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At least 19 recordsLinked to original sources
PubMed1994

[Characteristics of blood pressure regulating endocrinological factors in elderly essential hypertensives].

Plasma renin activity (PRA) was lower in elderly normotensive subjects and essential hypertensives (EHT), and a significant negative correlation was found between PRA and age in both groups. In EHT, the proportion of the low renin group to total EHT increased with aging. There was a significantly positive correlation between plasma norepinephrine (PNE) and age in NT, but not in EHT. The mean value of PNE in young subjects was significantly higher in EHT than in NT, but not in the middle-aged and elderly groups, suggesting the important role of PNE in young EHT. Power spectral analysis revealed a significant reduction of both sympathetic and parasympathetic activity with aging in NT and EHT, indicating much caution may be required if sympathetic nerve activity is evaluated only by PNE levels in elderly EHT. The expanded plasma volume was another characteristic in elderly EHT, and suppressed activity of renal kallikrein-kinin, prostaglandin and dopamine may be involved with its mechanisms. Regarding insulin sensitivity in elderly EHT, it was shown that 1) the reduction of insulin sensitivity plays some role in age related acceleration of hypertension and glucose intolerance, 2) selective insulin resistance with respect to glucose metabolism already exists at lower ages in EHT, and 3) both Na retention and pressor system activation via insulin action might be a cause of blood pressure elevation in EHT.

Adult↗
PubMed2026

Hypertensive disorders of pregnancy and the risk for hypertension and cardiovascular and kidney disease. International Society of Hypertension position paper, endorsed by the World Hypertension League and European Society of Hypertension.

Hypertensive disorders of pregnancy (HDP) remain a leading cause of maternal and perinatal morbidity and mortality worldwide, especially in low- and middle-income countries. Moreover, HDP are directly linked to an increased risk of long-term cardiometabolic and kidney disease in mothers and offspring. Since prevention, diagnosis, and treatment of HDP remain suboptimal globally, enhanced understanding and implementation of current guidelines on HDP present a substantial opportunity to significantly reduce maternal and fetal morbidity and mortality. This position paper by the International Society of Hypertension reviews current knowledge in the field, identifies knowledge gaps and provides recommendations on the care of women with HDP and lifelong care, thereafter.

AT1R-Aas↗
PubMed2000

Calcium supplementation during pregnancy for preventing hypertensive disorders and related problems.

BACKGROUND: Calcium supplementation may prevent high blood pressure through a number of mechanisms and may help to prevent preterm labour. OBJECTIVES: The objective of this review was to assess the effects of calcium supplementation during pregnancy on hypertensive disorders of pregnancy and related maternal and child adverse outcomes. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group trials register and the Cochrane Controlled Trials Register and we contacted study authors. SELECTION CRITERIA: Randomised trials comparing at least one gram daily of calcium during pregnancy compared to placebo. DATA COLLECTION AND ANALYSIS: Eligibility and trial quality were assessed. Data extraction was carried out independently by two reviewers. MAIN RESULTS: Nine studies were included, all of good quality. There was a modest reduction in high blood pressure with calcium supplementation (relative risk 0.80, 95% confidence interval 0.73 to 0.88). The effect was greatest for women at high risk of hypertension (relative risk 0.35, 95% confidence interval 0.21 to 0.57) and those with low baseline dietary calcium (relative risk 0.49, 95% confidence interval 0.38 to 0.62). There was also a modest reduction in the risk of pre-eclampsia with calcium supplementation (relative risk 0. 72, 95% confidence interval 0.60 to 0.86). The effect was greatest for women at high risk of hypertension (relative risk 0.22, 95% confidence interval 0.11 to 0.43) and those with low baseline calcium intake (relative risk 0.32, 95% confidence interval 0.21 to 0.49). There was no overall effect on the risk of preterm delivery, although there was a reduction in risk amongst women at high risk of hypertension (relative risk 0.42, 95% confidence interval 0.23 to 0. 78). There was no evidence of any effect of calcium supplementation on stillbirth or death before discharge from hospital. REVIEWER'S CONCLUSIONS: Calcium supplementation appears to be beneficial for women at high risk of gestational hypertension and in communities with low dietary calcium intake. Optimum dosage requires further investigation.

Calcium↗
PubMed1989

Changes in platelet function due to hypertension: comparison of experimental hypertension with spontaneous hypertension in rats.

