| For medical practitioners and the general public - High Blood Pressure Journal Article Catalog. |
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| High blood pressure maintaining mechanisms in chronic one-kidney, one clip and two-kidney, one clip hypertensive rats. I. Roles of the renin-angiotensin, kallikrein-kinin and prostaglandin systems Hashimoto, H. (1983), Nippon Jinzo Gakkai Shi 25(2): 143-51. |
| High blood pressure maintaining mechanisms in chronic one-kidney, one clip and two-kidney, one clip hypertensive rats. II. Roles of the sympathetic nervous system and renin-angiotensin system Hashimoto, H. (1983), Nippon Jinzo Gakkai Shi 25(2): 153-61. |
| High blood pressure maintenance in transgenic mRen-2 vs. Lyon genetically hypertensive rats Lo, M., I. A. Medeiros, et al. (1993), Am J Physiol 265(1 Pt 2): R180-6. Abstract: The present work was aimed to assess the factors involved in the maintenance of hypertension in adult transgenic mRen-2 (TG) rats. Special attention was paid to the renal handling of sodium, the sympathetic, and the renin-angiotensin system (RAS) activity. TG rats were compared with age-matched Lyon genetically hypertensive rats (LH), as both are of Sprague-Dawley origin. Blood pressure (BP), heart rate, and renal sympathetic nerve activity (RSNA) were recorded in conscious freely moving animals. Kidneys were isolated and single-pass perfused at different pressure levels. It was observed that the peripheral sympathetic drive was identical in TG and LH rats as indicated by their similar 24-h urinary excretion of catecholamines and methoxylated metabolites, baseline RSNA and its control by the baroreflex, and hypotensive response to ganglion-blockade. On the contrary, TG rats differed from LH rats by a more rapid excretion of an oral isotonic sodium load, a greater hypotensive and natriuretic response to furosemide, and a more marked BP response to acute RAS blockade. The TG kidney responses to stepwise changes in renal perfusion pressure (RPP) differed from those of LH rats by significantly higher perfusate flow and glomerular filtration rate. However, the pressure natriuresis curve of TG kidneys did not differ from that of LH rats because of an elevated tubular sodium reabsorption rate. These results suggest that adult TG rats, compared with LH rats, exhibit a tendency toward sodium and water retention, which may explain that despite low renal and circulating renin levels, the RAS remains involved in the maintenance of high BP in that model. |
| High blood pressure management: potential benefits of I1 agents Esler, M. (1998), J Hypertens Suppl 16(3): S19-24. Abstract: SYMPATHETIC NERVOUS SYSTEM AND HYPERTENSION: Biochemical, electrophysiological, pharmacological and haemodynamic findings support the existence of sympathetic nervous system activation in primary human hypertension. Analysis of regional sympathetic nervous system function, using both neurophysiological methods for measuring sympathetic nerve firing rates, and neurochemical techniques for quantifying regional noradrenaline spillover to plasma has demonstrated activation of the sympathetic nervous outflows to the heart, the kidneys, and skeletal muscle vasculature, particularly in younger patients. The initiating cause of this sympathetic nervous stimulation is unknown, but estimation of central nervous system noradrenaline turnover in hypertensive patients, using measurements of the washout of noradrenaline and its lipophilic metabolites into the internal jugular veins, indicates that activation of forebrain pressor noradrenergic nuclei is the probable underlying mechanism. CONSEQUENCES OF INCREASED SYMPATHETIC ACTIVITY: The sympathetic activation present in human hypertension no doubt contributes to the blood pressure elevation, and is a legitimate target for therapeutic intervention with imidazoline receptor-binding agents such as rilmenidine. In addition, the sympathetic nervous activation seems to have adverse consequences in hypertensive patients beyond initiating the blood pressure elevation. There is evidence that neural vasoconstriction has metabolic effects, in skeletal muscle impairing glucose delivery to muscle, causing insulin resistance and hyperinsulinaemia, and in liver retarding postprandial clearing of lipids, contributing to hyperlipidaemia. Cardiac sympathetic activation