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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nephrosclerosis, the morbid condition of the kidney that accompanies essential hypertension, is characterized by thickening of the walls of cortical arteries. According to the law of Laplace, the tension in the wall of an artery should be proportional to the product of pressure (P) times diameter (D). Thus, if wall thickness (T) is governed by wall tension, then it should be proportional to the same product: T = kPD, where k is a proportionality constant. A comparison of immersion-fixed kidneys in normotensives aged 75 to 90 years with those aged 19 to 34 years showed the magnitude of k to increase with age. The increase was 41% in vessels that were relatively close to the heart (outer diameter, 150 to 300 microns) and 30% at the more remote level (outer diameter, 80 to 140 microns). In perfusion-fixed specimens, k also increased with age, being 77% and 35% greater, respectively, for the comparison between normotensives in the two age groups. Normotensives were defined to be those with mean blood pressure less than 115 mm Hg. A similar result was found by defining normotension to be systolic pressure less than 140 mm Hg. Wall thickness was not proportional to pressure in hypertensive compared with normotensive subjects, but rather to a quadratic function that combined age and blood pressure taken together. The law of Laplace did not fully encompass the data that relate the thickening of renal arterial walls to hypertension or to aging in the absence of hypertension. The thickening with age is structurally a metaplasia that exchanges fibrotic intima in the elderly for muscular media in the young. The result was reproduced in perfusion- as well as immersion-fixed specimens and is therefore not distorted by postmortem collapse. The results favor the conclusion that arterial wall thickening in hypertensive and aging normotensive kidneys is sclerosis and not adaptive hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evidence for the failure of the Laplace law as a sole explanation for wall thickening of arteries in hypertensive and aging normotensive kidneys. 270 66

In hypertension, coronary flow is augmented and oxygen balance is adequate despite an increase in coronary resistance. For the maintenance of flow in the presence of and after regression of ventricular hypertrophy, the ratio of pressure and ventricular mass must remain normal. Coronary reserve would be altered if treatment normalized pressure but not ventricular mass or if pressure were lowered too fast. We investigated 42 patients with primary hypertension. In 28 (Group I) left ventricular mass index (by ultrasound) was within the mean value +2 SD (96 + 38 g/m2) of 145 controls and exceeded these values in the remaining 14 patients (Group 2). The diastolic pressure was lowered rapidly to between 85 and 90 mm Hg with two potent vasodilators, nifedipine (sublingually) and nitroprusside, while a 12-lead electrocardiogram was recorded continuously. During both tests, seven patients in Group 2 (responders) showed inversion of normal T waves, in lead I, aVL, and V3-6. These changes waxed and waned in parallel with the pressure fall and recovery and were not attributable to alterations in adrenergic tone, conduction disturbances, variations, or group differences in the QRS axis, QTc interval, heart rate, left ventricular fractional shortening, wall stress, rate of dimension increase in early diastole, or isovolumic relaxation. A ""steal phenomenon'' or passive collapse in compliant coronary lesions during vasodilatation seems unlikely; in fact, patients were free from coronary symptoms, and the electrocardiographic alterations occurred only in seven patients in Group 2, who had a greater left ventricular mass index and required a larger pressure drop to return the diastolic pressure to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiac hypertrophy in hypertension. Repolarization abnormalities elicited by rapid lowering of pressure. 296 41

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

In focal segmental glomerulosclerosis (FSGS), a biphasic change in glomerular size is described in which glomeruli are enlarged with early glomerulosclerosis. Hyperperfusion of larger glomeruli is believed to contribute to progressive glomerular injury. This study was undertaken to investigate whether similar alterations in glomerular size can be found in other renal diseases. Volumes of sclerotic and nonsclerotic glomeruli were estimated in renal biopsy specimens using the Weibel and Gomez method (1962). Glomerulosclerosis was graded on individual glomeruli from 0 to 4, with 0 as no sclerosis and 4 as 76% to 100% sclerosis. Primary and secondary FSGS showed a biphasic change in which grade 2 glomeruli were 50% larger than grade 0 glomeruli and grades 3 and 4 glomeruli were solidified and smaller than grade 0 glomeruli. In essential hypertension, no increase in glomerular size was seen with early glomerulosclerosis, and the latter stages consisted of ischemic obsolescence in which collapsed tufts were 50% smaller than solidified glomeruli of FSGS. Grade 0 glomeruli of membranous glomerulonephritis (MGN) were significantly larger than grade 0 glomeruli of FSGS, and no significant difference in size was seen between grades 0 and 2 glomerulosclerosis. Solidified diabetic glomeruli maintained a large size with grades 3 and 4 sclerosis. Glomeruloscleroses of FSGS, hypertension, MGN, and diabetes have stereologically distinct features. A biphasic change in glomerular size is characteristic of primary and secondary FSGS, but not hypertension, in which tuft collapse supports reduced rather than increased perfusion in the pathogenesis of its glomerular obsolescence.
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PMID:Glomerular size and glomerulosclerosis: relationships to disease categories, glomerular solidification, and ischemic obsolescence. 1192 Mar 32