In washed platelets both from DOCA-salt and renal hypertensive rats, there was a marked decrease in thrombin-induced aggregation and secretion responses compared with those of respective controls. Concomitantly, the platelets showed attenuated malondialdehyde (MDA) formation and reduced serotonin contents, suggesting the presence of degranulated platelets in the circulation due to hypertension. In platelets from stroke-prone spontaneously hypertensive rats (SHRSP) at early hypertensive stages, thrombin-induced aggregation and secretion responses were similarly reduced. However, the platelet hypofunctions did not accompany reduced MDA formation and serotonin contents. Properties of platelets obtained from SHRSP at late hypertensive stages resembled those of platelets from experimentally hypertensive rats. These results suggest that the mechanisms of platelet hypofunction differ between experimental hypertension and spontaneous hypertension in their early stages. The hypo-aggregability observed in experimental hypertension appears to be secondary to the hypertension, whereas that seen in spontaneous hypertension seems to be a primary defect and not secondary to hypertension at early stages of hypertension.

Animals↗
PubMed1985

Plasma prolactin levels in patients with essential hypertension, malignant hypertension and secondary hypertension.

Plasma prolactin level and plasma renin activity were determined in normal subjects and patients with low and normal renin essential hypertension, renal hypertension, renovascular hypertension, primary aldosteronism, Cushing syndrome, pheochromocytoma and malignant hypertension. In both normal subjects and the normal renin essential hypertensives, plasma prolactin was significantly higher in females than in males. Plasma prolactin was also significantly higher in the normal renin essential hypertensives than in normal subjects of both sexes, while no significant difference was found between the low renin group and normal subjects of either sex. A significantly positive correlation was observed between plasma renin activity and the plasma prolactin level in male essential hypertensives, but not in females. Although no significant difference in plasma prolactin level could be detected between patients with secondary hypertension and normal subjects, this level was significantly higher in malignant hypertensives than in normotensives. From these results, it was shown that significant differences of plasma prolactin levels exist between normal renin essential hypertensives, and low renin essential hypertensives or normal subjects, and that these differences may partly depend on renin status which might be related to the central dopaminergic activity. In malignant hypertensives, the high level of plasma prolactin may be caused by diminished renal function, but the suppression of central dopaminergic activity cannot be excluded in the mechanism of plasma prolactin increment.

Adolescent↗
PubMed2000

Do patients with de novo hypertension differ from patients with previously known hypertension when malignant phase hypertension occurs?

Malignant phase hypertension (MHT) represents the most severe form of hypertension, and many consider that this condition only occurs in poorly managed patients with previously known hypertension. To investigate this further, we studied 350 patients with MHT on the West Birmingham MHT database: 195 (55.7%) of these presented de novo, without any known past history of hypertension (Group 1), and 146 (41.7%) were previously known hypertensives (Group 2), of whom 86 were receiving antihypertensive therapy; in 9 patients, the status was uncertain. Median duration of clinical followup was similar in both groups (36.0 v 37.5 months, Mann-Whitney test P = .795). Patients presenting de novo with MHT (Group 1) were younger, with a predominance of whites and men. Nevertheless, the clinical features, blood pressures, and renal function at presentation were similar to MHT patients with previously known hypertension. Renal function at follow-up was also similar in both groups. There was an excess of women and nonwhites in MHT patients with previously known hypertension (Group 2), who also had higher mean follow-up blood pressures. On univariate life-table analysis, there was no statistically significant difference in survival time between Groups 1 and 2 (mean 57.5 v 63.5 months, median 36.0 v 37.0 months; log-rank test, P = .456). Using a multivariate Cox analysis of baseline variables, the independent predictors of outcome (death or dialysis) were age at presentation (P = .0019), diastolic blood pressure (P = .0466), serum urea (P = .006), and serum creatinine (P < .001). Whether the patient had presented de novo, without any known history of hypertension (Group 1) or had previously known hypertension (Group 2) did not independently predict outcome (P = .6549). We suggest that MHT can occur de novo in patients without previously known hypertension, and the clinical characteristics and prognosis in such patients were similar to MHT patients with previously known hypertension.

Diagnosis, Differential↗
PubMed1994

Prevalence of mixed hypertension, isolated systolic hypertension and isolated diastolic hypertension in the elderly population in the community.

