Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pharmacological effects of 1-Sar-8-Ile-angiotensin II on blood pressure and plasma renin activity (PRA) were studied in 5 normal subjects and in 19 patients with hypertension of various etiologics including malignant hypertension, renovascular hypertension, essential hypertension, and primary aldosteronism. Intravenous administration of this peptide induced a significant pressor response in normal or low PRA subjects at infusion rates of 100-600 ng/kg/min. Similar pressor response was also observed in renovascular hypertensives with normal PRA who were cured later by surgical treatment. The blood pressure in high PRA group was lowered remarkably by infusion of this angiotensin II inhibitor. A significant increase in PRA was obtained in subjects with malignant hypertension following the infusion of this peptide. However, there was no detectable rise in PRA in other subjects with normal or high PRA. The present data show that circulating angiotensin II plays an important role in maintaining high blood pressure in high PRA patients, especially in malignant hypertension, while it is not directly involved in the maintenance of high blood pressure in human chronic renovascular hypertension.
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PMID:Effects of 1-sarcosine-8-isoleucine-angiotensin II on blood pressure and plasma renin activity in various types of hypertension. 117 25

Renal hypertension can usually be recognized only by examining all the features of the hypertensive illness. On the other hand, the investigation of a case of hypertension whose genesis was previously unclear can lead to the diagnosis of a hitherto unrecognized renal disease. The blood pressure values found in patients with renal hypertension are of widely differing degrees of severity. Slight rises in blood pressure (e.g. 140/90 mm Hg), can be a sign of renal disease in adolescent patients. 10-15% of the cases of chronic renal hypertension develop into malignant hypertension. High diastolic values above 120 mm Hg without renal symptomatology and without reduced renal function speak against a primary renal cause of the rise in blood pressure. The finding of hypertension developing during the course of renal disease is, with respect to the hypertensive cardiovascular complications, just as important as in the case of essential hypertension. Complications which can occur during renal hypertension include cardiac insufficiency, hypertensive encephalopathy, retinopathy, hypertensive crises and acceleration of the renal disease.
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PMID:The clinical picture of renal hypertension. 119 21

Renal dysfunction as a consequence of malignant hypertension has been recognized for decades in patients with essential hypertension. It has been shown only recently, however, that albuminuria (including underlying albuminuria not detectable by conventional tests, i.e. microalbuminuria) has emerged as a frequent sequela of essential hypertension. Furthermore, renal dysfunction of the elderly as a result of ischemic nephropathy, in the absence of malignant hypertension, has turned out to be an important long-term outcome in the patient with essential hypertension. The presence of albuminuria is a strong predictor of cardiovascular events. Albuminuria is associated with more severe hypertension and with evidence of more advanced target organ damage (e.g. LVH). It is more prevalent in the elderly. It is unknown whether the predictive value of albuminuria reflects its association with more severe hypertension and end-organ damage, or whether albuminuria serves as an indicator of capillary leakiness which causes detectable abnormalities in the renal microcirculation but reflects more generalized endothelial barrier dysfunction predisposing to accelerated atherogenesis.
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PMID:Albuminuria of hypertensive patients. 129 7

Angiotensin-converting enzyme (ACE) inhibitors act by lowering the level of angiotensin II. The therapeutic benefits of these drugs and their potential side-effects therefore result from suppression of the physiological effects of angiotensin II. It is rational to prescribe an ACE inhibitor when the renin-angiotensin system is activated, as in renin-dependent essential hypertension, malignant hypertension and hypertension associated with heart failure. The beneficial effects of ACE inhibitor must be weighed against the special risks of renovascular hypertension: risk of renal artery thrombosis in case of unilateral stenosis and risk of renal failure if the stenosis is bilateral or affects a solitary kidney. In some situations the renin-angiotensin system is not directly involved in hypertension but may play a local haemodynamic role, as in some cases of primary or diabetic nephropathy. In such case the ACE inhibitors are thought to exert a protective effect. ACE inhibitors were reputed to be less effective in the elderly than in younger patients, but we now know that they can be prescribed with equal success in both instances to reduce peripheral resistance and improve regional blood flow as well as arterial compliance. Finally, ACE inhibitors can be prescribed, albeit with limited effectiveness, when the renin-angiotensin system is not activated, as in low renin hypertension and idiopathic hyperaldosteronism due to adrenal hyperplasia. They are ineffective in case of Conn's adenoma and contra-indicated in pregnant women.
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PMID:[For which hypertensive patient should angiotensin-converting enzyme inhibitor be prescribed or forbidden?]. 129 38