We report on a 36 year old patient who collapsed at home and was resuscitated by prehospital medical emergency services. He presented on scene unconscious with severe ST-elevations on the ECG and hardly palpable pulses. His previous medical history included only idiopathic hypertension and his professional background as manager of a company was associated with high stress levels. The prehospital diagnosis was myocardial infarction with cardiogenic shock. A hypovolemic shock was excluded from the differential diagnosis because of the age of the patient, lack of a precipitating trauma and inconsistent symptoms. The patient died after terminating prolonged resuscitation. A post mortem showed as cause of death the rupture of a splenic artery aneurysm. We emphasize that a cardiovascular collapse in a young patient without specific history or trauma still can be caused by hypovolemic shock due to intra-abdominal or -thorac bleeding.
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PMID:[Rupture of a splenic aneurism in an emergency situation]. 1560 97

This review examines 2 potentially important morbid changes that may precede the onset of hypertension-capillary rarefaction (CR) and large artery rigidity (LAR). The mechanisms responsible for CR, currently measured in the skin microcirculation, as well those responsible for LAR, have yet to be fully delineated. Nor has the duration been determined of the latent period between the occurrence of these lesions and the onset of blood pressure elevation. It has been known for 2 decades that, because of the kidney's relatively rigid capsule, alterations in the abundant postglomerular microcirculation network (which can accommodate circa 80% of total renal blood flow) can lead to endothelial plasma leakage. Even a small amount of plasma leakage can increase interstitial pressure and lead to capillary collapse and CR. Simultaneously, or at a later time, these alterations could have an impact on the reflection wave profile in the thoracic aorta and, via abnormal endothelial proliferation and other vascular effects, give rise to LAR. Nonpharmacologic and/or pharmacologic interventions have been shown to exert positive effects on CR and/or LAR. Recent studies have demonstrated the beneficial actions of a bradykinin B2-receptor antagonist (HOE140) in the spontaneously hypertensive rat, the classic rat model for essential hypertension. The fact that CR and LAR both precede blood pressure elevation could serve as a basis for designing strategies to prevent hypertension from occurring. Because modern tools capable of measuring CR and LAR noninvasively have been developed, it should soon be feasible to identify these 2 prehypertension markers in individual patients.
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PMID:Predisease biological markers: early diagnosis and prevention of arterial hypertension. 1880 64

The cause of variant angina is localized hyperresponsiveness of the vascular smooth muscle cells caused by non-specific stimuli of vasoconstriction. Autonomic imbalance can be one of the mechanisms of spontaneous vasospasm, and sympathetic or parasympathetic stimulation can induce Coronary Artery Spasm (CAS). Although various reports of CAS events have been described, episodes associated with untwisting or manipulation of a visceral structure remains unique. We report one such case of CAS in association with intraoperative untwisting of a torted ovarian cyst treated with intracoronary nitroglycerine in the catheterization laboratory. Vasospastic or variant angina is a well known clinical condition first described by prinzmetal and colleagues, characterized by CAS in normal and diseased coronary arteries. General anesthesia can be a triggering event. This case demonstrates unique etiology in that spasm was provoked by surgical manipulation of a torted ovarian cyst. CAS has been implicated as a cause of sudden, unexpected circulatory collapse and death during surgery, cardiopulmonary bypass, and other non-cardiac surgical procedures. There are few reports of coronary vasospasm during regional anesthesia and neuroaxial block. Many factors are involved in the occurrences of perioperative CAS including activated sympathetic activity, activated parasympathetic activity, cocaine, alkalosis, hypercalcemia, magnesium deficiency, succinylcholine, vasopressors, essential hypertension, Hyperthyroidism, epidural anesthesia, spinal anesthesia, smoking, lipid metabolic disorder, coronary artery aneurysm, commercial weight loss products. We describe a rare case of CAS during general anesthesia, in a patient with no past history of coronary artery disease, possibly provoked by surgical manipulation ofa torted ovarian cyst, which was diagnosed and treated promptly via cardiac catheterization. Intraoperative coronary artery vasospasm: a twist in the tale!
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PMID:Intraoperative coronary artery vasospasm: a twist in the tale! 2243 84

Pheochromocytoma during pregnancy is extremely rare. Its clinical manifestation includes hypertension with various clinical presentations, possibly resembling those of pregnancy-induced hypertension. The real challenge for clinicians is differentiating pheochromocytoma from other causes of hypertension (preeclampsia, gestational hypertension, and pre-existing or essential hypertension), from other cause of pulmonary edema (preeclampsia, peripartum cardiomyopathy, stress or Takotsubo cardiomyopathy, pre-existing cardiac disease [mitral stenosis], and high doses betamimetics), and from other causes of cardiovascular collapse (pulmonary embolism, and amniotic fluid embolism). Although, several cases of pheochromocytoma during pregnancy have been published, fetal and maternal mortalities due to undiagnosed cases are still reported. We report a case of a patient whose delivery by cesarean section was complicated by severe hemodynamic instability resulting in a cardiac arrest. Later on, pheochromocytoma was suspected based on computed tomography (CT) scan findings. Diagnosis was confirmed with special biochemical investigations that showed markedly elevated catecholamines in urine and metanephrines in serum, and later by histopathology of the excised left adrenal mass. This case illustrates the difficulty of diagnosing pheochromocytoma in pregnancy and raises the awareness to when this rare disease should be suspected.
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PMID:Cardiorespiratory crisis at the end of pregnancy: a case of pheochromocytoma. 2418 Jan 71