The prevalence of mixed hypertension (MHT), isolated systolic hypertension (ISH) and isolated diastolic hypertension (IDH) was estimated in the elderly population in the register of a large general practice in Wrexam, North Wales. Of the 3289 elderly patients, born in 1927 or before, entered in the register of surgery, 1901 attended for the first screening. The mean SBP rose with age until the age of 80-84 years in males and 75-79 years in females and then gradually declined. The mean DBP showed an earlier decline in males than in females. The prevalence of hypertension at first screening was: mixed hypertension 9.8%, ISH 19.1% (DBP < 95 mmHg*, 23.1%*) and IDH 5.7% with a total prevalence of hypertension of 52.2%. The prevalence fell at each subsequent screening so that at the third screening MHT was 3.9%, ISH 4.2% (5.4%)* and IDH 1.0%, with a total prevalence of hypertension of 10.3%. The prevalence of ISH rose with age until 70-74 years of age and with the maximum prevalence in this age group and then gradually declined. There was a drastic drop in the prevalence of both mixed hypertension and IDH after the age of 70-74 years. This study provides data for this community and also supports earlier observations that hypertension is a common problem in the elderly and that ISH is the commonest form of hypertension in the elderly. It confirms the fall in mean DBP with age but reports a decline also in mean SBP after the age of 80-84 years in males and 75-79 years in females.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Distribution↗
PubMed1993

Hypertensive sodium-proton exchanger phenotype persists in immortalized lymphoblasts from essential hypertensive patients. A cell culture model for human hypertension.

An enhancement of sodium-proton exchange activity is a frequently observed ion transport abnormality in essential hypertension. The cellular basis for this has not yet been elucidated. Due to the lack of a specific cell culture system it has been impossible to distinguish between intrinsic cellular abnormalities and influences exerted by the hypertensive neurohumoral milieu. Using Epstein-Barr virus we have immortalized lymphocytes from controls and from patients with essential hypertension that exhibited enhanced sodium-proton exchanger activity. Sodium-proton exchanger activity was determined in cells loaded with the fluorescent cytosolic pH indicator 2'7'-biscarboxyethyl-5,6-carboxyfluorescein acetoxymethylester (BCECF) after pretreatment with 250 nM of the phorbol ester 12-O-tetradecanoylphorbol-13-acetate for 10 min. Cell lines from hypertensive patients displayed higher Vmax values of sodium-proton exchange than those from normotensive controls (129.6 +/- 30.0 vs. 77.1 +/- 13.2 mmol H+/min.; P < 0.001). Hill coefficients for H+ were distinctly lower in hypertension compared to normotension (1.12 +/- 0.12 vs. 1.50 +/- 0.14; P < 0.0001). The enhanced antiporter activity in cell lines from hypertensive patients was not accompanied by a corresponding increase in steady-state NHE-1 mRNA transcript levels, which argues against overexpression of antiporter protein in hypertension. The cells from hypertensive patients with high sodium-proton exchange activity proliferated distinctly faster than those from normotensive controls. These human cell lines represent a novel model to study the mutual interaction between sodium-proton exchange and cell proliferation, and may provide insights into the alterations in ion transport observed in a group of patients with essential hypertension.

Adult↗
PubMed1995

Hypertension in acromegaly: hereditary hypertensive factor produces hypertension by enhancing IGF-I production.

Sixty-four patients with acromegaly were retrospectively analyzed to study the incidence and cause of hypertension in acromegaly. WHO criteria indicate that 37.5% patients with acromegaly have hypertension. The blood pressure was positively correlated with age, the insulin-like growth factor I (IGF-I) and serum sodium (Na) concentration. In addition, IGF-I and Na were significantly different in hypertensive and normotensive groups. Seventy-five percent of hypertensive patients had a family history of hypertension. IGF-I, Na and blood pressure were significantly higher in patients with a family history of hypertension than in those without it. In patients with a family history of hypertension, blood pressure was positively correlated with IGF-I and serum Na, but IGF-I was not correlated with serum Na. In patients without such a family history, blood pressure had a good correlation only with age, and IGF-I was not significantly correlated with blood pressure. In addition, the incidence of hypertension in this group was the same as or lower than that in the general population. The above results suggest that the genetic factor produces hypertension in acromegaly by two ways, by increasing Na and enhancing IGF-I production by GH.

Acromegaly↗
PubMed1980

Transfer of arterial hypertension by splenic cells from DOCA-salt hypertensive and renal hypertensive rats to normotensive recipients.