is demonstrably a cause of sudden death in heart failure patients; a comparable arrhythmogenic effect is probable in hypertension. A trophic effect of sympathetic activation on cardiovascular growth is also likely, contributing to the development of left ventricular hypertrophy. Rilmenidine, through its central nervous system actions, has been demonstrated to powerfully reduce sympathetic nervous activity in essential hypertension patients. INHIBITING THE SYMPATHETIC SYSTEM: As the clinical consequences of sympathetic nervous activation in essential hypertension appear to go beyond that of hypertension pathogenesis, extending to a causal influence in atherosclerosis development, cardiovascular hypertrophy and cardiac arrhythmias, it is possible that, of all antihypertensive drugs, those inhibiting the sympathetic nervous system might best reduce cardiovascular risk. This remains to be tested. |
| High blood pressure of hypertriglyceridaemic rats is related to metabolic disturbances Kunes, J., Z. Dobesova, et al. (1995), Physiol Res 44(6): 421-4. Abstract: A set of 131 F2 hybrids, obtained from a cross between normotensive Lewis and hypertensive hypertriglyceridaemic (HTG) rats, was studied in order to assess the relationship between blood pressure, plasma triglycerides and plasma uric acid. In progenitors, the plasma levels of triglycerides and uric acid were twice as high in HTG rats than in the Lewis rats. It was observed in the F2 cohort that high mean arterial pressure (MAP) was unrelated to body weight and relative heart or kidney weights. On the other hand, there were significant correlations between MAP and plasma triglycerides (r = 0.420, n = 131, p < 0.0001) and between MAP and plasma uric acid (r = 0.325, p < 0.001). Plasma triglycerides of F2 hybrids were below the midparental values, suggesting a stronger influence of normotensive Lewis alleles. In conclusion, hypertension in hypertriglyceridaemic rats strongly cosegregated with plasma triglycerides and plasma uric acid. Our results indicated a linkage between high blood pressure and several metabolic alterations characteristic for the X syndrome. |
| High blood pressure reduction reverses angiotensin II type 2 receptor-mediated vasoconstriction into vasodilation in spontaneously hypertensive rats You, D., L. Loufrani, et al. (2005), Circulation 111(8): 1006-11. Abstract: BACKGROUND: We have previously shown that angiotensin II type 2 receptor (AT(2)R) stimulation causes endothelium-dependent vasodilation that does not desensitize after chronic angiotensin II type 1 receptor (AT1R) blockade, suggesting a role for AT2R in antihypertensive treatment. METHODS AND RESULTS: We recorded mean arterial pressure (MAP) and investigated AT2R by Western blot analysis, immunohistochemistry, and function in isolated mesenteric resistance arteries (205 microm in diameter) from Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) receiving the following for 4 weeks in drinking water: placebo, AT1R blockade (candesartan; 2 mg/kg per day), ACE inhibitor (perindopril; 3 mg/kg per day), nonselective vasodilator (hydralazine; 16 or 24 mg/kg per day), or candesartan plus hydralazine (16 mg/kg per day). In precontracted isolated arteries, AT2R stimulation (angiotensin II in the presence of candesartan) caused vasodilation in WKY rats (MAP=118 mm Hg) and vasoconstriction in SHR (MAP=183 mm Hg). In SHR treated with candesartan (MAP=146 mm Hg) or hydralazine (16 mg/kg per day; MAP=145 mm Hg), AT2R-induced contraction was reduced by 50%. In SHR treated with perindopril (MAP=125 mm Hg), AT2R stimulation induced vasodilation. In SHR treated with hydralazine (24 mg/kg per day; MAP=105 mm Hg) and in SHR treated with hydralazine (16 mg/kg per day) plus candesartan (MAP=102 mm Hg), an AT2R-mediated vasodilation was restored. Immunochemistry and Western blot analysis showed that AT2R expression, lower in SHR than in WKY rats, was restored to normal levels by treatments reducing arterial pressure in SHR. CONCLUSIONS: Our results suggest that in resistance arteries of SHR, (1) AT2R is downregulated by hypertension, and (2) specific and nonspecific antihypertensive treatments restore AT(2)R expression and vasodilator functions. |
