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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The treatment of high blood pressure prevents death from congestive heart failure, hypertensive nephropathy, and encephalopathy, and strokes from cerebral arteriolar disease (lacunes, hemorrhage from microaneurysms). However, atherosclerosis, manifested as coronary artery disease is just as frequent a cause of death in well-controlled hypertensives as in poorly-controlled patients. Increasing evidence suggests that increased blood velocity, by causing turbulence and high shear rates at the endothelial surface of arteries, may be important in the pathogenesis of atherosclerosis. Turbulence has been observed in cerebral berry aneurysms. In order to measure the effects of antihypertensive agents on blood velocity, a new method of analysing Doppler ultrasound velocity recordings has been developed. Studies in Rhesus monkeys show the following: In doses which reduce diastolic pressure by 13-28%, propranolol decreased mean blood velocity (MV) by 17%, clonidine decreased MV by 14%, while methyldopa increased MV 12%, and hydralazine increased MV by 52%. (p less than .00001). It is hypothesized that enlargement of berry aneurysms, the progression of cerebral atherosclerosis, and embolism from carotid lesions might all be decreased by the selection of antihypertensive agents which decrease blood velocity.
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PMID:Effects of antihypertensive drugs on blood velocity: implications for prevention of cerebral vascular disease. 40 9

Eleven patients with hypertension secondary to renal disease were treated with hydrochlorothiazide or furosemide plus other drugs to normalize blood pressure. Creatinine clearance fell during the initial treatment period, but then either remained constant or rose toward pretreatment levels in spite of continued therapy. Plasma renin activity was low-normal to subnormal in eight of the 11 patients prior to therapy and did not rise significantly with therapy. Aldosterone excretion was within the normal range prior to treatment and remained normal or increased moderately with treatment. This study demonstrates that diuretics effectively reduce blood pressure in patients with hypertension secondary to renal disease without producing severe volume depletion or clinically significant reduction in renal function. The low renin levels are consistent with other evidence that hypertension in these patients is related to salt and water retention.
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PMID:Use of diuretics in treatment of hypertension secondary to renal disease. 70 75

Urinary excretion of tissue kallikrein is reduced in essential hypertension. Although a similar finding has been reported in spontaneously hypertensive rats (SHR), only a few studies have been concerned with the amount of enzyme within the kidney both at the time of onset and during progression of the hypertension. We have performed an ontogenic study on the renal parenchymal values and immunoreactivity of tissue kallikrein in Okamoto SHR aged 4-78 weeks. Additionally, these two parameters were analysed in human biopsies taken from patients with hypertensive nephropathy. The enzymatic activity of renal tissue kallikrein (active and total; specifically antagonized by anti-tissue kallikrein antibodies), increased from 4 to 52 weeks in SHR when compared to normotensive Wistar Kyoto (WKY) rats; this increase was associated with a significant increase in blood pressure. In contrast, 78 weeks SHR and human biopsy tissue showed a substantial reduction in tissue kallikrein values. Also, both renal tissues showed a reduction in immunoreactivity in the cells of the connecting tubules that specifically store the enzyme. In advanced hypertension the observed reduction in tissue kallikrein was probably secondary to a loss of distal tubular mass, as a result of tubular atrophy and fibrosis. The greater values for renal tissue kallikrein in the kidney and reported reduced urinary excretion during the early phases of spontaneous hypertension may be explained by a primary defect in the mechanisms that regulate release of tissue kallikrein from the connecting tubule cells.
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PMID:An ontogenic study of renal tissue kallikrein in Okamoto spontaneously hypertensive rats: comparisons with human hypertensive nephropathy. 132 Feb 31