Arterial hypertension was transferred from DOCA-salt hypertensive and renal hypertensive rats to normotensive rats by intravenous injection of splenic cells. Thirteen normotensive recipients were injected intravenously with splenic cells from the hypertensive donors. Eleven developed arterial hypertension (85%), that is, with a systolic blood pressure exceeding 140 mm Hg. Three of the recipients developed hypertensive levels up to 155-160 mm Hg, which was almost up to the levels in the donors. The increase of the blood pressure in the recipients was significant when compared to controls injected intravenously with splenic cells from normotensive donors (p less than 0.001). Skin tests, performed by intracutaneous injection of homogenized common carotid arteries in half of the recipients, showed positive reactions 24 hours after the injection. Microscopical examination of heart and kidney from the other half demonstrated mononuclear infiltration into arterial and arteriolar walls and exudative changes in these walls. Due to exudative thickening of the vessel walls the lumina were narrowed. The hypothesis is advanced that the recipient rats developed arterial hypertension as a result of a transferred delayed hypersensitivity directed against the arterial walls. This hypersensitivity reaction caused insudation of plasma components into the arterial walls, narrowing of their lumina and an increased peripheral resistance to the blood flow, so that arterial hypertension developed.

Animals↗
PubMed1994

[Correlation between pulmonary hypertension and portal hypertension--2 case reports of different forms of pre-sinusoidal portal hypertension].

Since its first description in 1951 by Mantz and Craig pulmonary hypertension in combination with portal hypertension has been observed more and more frequently. In a recent prospective study Hadengue et al. reported an incidence of 2%. Thus this simultaneous occurrence can no longer be considered to be coincidental. The etiology remains still unclear. It is most probable that the development is due to vasoactive substances which bypass the liver or which are produced in the lung itself, and which, due to a long-term vasoconstriction, causes irreparable damage to the arterioles and arteries in the lung. Such pulmonary hypertension can develop in the presence of a pre- as well as an intrahepatic block, even when the portal hypertension is partially or completely alleviated by a portosystemic anastomosis. This last circumstance can be illustrated by two cases which were observed by our group. Case A is of particular interest because it is the first documentation of a case of an intrahepatic block due to a (so-called) macronodular transformation of the liver in the absence of portal thrombosis (a so-called NRH: nodular regenerative hyperplasia) in combination with pulmonary hypertension. This type of non-cirrhotic portal hypertension can be associated with micronodular transformation of the liver as well. Post-hepatic blocks or the so-called BUDD-CHIARI Syndrome type appear to carry no risk of development of pulmonary hypertension. It remains unclear which particular etiologies increase susceptibility to later development of pulmonary hypertension.

Adolescent↗
PubMed1997

Aminoguanidine corrects hyperdynamic circulation without ameliorating portal hypertension and portal hypertensive gastropathy in anesthetized portal hypertensive rats.

BACKGROUND/AIMS: Portal hypertension and hyperdynamic circulation (i.e. generalized vasodilation and increased cardiac output and regional organ blood flows) may play an important role in the development of portal hypertensive gastropathy. This study investigated the effect of chronic administration of aminoguanidine, a selective inducible nitric oxide synthase inhibitor, to portal hypertensive rats on hemodynamics and the development of portal hypertensive gastropathy. METHODS: Partial portal vein-ligated or sham-operated rats were randomly assigned to receive either placebo (distilled water) or aminoguanidine (approximately 100 mg/kg per day subcutaneously) for 2 days prior to and 14 days. Hemodynamic studies with a thermodilution technique and gastric morphometric analysis were performed at 14 days after the operation. RESULTS: In rats given placebo, portal vein-ligated rats had a significantly lower mean arterial pressure and systemic vascular resistance associated with a significantly higher cardiac index and portal pressure than sham-operated rats (p<0.05). In portal vein-ligated rats aminoguanidine induced a significant increase in mean arterial pressure and systemic vascular resistance accompanied by a significant decrease in cardiac index (p<0.05) without changes in portal pressure (p>0.05). Despite persistence of portal hypertension, the aminoguanidine-treated portal vein-ligated rats had similar mean arterial pressure, cardiac index, and systemic vascular resistance as seen in placebo-treated sham-operated rats. The mean cross-sectional area of gastric mucosal vessels was significantly higher in placebo-treated portal vein-ligated than in placebo-treated sham-operated rats (p<0.05). Treatment with aminoguanidine did not induce changes in the mean cross-sectional area of gastric mucosal vessels in either portal vein-ligated or sham-operated rats (p>0.05). CONCLUSIONS: The results show that in portal hypertensive rats long-term aminoguanidine therapy corrects the hyperdynamic circulation without inducing changes in portal pressure and ameliorating the development of portal hypertensive gastropathy. This study suggests that, instead of correcting hyperdynamic circulation, treatment of portal hypertensive gastropathy should be aimed at reducing portal pressure.