| High blood pressure related to carcinogen-induced unscheduled DNA synthesis, DNA carcinogen binding, and chromosomal aberrations in human lymphocytes Pero, R. W., C. Bryngelsson, et al. (1976), Proc Natl Acad Sci U S A 73(7): 2496-500. Abstract: Unscheduled DNA synthesis (excision-repair) of N-acetoxy-2-acetylaminofluorene (NA-AAF) damage to the DNA of human lymphocytes was determined quantitatively for 92 individuals with diastolic blood pressures ranging from 65 to 120 mm of Hg (8,7 to 16 kPa). Measurements of NA-AAF-induced repair synthesis (incorporation of3Hthymidine in the presence of 10 mM hydroxyurea) showed linear increase with the blood pressure in the individuals under study. Concurrent determinations for the levels of 3H-labeled 7,12-dimethyl-benzaanthracene bound to the DNAs of lymphocytes after 18 hr of culturing have shown that increased amounts of DNA bound carcinogen were linearly proportional to increased NA-AAF-induced repair synthesis values, and therefore were correlated to high blood pressure. The number of NA-AAF-induced chromosomal abberations in lymphocytes increased linearly with the diastolic blood pressures of the individuals. High NA-AAF-induced repair synthesis values also tended to be associated with increased NA-AAF-induced chromosomal damage. Together, these results suggest that individuals with elevated blood pressures have a greater potential for accumulating DNA damage, because of an increased chemical reactivity of lymphocytes to carcinogen exposure, than do individuals with normal blood pressure. |
| High blood pressure research in Australian general practice Nelson, M. (2003), Aust Fam Physician 32(4): 277. |
| High blood pressure screening and referral by dentists. Legal implications of blood pressure measurement in the dental practice Conway, B. J. (1980), R I Dent J 13(4): 16-8. |
| High blood pressure screening in the dental office: a survey among Dutch dentists Gortzak, R. A., L. Abraham-Inpijn, et al. (1993), Gen Dent 41(3): 246-51. |
| High Blood Pressure Therapy Without Reserpine? A Contribution To The Therapy Of Hypertension. Grafzudohna, P. and A. Pfisterer (1965), Landarzt 41: 435-6. |
| High blood pressure treatment facilities. Survey in greater New York area Alderman, M., J. Rafter, et al. (1979), N Y State J Med 79(5): 754-7. |
| High blood pressure treatment in the elderly Applegate, W. B. (1992), Clin Geriatr Med 8(1): 103-17. Abstract: Clinicians should clearly understand the magnitude of the clinical benefits attributable to the treatment of hypertension in the elderly so that appropriate tradeoffs can be made between benefits and side effects. Potential types of overtreatment of elevated blood pressure in older persons include inaccurate measurement technique, insufficient numbers of readings, and too great a lowering of blood pressure. |
| High blood pressure upregulates arterial L-type Ca2+ channels: is membrane depolarization the signal? Pesic, A., J. A. Madden, et al. (2004), Circ Res 94(10): e97-104. Abstract: Long-lasting Ca2+ (Ca(L)) channels of the Ca(v)1.2 gene family contribute to the pathogenesis of abnormal arterial tone in hypertension. The physiological stimulus that enhances Ca(L) channel current in the vascular smooth muscle cells (VSMCs) remains unknown. The present study investigated if high blood pressure triggers an upregulation of vascular Ca(L) channel protein. Rat aortae were banded between the origins of the left renal (LR) and right renal (RR) arteries to selectively elevate blood pressure in the proximal RR arteries. After 2 days, the immunoreactivity on Western blots corresponding to the pore-forming alpha1C subunit of the Ca(L) channel was increased 3.25-fold in RR compared with LR arteries. This finding persisted at 28 days and was associated with abnormal Ca2+-dependent tone and higher Ca(L) currents in the VSMCs exposed to high pressure. Based on microelectrode studies indicating that RR arteries were depolarized compared with LR arteries, further studies examined if membrane depolarization, an inherent response of VSMCs to high blood pressure, increased alpha1C expression. Isolated rat renal arteries were cultured for 2 days in low K+ (4 mmol/L) or depolarizing high K+ (30 mmol/L) media. Arteries preconditioned in high K+ showed a 5.47-fold increase in alpha1C expression, enhanced Ca(L) channel current, and elevated Ca2+-dependent tone. These findings provide the first direct evidence that high blood pressure upregulates the Ca(L) channel alpha1C subunit in VSMCs in vivo and suggest that membrane depolarization is a potential signal involved in this interaction that may contribute to the development of abnormal vascular tone. |
