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)

Although free and conjugated dopamine (DA) constitute most of the plasma and urine catecholamine pool, the diagnostic significance of DA estimation for the evaluation of illness is not clear. We evaluated the clinical utility of DA estimation by measuring free and conjugated DA in patients with various illness. Patients with adrenal insufficiency did not show decreases in DA concentrations but did demonstrate reductions in free and conjugated plasma adrenaline (Ad). Patients with established stage of essential hypertension exhibited decreased plasma concentrations of free and conjugated DA, although they were hyperadrenergic. In patients with chronic renal insufficiency and failure, the free DA concentration in the urine decreased depending on the severity of renal impairment. Conversely, plasma concentrations of conjugated DA are higher in patients with chronic renal failure than in normal subjects. The high plasma concentrations of conjugated DA decreased dramatically following hemodialysis and renal transplantation. Urinary free DA excretion increased markedly following renal transplantation. In conclusion, the estimation of the free and conjugated DA in plasma and urine is clinically useful for the diagnosis of adrenal insufficiency, essential hypertension, and renal insufficiency and failure. It also can be used to monitor the effectiveness of hemodialysis and renal transplantation.
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PMID:Diagnostic significance of dopamine estimation using plasma and urine in patients with adrenal and renal insufficiency, renal transplantation and hypertension. 852 80

It is now well-established in experimental models in rodents that increased glomerular pressure results in the development of focal and segmental glomerulosclerosis, proteinuria and progressive renal functional deterioration. In humans, direct measurement of glomerular capillary pressure is impossible. However, it is widely accepted that glomerular hypertension is present in different clinical situations, like diabetic nephropathy, chronic renal failure associated with glomerulonephritides, some forms of essential hypertension and cadaveric kidney transplantation. Many studies were performed on the effects of protein-restricted died and/or angiotensin converting enzyme inhibition on the rate of progression of renal failure in these renal diseases. Although controversial, the overall results suggest that these therapeutic strategies may reduce the rate of progression, particularly in diabetic nephropathy.
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PMID:[Intraglomerular hypertension. Physiopathology and therapeutic implications]. 868 50

Positive correlation between blood pressure and insulin is well established in patients with essential hypertension. The aim of the present study was to examine the relationship between fasting plasma insulin level and ambulatory blood pressure (ABPM) in patients with chronic renal failure. The study group consisted of 20 patients (11 females, 9 males, mean age 39 +/- 12 years) on chronic haemodialysis (mean 2.5 years). Fasting plasma insulin (FPI) was measured by radioimmunoassay. The patients were investigated before and after haemodialysis. FPI significantly increased after haemodialysis from 18.4 +/- 12.0 to 40.1 +/- 31.9 mIU/l (p < 0.01), while creatinine concentration decreased from 1158 +/- 130 to 910 +/- 159 mumol/l (p < 0.001). Night-time systolic blood pressure (SBP) was significantly lower during the day of haemodialysis (141.9 +/- 19.6 mmHg vs. 136 +/- 27.7 mmHg, p < 0.05). 24-hour and daytime SBP was nonsignificantly lower after haemodialysis. 24-hour diastolic blood pressure (DBP) was significantly lower during the day of haemodialysis (92.9 +/- 12.5 mmHg vs. 87.3 +/- 14.3 mmHg, p < 0.05), as well as daytime (94.9 +/- 12.1 mmHg vs. 88.8 +/- 14.6 p < 0.05) and night-time DBP (88.9 +/- 16.0 mmHg vs. 83.8 +/- 17.4 mmHg p < 0.05). FPI was found to be significantly negatively correlated with 24-hour, daytime and night-time SBP on the day of haemodialysis (r = -0.63, p < 0.005; r = 0.64, (p < 0.005 and r = -0.54, p < 0.05, respectively). The significant negative correlation between FPI and 24-hour SBP suggests that insulin could reveal its hypotensive effect after the haemodialysis.
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PMID:[Significant negative correlation between fasting plasma insulin and ambulatory blood pressure in patients on chronic hemodialysis]. 875 39

Obstructive sleep apnea (OSA) is a disorder in which there is repetitive collapse and closing of the pharynx during sleep. There is growing evidence to suggest that this disorder is a major cause of essential hypertension (EH) and that successful treatment of OSA can reduce the blood pressure (BP) significantly. In addition many other patients with EH have milder forms of sleep related breathing disorders (SRBD) like snoring, and upper airway resistance syndrome (UARS) which, while not as severe as OSA, may be severe enough to also cause systemic hypertension. We therefore propose a unifying hypothesis-that many patients with EH may have sleep related breathing disturbances (SRBD) and treatment of these disorders may improve the BP. SRBD could also explain many of the epidemiological, clinical, hereditary, biochemical, hematological and physiological characteristics seen in EH. In addition, many types of secondary hypertension (those caused by excessive alcohol intake, chronic renal failure, diabetes, hypothyroidism or acromegaly) have a higher than normal prevalence of OSA and OSA may contribute to the hypertension and organ damage found in these conditions as well. Thus SRBD may play an important role in the production of many cases of essential and secondary hypertension, and their early detection and treatment could reduce the hypertension and organ damage seen in these conditions.
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PMID:Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis. 887 97