Animals↗
PubMed1991

Why do lean hypertensives have higher mortality rates than other hypertensives? Findings of the Hypertension Detection and Follow-up Program.

Specific causes of death were analyzed for 10,908 participants in the Hypertension Detection and Follow-up Program, to explore possible explanations for the observed excess 8.3-year mortality from all causes in hypertensives with low body mass. Although the cardiovascular mortality rate among men in the lowest decile of body mass (body mass index 21.96 or less) was 50% higher than that of men in the median class (body mass index 26.4-28.8), death rate for noncardiovascular deaths was more than 2 1/2 times higher in men with lean versus median body mass. The pattern was similar among women. Among noncardiovascular causes, striking differences in mortality rates between lean hypertensives and those of average body mass were observed for cirrhotic death (relative risk of 12+ in men and 11+ in women), for nonmalignant respiratory disease in men (relative risk of 7+), for violent death (both sexes), and for malignant neoplasms in men. Prevalence of smoking was almost twice as high in the lowest compared with the median body mass group; among the lean, excess deaths, particularly noncardiovascular deaths, were concentrated among smokers. Thus, male smokers in the lowest decile of body mass constituted only 3% of the study population, but contributed 8% of all deaths, 11% of all noncardiovascular deaths, and 22% of all cirrhotic deaths. A larger proportion of deaths occurred early in follow-up in the lean versus other hypertensives, suggesting occult disease among the lean at baseline. There was no evidence that more severe or treatment-resistant hypertension was present in or could explain excess mortality among the hypertensives with low body mass. The inference from the findings is not that overweight is protective for hypertensives nor that excess risk is due to leanness per se. Rather, a reasonable hypothesis, particularly from findings on specific causes of death, is that excess mortality in lean hypertensives is due to deleterious lifestyles, particularly smoking and excess alcohol intake, contributing to both leanness and risk of death.

Adult↗
PubMed1990

[Adrenal regeneration hypertension--effects of vascular connective tissue protein and plasma corticosterone on hypertension in rats with adrenal regeneration hypertension].

In young rats consuming 1% NaCl drinking solution, unilateral nephrectomy and bilateral adrenal enucleation caused a hypertension. Plasma corticosterone concentration in hypertensive rats was not significantly higher than that of normotensive control rats in early hypertensive or chronic hypertensive stage. At the end of experiment, each rat received an intravenous injection of 0.4 microCi/g of 3H-lysine and was sacrificed 2 hours after the injection. Incorporation of 3H-lysine into collagen or elastin of the mesenteric artery and heart in hypertensive rats was greater than that of normotensive rats. Administration of phenoxybenzamine hydrochloride lower the blood pressure of hypertensive rats and reduced the incorporation of 3H-lysine into collagen and elastin of the mesenteric artery and heart. From these findings, increased protein synthesis of collagen and elastin in hypertensive rats appears to play an important role for the maintenance of adrenal regeneration hypertension.

Adrenal Glands↗
PubMed1979

Heart and kidney involvement and prognosis in hypertension. A study concerning referred hypertensive patients and hypertensive patients found by blood pressure screening.

Severity of hypertension, frequency of secondary hypertension and prognosis have been compared in two groups of hypertensive men. The first group (n=686) was taken from a blood pressure screening of a total population sample. The other group (n=154) consisted of hypertensive men, referred to a hypertension clinic by physicians. The mean age of the groups was the same, (X=52 years, range 46--59 years). All went through the same investigations and were followed up and treated in a similar way at the hypertension clinic. The referred men had more severe hypertension, as shown by significantly more heart and kidney involvements. They also had a higher incidence of myocardial infarction, implying a poorer prognosis with regard to cardiovascular disease. The analysis shows the importance of a detailed description of studied groups, not only in terms of blood pressure, age and sex, but also with respect to the frequency and degree of present and previous signs of heart and kidney involvement. With such a description it is possible to compare results from different studies regarding pathophysiological mechanisms and the effect of treatment in hypertension.