It is well known that hypertension (HT) is frequently accompanied with diabetic nephropathy (DN) and that HT contributes to progression of DN. Thus, proper anti-hypertensive therapy is required in hypertensive patients with DN. However, there is so far no consensus of optimal blood pressure (BP) level to maintain the renal function in these patients. In order to evaluate the optimal BP level in the patients with renal insufficiency, we investigated the relation between BP and renal function in 15 DN patients with HT (aged 56.9 +/- 11.7 years at the first medical examination; 6 male and 9 female, total 117 patient-years) and 20 patients with hypertensive nephropathy (aged 44.3 +/- 13.0 years at the first medical examination; 17 male and 3 female, total 207.5 patient-years) as the control, who receive antihypertensive therapy for more than 4 years as outpatients at the second department of internal medicine of Tohoku University Hospital between 1974 and 1990. During this period 7 patients with DN came to receive hemodialysis therapy 2 to 6 (average 3.8 +/- 1.3) years after the first medical examination. As a result, in patients with hypertensive nephropathy, there was a tendency to show that the lower the mean BP was, the better the renal function. On the contrary, in DN patients there was an optimal mean BP (MBP) range; i.e, when MBP was controlled in this range, the deterioration rate of renal function was delayed, while deviation of MBP from this range made the renal function worse (p less than 0.01). However, this range varied with the serum creatinine (SCr) concentration level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The treatment of hypertensive patients with renal insufficiency--a comparison of the blood pressure management in patients with diabetic nephropathy and patients with hypertensive nephropathy]. 177 Jun 21

Casual blood pressure does not provide an adequate estimation for the hemodynamic load of 24 hours upon the cardiovascular system. Hence, cardiovascular complications are loosely correlated to casual blood pressure measurements in arterial hypertension. In contrast, ambulatory blood pressure measurements have been repeatedly found to be closely related to signs of target organ damage such as left ventricular hypertrophy, hypertensive nephropathy and impaired arterial compliance. Furthermore, monitoring of blood pressure over 24 hours allows assessment of hazardous nocturnal declines in perfusion pressure with the risk of fatal coronary or cerebrovascular events. A blunted nocturnal decline in blood pressure has been suggested to indicate secondary forms of arterial hypertension or severe hypertensive disease. In conclusion, ambulatory blood pressure monitoring, nowadays reliably assessed by non-invasive tools, improves the estimation of the hemodynamic load imposed on the cardiovascular system and thereby the risks attributed to arterial hypertension.
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PMID:[Importance of 24-hour blood pressure monitoring in detection of hypertension-induced end organ damage]. 202 33

Ketanserin is a 5-HT2 antagonist with alpha-adrenoreceptor blocking activity. This study examines the efficacy and safety of ketanserin in the control of severe primary and secondary hypertension, including renal hypertension. Patients with uncontrolled hypertension were admitted to hospital and entered the study if the supine diastolic blood pressure phase V (SDBP) was greater than 110 mm Hg after 2 h continuous BP monitoring (Dynamap). Ketanserin was administered as an intravenous (i.v.) 5 mg bolus every 60 s until SDBP fell greater than 15 mm Hg or maximum dose (30 mg) was reached, then by i.v. infusion at 4-20 mg/h to maintain SDBP fall greater than 15 mm Hg over 6 h. Twenty five patients were monitored and 20 (seven men, 13 women, ages 14-65 years) fulfilled the entry criteria. Seventeen of 20 were on antihypertensive medication, and 14 had underlying renal disease. Preinjection mean BP was 188/123 mm Hg for the 20 patients, falling at 5 min to 175/103 mm Hg. Supine diastolic blood pressure fell greater than 15 mm Hg in 16 of 20 patients. In these patients, BP remained satisfactorily controlled over the 6-h ketanserin infusion. Heart rate was unchanged. The four patients who did not respond were receiving the alpha-blocker prazosin, but seven other patients on high-dose prazosin did respond. We conclude that i.v. ketanserin is effective in the acute management of severe hypertension, including hypertension secondary to renal disease.
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PMID:Ketanserin in the acute management of severe hypertension. 241 44

