p less than 0.01) and inactive renin (20.5 and 18.9, p less than 0.03) towards the side of the ischemic kidney. After captopril, the values for total renin and active renin increase (p less than 0.001), and the side difference for active renin becomes still more pronounced (33.0 vs 14.2; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Conversion of inactive renin to active renin following acute angiotensin converting enzyme inhibition in essential hypertension and renovascular hypertension]. 265 7


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