Eye-ground-photos were taken in twenty-eight previously untreated men with mild to moderate essential hypertension. The same eye was evaluated before and after 26 weeks of double-blind treatment with Enalapril or Hydrochlorothiazide. The vascular changes were assessed by using a more elaborate and refined grading than the Keith-Wagener-Barker scale. All photos were examined by the same observer without knowledge of blood pressure, type of treatment or the order in which the photos had been taken. There were significant positive correlations between the vascular alterations in the retina in the untreated state and left ventricular wall thickness (echocardiography), minimal vascular resistance in the calf (plethysmography) and blood pressure respectively. Treatment with Enalapril decreased the reflection of the retinal arterial wall significantly and reduced the narrowing of arteries and arterio-venous crossing phenomena non-significantly. Hydrochlorothiazide did not affect any of the retinal vascular changes. It can be concluded that this relatively simple technique of evaluating eye-ground-photos with a new grading scale, when used in non-malignant hypertension, gives a useful assessment of the degree of hypertensive target organ damage in the retina as well as in other important target organs, i.e. the heart and vascular beds. In addition, Enalapril positively affects hypertensive retinopathy in contrast to Hydrochlorothiazide, reflecting what happens to structural cardiovascular changes in the rest of the body.
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PMID:Hypertensive retinal vascular changes: relationship to left ventricular hypertrophy and arteriolar changes before and after treatment. 134 41

In many different clinical situations, including some cases of secondary hypertension, nighttime blood pressure (BP) is abnormally increased in the majority of patients, with consequent flattening of the 24-hour BP profile, but the clinical importance of this finding in such conditions is unknown. In patients with essential hypertension, ambulatory BP has been shown to decrease by 10-20% from day to night, but in severe or malignant hypertension this diurnal BP rhythm may be blunted or even abolished. One of the reasons why the noninvasive monitoring of BP may be a reliable tool in assessing the day-night BP changes is the demonstration that frequent cuff inflations do not interfere to a significant extent with the haemodynamic effects of sleep. Part of the differences between the studies in the reported day-night BP drop may be artifactual, owing to the very different time intervals defining the daytime and nighttime subperiods in the single studies. In unselected patients with essential hypertension, a sizable proportion of subjects (17 to 40%) shows abnormally high nighttime BP, with consequent flattening of the 24-hour BP profile (the so called "non dippers", as opposed to the "dippers" who show a maintained diurnal BP rhythm). Several clinical studies carried out in independent laboratories show that the target organ damage induced by hypertension (left ventricular hypertrophy, cerebrovascular lesions) is more severe in hypertensive "non dippers" than in "dippers", possibly because of the different duration of exposure to high BP levels over the 24 hours.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The day-night changes in ambulatory blood pressure: another risk indicator in hypertension?]. 147 64

The discovery and clinical availability of ACE inhibitor drugs is a triumph of rational drug development and a land-mark in biochemical pharmacology and hypertension research. The clinical pharmacological properties and haemodynamics of the clinically available drugs, captopril and enalapril, are reviewed, as is their therapeutic efficacy in African patients with essential and renal hypertension and chronic congestive heart failure. ACE inhibitors act as balanced arteriolar vasodilators and venular dilators and do not excite a reflex tachycardia in contrast to other vasodilator drugs. Their efficacy is, at least in part, dependent on plasma renin activity, which is low in Blacks and in Africans. Consistent with this, is the poor response to ACE inhibitor monotherapy of essential hypertension in controlled studies in Africans. However, the compensatory neuroendocrine activation which occurs in malignant hypertension, renal failure and congestive heart failure and concurrent diuretic therapy appears to enhance the clinical response to ACE inhibitors in African patients.
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PMID:Angiotensin converting enzyme inhibitors in cardiovascular and renal disease in Africans: a review. 190 20