Sodium-lithium countertransport (Na-Li CT) has been reported to be increased in essential hypertension (EHT) but the nature and degree of distinction from normal controls in unclear. Of 44 unselected patients with EHT in the hospital hypertension clinic 36% had Na-Li CT greater than the normal control range and 70% of these had a family history of hypertension. Almost all the patients with normal Na-Li CT had no family history of hypertension. Analysis of variance showed that raised Na-Li CT was related to both a family history of hypertension and a family history of a cardiovascular event. Of 23 patients with hypertension secondary to renal disease, 43% had Na-Li CT greater than the normal control range and raised Na-Li CT was related to both a family history of hypertension and a family history of cardiovascular event in the same way as EHT. Raised Na-Li CT was not characteristic of EHT but identified a subgroup of patients with EHT and a family history of hypertension, some of whom also had renal disease.
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PMID:Erythrocyte sodium-lithium countertransport in primary and renal hypertension: relation to family history. 249 56

Chronic lead exposure resulting in blood lead concentrations that exceed 1.93 mumol/l (40 micrograms/dl) or chelatable urinary lead excretion greater than 3.14 mumol (650 micrograms) per 72 h has been associated with renal disease. A previous study had found greater chelatable urine lead excretion in subjects with hypertension and renal failure than in controls with renal failure due to other causes, although mean blood lead concentrations averaged 0.92 mumol/l (19 micrograms/dl). To determine if chelatable urinary lead, blood lead, or the hematologic effect of lead (zinc protoporphyrin) were greater in hypertensive nephropathy (when hypertension precedes elevation of serum creatinine) than in other forms of mild renal failure, we compared 40 study subjects with hypertensive nephropathy to 24 controls having a similar degree of renal dysfunction due to causes other than hypertension. Lead burdens were similar in both the study and control groups as assessed by 72-h chelatable urinary lead excretion after intramuscular injection of calcium disodium EDTA (0.74 +/- 0.63 vs. 0.61 +/- 0.40 mumol per 72 h, respectively), and by blood lead (0.35 +/- 0.23 vs. 0.35 +/- 0.20 mumol/l). We conclude that subjects from a general population with hypertensive nephropathy do not have greater body burdens of lead than renal failure controls.
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PMID:Body burdens of lead in hypertensive nephropathy. 251 Jun 13

The effects of monotherapy with nicardipine, 20 mg three times a day, have been investigated in a 1-year study of 26 elderly (greater than 60 years) patients with hypertension with various types of renal dysfunction and seven without renal dysfunction. Parameters measured included blood pressure, blood chemistry (serum creatinine, uric acid, blood urea nitrogen, blood glucose total cholesterol, and electrolytes), plasma renin activity, and plasma aldosterone concentration. Nicardipine was effective in reducing blood pressure in all patients with diabetic nephropathy, parenchymal renal diseases, or hypertensive nephropathy, and in those without renal dysfunction. Serum creatinine and blood urea nitrogen levels were slightly elevated in some patients whose pretreatment serum creatinine level was greater than 2 mg/dl, regardless of the type of nephropathy. However, it was not determined whether this effect was the result of a reduction in blood pressure induced by nicardipine. Serum sodium, potassium, total cholesterol, and blood glucose levels were unchanged by the administration of nicardipine. Changes in plasma renin activity and aldosterone levels were not significant. These results suggest that nicardipine can be used safely in elderly patients with hypertension with renal dysfunction, regardless of the type of nephropathy.
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PMID:Effects of nicardipine on blood pressure and renal function in elderly hypertensive patients with renal dysfunction. 264 83

Heavy proteinuria in patients with essential hypertension raises the question of underlying primary renal disease. While malignant hypertension may be associated with proteinuria in the nephrotic range, it is generally held that protein excretion in benign nephrosclerosis is almost invariably less than 0.5-1.0 g/24 h. We report 18 patients with biopsy-proven hypertensive nephropathy and heavy proteinuria, of which only 6 had malignant hypertension. In the remaining 12 patients with benign nephrosclerosis, protein excretion reached up to 6.5 g/24 h, and nephrotic range proteinuria was present in 3 patients. All patients with heavy proteinuria suffered from long-standing moderate or severe, poorly controlled hypertension and were azotemic. We suggest that hypertensive nephrosclerosis be included in the differential diagnosis of massive proteinuria accompanying azotemia in poorly controlled hypertensives.
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PMID:Marked proteinuria in hypertensive nephrosclerosis. 316 Feb 40


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