The factors that initiate chronic renal failure in patients with hypertension, diabetes mellitus, and chronic glomerular disease are largely unknown. The likely genetic contribution to ESRD, particularly in African Americans, suggests that linkage analysis may be useful to evaluate the role of candidate genes in the pathogenesis of chronic renal failure. The renin-angiotensin-aldosterone (RAA) axis has been intensively evaluated for its contribution to cardiovascular disease and nephropathy. This study tested for linkage between candidate genes in the RAA axis and chronic renal failure, using 85 African-American sibling pairs (from 65 families) concordant for ESRD. Angiotensinogen was selected because of the putative link between it and mild to moderate essential hypertension and nephrosclerosis; angiotensin-converting enzyme because of its possible contribution to diabetic nephropathy; and renin, the angiotensin II receptor, and kallikrein because of their roles in hypertension and renal perfusion. These candidate loci did not demonstrate linkage to either diabetic or nondiabetic renal disease in this study's collection of sibling pairs. These results suggest that polymorphisms at these RAA axis loci do not make major contributions to the pathogenesis of renal disease in African Americans.
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PMID:Linkage analysis between loci in the renin-angiotensin axis and end-stage renal disease in African Americans. 898 34

1. Adrenomedullin is a potent vasodilating peptide first isolated from phaeochromocytoma and adrenal medulla but also found in the heart, lungs and kidneys. It may also be a paracrine factor because endothelial and smooth muscle cells synthesize adrenomedullin as well as express the receptors. Adrenomedullin induces vasorelaxation by activating adenylate cyclase and also by stimulating the release of nitric oxide. 2. We have developed a specific radioimmunoassay and measured the immunoreactivity of human adrenomedullin in the plasma of 58 male subjects: eight with essential hypertension, 12 with heart failure, 10 with ascites due to cirrhosis, 12 with chronic renal failure, four with hypoxia due to chronic obstructive pulmonary disease and 12 control subjects. 3. Plasma levels (mean +/- SEM) in patients with essential hypertension (16.3 +/- 1.9 pmol/l), congestive heart failure (17.5 +/- 2.8 pmol/l) and renal failure (17.7 +/- 2.5 pmol/l) were raised compared with control subjects (7.8 +/- 1.4 pmol/l, P < 0.05), confirming previous reports. 4. In addition, we observed that plasma levels of adrenomedullin were significantly raised in patients with ascites due to liver cirrhosis (15.5 +/- 1.9 pmol/l) and chronic obstructive pulmonary disease with hypoxia (20.0 +/- 1.5 pmol/l). 5. We concluded that the plasma level of adrenomedullin is raised in a variety of diseases.
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PMID:Elevated plasma levels of human adrenomedullin in cardiovascular, respiratory, hepatic and renal disorders. 903 92

Low intracellular free magnesium concentrations ([Mg2+]i) are associated with essential hypertension and may reflect a disordered cellular ionic environment. 31P magnetic resonance spectroscopy was used to study skeletal muscle [Mg2+]i in a group of chronic renal failure (CRF) patients and data were compared with a group of control subjects of similar age. Other data including the patients' blood pressure, medication and plasma biochemistry were collected. There was a significant inverse correlation of [Mg2+]i with systolic (p < 0.001) and diastolic blood pressure (p < 0.05) in the CRF population. In CRF [Mg2+]i was similar (0.52 +/- 0.01 mM, SEM) to controls (0.53 +/- 0.01 mM; p = 0.20), even if just the normotensive patients and controls were compared. There was no correlation of [Mg2+]i with plasma parathyroid hormone, total [Mg2+] or [Ca2+]. Similar to studies in subjects with essential hypertension, these data support a role for [Mg2+]i specifically, and an abnormal intracellular environment more generally, in the pathophysiology of hypertension in CRF.
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PMID:Intracellular free magnesium concentrations in skeletal muscle in chronic uraemia. 917 Dec 95