Cerebrovascular Disorders↗
PubMed1995

Is isolated systolic hypertension in the elderly more associated with left ventricular hypertrophy and significant carotid artery stenosis than mixed hypertension and isolated diastolic hypertension?

The association of electrocardiographic left ventricular hypertrophy (ECG-LVH) (212 subjects) and haemodynamically significant internal carotid artery stenosis (ICAS) (27 subjects) with isolated systolic hypertension (ISH), mixed hypertension (MHT) and isolated diastolic hypertension (IDH) was studied in untreated elderly patients. Subjects were those aged 67-86 years, drawn from a community screening programme for hypertension in Wales. The prevalence of ECG-LVH with or without repolarisation abnormalities was higher in subjects with ISH (16.6%) than in subjects with mixed hypertension (11.6%, NS). Partial correlation of SBP, DBP, voltage of lead I and SV1+RV5 for each hypertensive subtype showed a consistent positive correlation of DBP with the voltage of lead I and SV1+RV5 in all the subtypes except with the voltage of lead I in IDH subjects. In MHT, the SBP was inversely related to both the voltage of R-wave in lead I and SV1+RV5 (P < 0.03). In IDH, the SBP was positively correlated with the voltage of R-wave in lead I and inversely with SV1+RV5. Atheromatous plaque was present in 40 of 54 (74.1%) internal carotid arteries investigated. The homogeneous type of plaque was predominant in ISH (67%). Heterogenous type of plaque was predominant in the MHT group (50%) and IDH group (43%). The normotensive group did not show any predilection to any morphological type. Plaque was invariably present in the case of ISH, chi 2 = 12.29, 0.1 > P > 0.05. There was more smooth plaque surface in normotensives (79%) and more rough or pitted plaque surface in hypertensives (all types), chi 2 = 6.51, 0.1 > P > 0.05. All normotensives and IDH subjects had non-haemodynamically significant stenosis. Haemodynamically significant stenosis was found in cases of ISH (25%) and MHT (7%); chi 2 = 7.66, 0.1 > P > 0.05. ECG-LVH and haemodynamically significant internal carotid artery stenosis were more commonly found in subjects with ISH than in subjects with MHT. Further studies with larger numbers of patient in each hypertensive subtype would be desirable to confirm these observations.

Aged↗
PubMedDate not supplied

Effects of acute hypertension on brain metabolism in normotensive, renovascular hypertensive and spontaneously hypertensive rats.

Effects of angiotensin-induced acute hypertension on cerebral metabolism were studied in normotensive (NTR), spontaneously hypertensive (SHR) and experimental renovascular hypertensive rats (RHR). Lactate, pyruvate and adenosine triphosphate (ATP) concentrations in the brain frozen in situ at 18--20 min after angiotensin infusion, which raised mean arterial pressure (MAP) by 28--62% of control, were determined by enzymatic methods. Supratentorial lactate was significantly increased to 135% of control in RHR, its increase being correlated with the degree of hypertension, wherease it remained unchanged in NTR or SHR. Furthermore, RHR showed a tendency toward increase in lactate/pyruvate ratio with a decrease in ATP despite no change of arterial acid-base balance measured simultaneously before and after acute induced hypertension. From the present study, it is postulated that some renal factor seems to contribute ischemic metabolic changes in RHR following acute hypertension. The possible effect of renin on the vascular permeability is discussed as the pathogenesis of hypertensive encephalopathy.

Acute Disease↗
PubMed2002

Resistant hypertension, secondary hypertension, and hypertensive crises.

Resistant hypertension, secondary hypertension, and hypertensive crises are uncommon but potentially dangerous forms of hypertension that are associated with an increased risk of complications such as myocardial infarction, heart failure, stroke, and renal failure. Appropriate diagnostic screening and selective drug or surgical management can reduce the risk of these complications dramatically. In compliant patients, resistant hypertension occurs most often in obese patients receiving inadequate diuretic therapy. In patients with clinical clues to the diagnosis, the best current screening test for renovascular hypertension is probably the ACE-inhibitor renal scintiscan. Angioplasty is considerably more successful in younger patients with fibrous dysplasia than in older patients with the atherosclerotic variety. Hypertensive crises are divided into BP urgencies and emergencies. In both settings, the reduction in BP should generally be gradual rather than abrupt, with no intent to acutely normalize the BP.

Drug Resistance↗