| High blood pressure vs. hypertension Salomon, M. I. (1966), Med Times 94(5): 531-40. |
| High blood pressure vs. hypertensive disease Lockhart, J. C. (1957), Ill Med J 111(3): 119-21. |
| High blood pressure, alcohol and cardiovascular risk Estruch, R., A. Coca, et al. (2005), J Hypertens 23(1): 226-9. |
| High blood pressure, catecholamines and the sympathetic nervous system. I. Molecular-pharmacological insights Offerhaus, L. (1975), Ned Tijdschr Geneeskd 119(4): 144-53. |
| High blood pressure, other risk factors and longevity: the insurance viewpoint Lew, E. A. (1973), Am J Med 55(3): 281-94. |
| High blood pressure, oxygen radicals and antioxidants: etiological relationships Romero-Alvira, D. and E. Roche (1996), Med Hypotheses 46(4): 414-20. Abstract: This hypothesis proposes that high blood pressure is a pathological state associated with a loss of the balance between pro-oxidation and antioxidation, energy depletion, and accelerated aging in the target organs, such as heart, kidney and brain. Different nutritional, environmental, pharmacological factors and/or associated pathologies (diabetes, arteriosclerosis, cancer, alcoholism, etc.) and/or genetic components, can induce high blood pressure by breaking the redox equilibrium in the affected organs. Additional evidence, such as increase of oxidative damage, fibrogenesis, inhibition of the cardiocytic sodium-potassium pump, and heart hypertrophy, supports this hypothesis. These facts are analysed in the present paper, showing that they could contribute to the development of high blood pressure and associated pathologies by oxidative mechanisms. |
| High blood pressure, smoking and cardiovascular risk Pardell, H. and J. L. Rodicio (2005), J Hypertens 23(1): 219-21. |
| High blood pressure. A side effect of drugs, poisons, and food Grossman, E. and F. H. Messerli (1995), Arch Intern Med 155(5): 450-60. Abstract: A variety of therapeutic agents or chemical substances can induce either a transient or a sustained increase in blood pressure. These agents increase arterial pressure by either causing sodium retention and extracellular volume expansion or directly or indirectly activating the sympathetic nervous system. Some agents act directly on arteriolar smooth muscle. For certain agents, the mechanism of pressure elevation is mixed or unknown. Paradoxically, some agents that are used to lower arterial pressure may acutely increase arterial pressure. Also, a rebound increase in pressure may be encountered after discontinuation of certain antihypertensive agents. In general, these chemically induced increases in arterial pressure are small and transient; however, severe hypertension involving encephalopathy, stroke, and irreversible renal failure has been reported. Careful evaluation of a patient's drug regimen may identify chemically induced hypertension and prevent the need for evaluation and therapy. This study reviews the therapeutic agents or chemical substances that elevate blood pressure and their mechanisms of action. |
| High blood pressure. A side effect of drugs, poisons, and food Messerli, F. H. and E. D. Frohlich (1979), Arch Intern Med 139(6): 682-7. Abstract: Arterial hypertension, either transient or persistent, may be induced or aggravated by ingestion of various chemical agents, such as drugs, poisons, and food. Most of these agents either cause sodium retention and expand extracellular fluid volume or act as direct or indirect sympathomimetics. Others act directly on arteriolar smooth muscle. For a few agents, no precise mechanism has been ascertained. Hypertensive reactions may also occur as a result of drug interactions or food and drug interactions. In addition, paradoxical increases in pressure may be encountered during or after discontinuance of antihypertensive therapy. In general, these pressure increases are small and transient; however, a few have been associated with severe hypertension involving encephalopathy, strokes, and irreversible renal failure. Careful review of a patient's drug regimen, including over-the-counter preparations, may avoid chemically induced hypertension. Identification of any offending or incriminating agent will prevent the labeling of a chronic illness and obviate the need for lifelong antihypertensive therapy. |