1. Increased affinity for sodium (Km) at an external site of the sodium-lithium countertransporter and altered membrane microviscosity in the surface regions of the lipid bilayer identifies a group of essential hypertensive patients with a genetic predisposition to hypertension. The present study investigated the kinetic properties of the sodium-lithium countertransporter and membrane microviscosity in patients with hypertension, renal disease and impaired renal function. 2. Sixty patients with renal disease (28 chronic renal failure, 30 hypertensive, 23 family history of hypertension) were investigated. Standard erythrocyte sodium-lithium countertransport activity, sodium affinity constant (Km), maximum reaction velocity (Vmax) and membrane microviscosity were measured. 3. Patients with renal disease and a family history of hypertension had significantly lower Km (P < 0.05) values and raised membrane microviscosity measured by 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene anisotropy (P < 0.05) compared with patients without a family history of hypertension. 4. Uraemic subjects had low K(m) values compared with patients with renal disease and normal renal function (P < 0.05). However, there was no significant difference in membrane microviscosity between uraemic and non-uraemic subjects. 5. In patients with a family history of hypertension, sodium-lithium countertransport activity and 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene anisotropy are important markers of cellular changes in essential hypertension, independent of renal disease. Uraemia, independently of hypertension, produces an alteration in the function of the sodium-lithium countertransporter which has previously been associated with a genetic predisposition to hypertension and cardiovascular disease.
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PMID:Raised affinity for extracellular sodium of the sodium-lithium countertransporter is associated with a family history of hypertension and uraemia in patients with renal disease. 917 24

The prevalence and natural history of severe proteinuria in mild to moderate hypertension are not completely defined. We screened 1635 men with a history of hypertension and randomized 1292 with untreated diastolic blood pressure (DBP) 95-109 mmHg to single-drug treatment with either hydrochlorothiazide, atenolol, captopril, clonidine, diltiazem-SR, prazosin, or placebo in a double-blind prospective trial. Twenty-seven of 1635 patients (1.7%) satisfying clinical criteria for primary hypertension were found to have developed proteinuria > 1000 mg/24 hours and were removed from the study. Follow-up data were obtained on 19 of these 27 patients. One patient was found to have focal segmental sclerosis and progressed to end-stage renal disease. Three other patients developed severe (serum creatinine > 3.5 mg/dl) chronic renal failure (one with diabetic nephropathy), one progressed from serum creatinine 1.4 to 2.2 mg/dl, but 14 of the 19 remained with stable serum creatinine < 2.0 mg/dl on follow-up for 6-9 years. Data were available for 1076 of 1155 (93%) treated study patients at end titration, 522/600 (87%) at one year and 322/444 (73%) at two years. There were significant associations for proteinuria with obesity and higher systolic blood pressure. There was a trend toward significant difference in mean 24-hour protein excretion rates at baseline between black (127 mg) and white (139 mg) patients (p = 0.07). There were no statistically significant changes in urinary protein excretion/24 hours between or within the different treatment groups (including placebo). Eighteen patients were removed from the study during the active treatment phase for proteinuria > 1000 mg/24 hours: hydrochlorothiazide 4, placebo 3, diltiazem 3, prazosin 3, atenolol 2, clonidine 2, and captopril 1. We conclude: (1) the prevalence of severe (> 1 g/24 hours) proteinuria in the hypertensive population is significant but does not necessarily imply a poor prognosis; (2) mean 24-hour urinary protein excretion rates did not vary in response to the different classes of antihypertensive drugs; and (3) there was no drug-specific increase in proteinuria detected in this study.
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PMID:Proteinuria in mild to moderate hypertension: results of the VA cooperative study of six antihypertensive agents and placebo. Department of Veterans Affairs Cooperative Study Group on Antihypertensive Agents. 918 Dec 78

GENETIC DISEASE MODELS: A certain proportion of hypertension cases are due to renal disease. Recent advances in genetics has improved our knowledge of the pathophysiological mechanisms involved in certain rare diseases including apparent overproduction of mineralocorticoids, Liddle syndrome and Gitelman syndrome, and to hypothesize on the mechanism of primary hypertension. EFFECT ON PROGNOSIS: Onset of renal disease in hypertensive patients, whether expressed by proteinuria or the early stages of renal failure, worsens cardiovascular prognosis. FREQUENCY OF RENAL DISEASE: Renal disease is relatively rare in hypertensive patients, but as the general hypertensive population becomes older, there is a considerable rise in the prevalence of hypertensive renal disease as the underlying cause leading to dialysis. The risk of progressing to renal failure appears to be related to the level of the blood pressure, especially systolic pressure, at disease onset. Hypertension black subjects have a higher risk of developing chronic renal failure. THERAPEUTIC BENEFIT: Several studies have shown that lowering blood pressure with antihypertensive drugs lowers the risk progressing with primary hypertension.
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PMID:[Renal involvement in essential arterial hypertension]. 920 91


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