We reviewed the data of 3,632 patients with end-stage renal failure entered into the South African Dialysis and Transplantation Registry over a six-year period. The male to female ratio was 1.4:1. Of these patients, 48.8% were white, 26.2% black, 17.6% coloured and 7.4% Asian. Essential hypertension was the cause of end-stage renal failure in 15.9% of patients. Malignant hypertension was the diagnosis in 57% of the essential hypertensives. Hypertension was responsible for 34.6% of end-stage renal failure in blacks, 20.9% in coloureds, 4.3% in whites and 13.8% in Asians. In the age group 30-39 years, 37.4% of patients with malignant hypertension commenced dialysis, while 28.4% and 28.8% of benign hypertensives commenced dialysis in the 30-39 and 40-49 age groups, respectively. The survival at 36 and 72 months was the same whether hypertension was the cause of end-stage renal failure or not, and whether the hypertension was malignant or benign. Cardiac causes were responsible for most of the deaths. The percentage of deaths from cardiac causes was similar in patients with renal failure from essential hypertension and other causes (33.2% and 29.3% respectively). Hypertension is the commonest cause of end-stage renal failure in black South Africans and the most common preventable cause of end-stage kidney disease in the country.
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PMID:Hypertension as a cause of end-stage renal failure in South Africa. 225 79

The role of vasopressin in human hypertension was examined in a series of studies. In patients with primary hyperaldosteronism and benign essential hypertension, circulating vasopressin was generally lower than in normotensive subjects. In contrast, plasma vasopressin was increased (p less than 0.001) in patients with malignant-phase hypertension. However, compared to infused vasopressin in normal subjects, when plasma levels of up to 120 pg/ml did not affect blood pressure, the increased levels found in malignant hypertension could not account for the hypertension. The possibility that there may be an increased pressor sensitivity to vasopressin in hypertension was examined by infusing the peptide into nine patients with essential hypertension. This showed a slight increase in sensitivity compared to normotensive subjects, but again this was insufficient to account for the discrepancy between the circulating level of vasopressin and the extent of the raised blood pressure in the hypertensive patients. The effect of chronically elevated levels of vasopressin was studied in a group of patients with the syndrome of inappropriate ADH excess as a consequence of bronchogenic carcinoma. In spite of having chronically elevated levels of vasopressin, these patients had normal blood pressures for their age and sex. Our results suggest that, although vasopressin is elevated in malignant hypertension, it does not contribute significantly to the raised blood pressure, and its increase is probably a consequence of volume shrinkage through renal salt and water loss.
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PMID:Vasopressin and hypertension in man. 243 62

A 3-fold higher concentration of "endogenous digitalis" is found in the serum of patients with essential hypertension than in the serum of normotensives, whose concentration was determined in 22 normotensive probands by an receptor assay using isolated (Na+ + K+)-ATPase as 76.3 +/- 9.3 nM ouabain equivalents. Since the concentration of "endogenous digitalis" was 7-19 fold higher in 2 patients, who had become uremic due to a malignant hypertension and since their serum levels fell 3-fold by hemodialysis, the hemofiltrate was used for partial purification of the substance. This was possible by hydrophobic chromatography on Amberlite XAD-2, octadecyl-coated silica gel, anion exchange chromatography and affinity chromatography on membrane-bound (Na+ + K+)-ATPase. The partially purified substance behaved like the material described by Cloix et al. (1985) Biochem. Biophys. Res. Commun. 131:1234-1240 and competed with digoxin for digoxin antibodies. Ascorbic acid isolated on the search for an inhibitor of (Na+ + K+)-ATPase from beef brain inhibited [3H]ouabain binding due to a decrease of the ouabain binding sites by a reduction of a group within the ATP binding site of the enzyme. Unsaturated fatty acids claimed to be "endogenous digitalis (Tamura et al. [1985] J. Biol. Chem. 260:9672-9677)" also lowered the capacity of the cardiac glycoside binding site but did not compete with ouabain.
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PMID:Sodium pump inhibitor in the serum of patients with essential hypertension and its partial purification from hemofiltrate. 243 45


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