| High blood pressure. detection and treatment by general practitioners Hodes, C., P. A. Rogers, et al. (1975), Br Med J 2(5972): 674-7. Abstract: A questionnaire was sent to a 10% random sample of general practitioners in England and Wales on their attitudes to the detection and treatment of hypertension; 62% responded and no further inquiry was made. Their view on detection and criteria for treatment and investigations performed were considered in relation to their background. More of the older practitioners always measured blood pressure and 36% of all practitioners believed that hypertensive patients usually present with symptoms. Altogether 91% thought that strokes could be prevented by treating hypertension, and only 18% reported difficulty in keeping patients on treatment. Older practitioners preferred to measure the distolic pressure using phase five, while the younger preferred phase four. Nearly all doctors were satisfied with their current sphygmomanometers. |
| High blood pressure. Measurement or management? Hutchison, J. C. (1966), Pa Med 69(9): 37-40. |
| High blood pressure: a national concern Chenoweth, A. D. (1973), J Sch Health 43(5): 307-8. |
| High blood pressure: A time for action Berman, C. L. (1975), J Prev Dent 2(1): 4-6. |
| High blood pressure: can we close the gap between what we know and what we do? Peacock, P. B. (1974), Prev Med 3(3): 312. |
| High blood pressure: definitions, prognostic, and therapeutic implications Birbari, A. E. (2001), J Med Liban 49(6): 338-41. Abstract: Although it is well established that high blood pressure (BP) levels of 140/90 mmHg or higher are associated with increased cardiovascular morbidity and mortality it has not been as well appreciated that lower BP levels, namely those considered to be in the "normotensive" range, also confer an increased risk of cardiovascular disease. Recent data from the Framingham Heart Study have demonstrated that high normal levels (i.e. SBP = 130-139 and/or DBP = 85-89 mmHg) frequently progress to hypertension, are associated with structural and functional cardiovascular alterations, an atherogenic metabolic profile and/or a comorbid condition, and an increased risk of cardiovascular outcomes. Factors that predispose to progression to hypertension include higher SBP and body weight at baseline and weight gain. In low risk subjects with high normal BP, nonpharmacologic measures, especially salt restriction and weight reduction are often adequate to lower BP to < or = 130/80. In those with a high cardiovascular risk profile, BP should be reduced to < or = 120/80 with nonpharmacologic measures and pharmacotherapy. |
| High blood pressure: hunting the genes Leckie, B. J. (1992), Bioessays 14(1): 37-41. Abstract: High blood pressure is a disease of unknown cause. Family history of the disease indicates higher risk, but it is not known which genes are involved or how they interact with environmental influences to produce the disorder. Molecular biology offers an approach to problems that have not so far been solved by classical physiology or biochemistry. By analysing polymorphic variation in chromosome markers such as minisatellite sequences, or by restriction fragment polymorphism analysis of candidate genes, attempts are being made to link genetic variations with hypertension. In genetically hypertensive rats, hypertension is associated with a polymorphism of the renin gene and with other loci on chromosomes 10 and 18. The role of these loci in human hypertension remains to be determined. Other genes such as sodium-lithium countertransport may be involved. Environmental factors such as stress or salt intake could influence the rate or timing of expression of certain genes and thus result in hypertension. |
| High blood pressure: its care and consequences in urban centres Apostolides, A., J. R. Hebel, et al. (1974), Int J Epidemiol 3(2): 105-18. |
| High blood pressure: new efforts in primary prevention and disease management Zelizer, G. (1993), J Tenn Med Assoc 86(4): 157-9. |
| High blood pressure: public views and knowledge Obrien, M. and C. Hodes (1979), J R Coll Gen Pract 29(201): 234-9. |
| High blood pressure: should dentists in Maryland be involved? Meiller, T. F., M. J. Kutcher, et al. (1980), J Md State Dent Assoc 23(3): 172-5. |
| High blood pressure: side effects of drugs, poisons, and food Oren, S., E. Grossman, et al. (1988), Cardiol Clin 6(4): 467-74. Abstract: A number of therapeutic agents, foods, chemicals, and poisons have been associated with the development or exacerbation of hypertension. This review discusses those identified in recent years. |
| High blood pressure: some answers, new questions, continuing challenges Lenfant, C. (1996), Jama 275(20): 1604-6. |
| High blood pressure: the foundation for epidemic cardiovascular disease in African populations Cooper, R. S., A. G. Amoah, et al. (2003), Ethn Dis 13(2 Suppl 2): S48-52. Abstract: High-blood pressure is a powerful independent risk factor for death from heart disease and stroke. It is also a common clinical condition affecting more than 600 million persons worldwide and seen in nearly all populations. Although reliable, large-scale, population-based data on high blood pressure in sub-Saharan Africa (SSA) are limited, recent studies provide important and worrisome findings in both epidemiology and clinical outcomes. Although overall hypertension prevalence is between 10%-15%, prevalence rates as high as 30%-32% have been reported in middle-income urban and some rural areas. Importantly, hypertension awareness, treatment, and control rates as low as 20%, 10%, and 1%, respectively have also been found. Stroke has been by far the most common clinical sequela. In most SSA settings, hypertension control assumes a relatively low priority and little experience exists in implementing sustainable and successful programs for drug treatment. Rapid urbanization and transition from agrarian life to the wage-earning economy of city life continue to fuel increases in average blood pressure levels and prevalence of hypertension. Although the true burden of high blood pressure in sub-Saharan Africa remains largely unmeasured, compelling preliminary evidence suggests that it is the foundation for epidemic cardiovascular disease in Africa and already contributes substantively to death and disability from stroke, heart failure, and kidney failure in this region. Success in limiting this epidemic in SSA will depend heavily on the implementation of sustainable and aggressive population-based programs for high blood pressure awareness, prevention, treatment, and control. It will be critical to obtain investments in improved surveillance and program-relevant research to provide the evidence base for policy development and effective hypertension prevention and control. |
| High blood pressure: the problem and the responsibility Thomson, G. E. (1976), Bull N Y Acad Med 52(6): 639-41. |
| High blood pressure: the silent killer Coleman, P. (1977), Imprint 24(2): 16, 69-71. |
| High blood pressure: what level to treat? Sleight, P. (1985), J Cardiovasc Pharmacol 7 Suppl 1: S109-11. Abstract: Recent trials of the treatment of mild hypertension have suggested that there may be benefit from drug treatment of quite modest or borderline levels of pressure. Drug treatment of subjects with diastolic pressures over 95 mm Hg would pose a major problem in the efficient organization of such a long-term program and would also be costly. Perhaps about 350 patient years of treatment might be necessary to prolong one patient's life by 1 year. The side effects as well as the costs of such a program should make us cautious about offering such treatment solely on the results of measurement of arterial pressure. In people with diastolic pressures in the range of 90-100 mm Hg we should carefully consider several factors such as age, sex, cholesterol concentrations, diabetes, family history, and smoking habit which might also interact to identify particularly high risks and exclude those individuals with a particularly benign prognosis. The results of the more recent trials can give very little information about such subgroup analysis, which would be possible only with much larger samples. The untreated subjects with raised pressure should be carefully followed and offered advice on nondrug strategies such as weight reduction, treatment of lipid abnormalities, and reduction in dietary salt intake. This type of program demands careful, possibly computerized, records and follow-up. |