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

Severe hypertension frequently requires hospitalization. Although hospital admission is undesirable for most patients, others are motivated to achieve hospitalization status for secondary gain. The authors present a case of a prison inmate who simulated severe hypertension with a combination of Valsalva's maneuver and arm flexion, on the background of preexisting essential hypertension and mitral valve prolapse. His secondary intent--to avoid his prison duties--classifies him as a malingerer. The differences between this malingering and the psychiatric diagnosis of Munchausen syndrome are discussed. The contributions of essential hypertension and mitral valve prolapse to the self-induced blood pressure elevations also are considered.
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PMID:Case report: stimulation of severe hypertension as a means of malingering. 141 22

Frederick Akbar Mahomed was an Englishman of mixed Indian and Irish descent who made substantial contributions to the study of high blood pressure in a short professional life from 1872 to 1884. He was strongly influenced by the previous work of Richard Bright on kidney disease at his own hospital (Guy's Hospital in London) and by the contemporary pathological studies of Gull and Sutton on arteriolar changes in persons with high blood pressure. In detailed clinical studies, he separated chronic nephritis with secondary hypertension from what we now term essential hypertension. He described the constitutional basis and natural history of essential hypertension and pointed out that this disease could terminate with nephrosclerosis and renal failure. His clinical studies were done without the benefit of a sphygmomanometer but with the aid of a quantitative sphygmogram that he had initially developed while a medical student. He described characteristic features of the pressure pulse in patients with high blood pressure and in persons with arteriosclerosis consequent on aging. These pressure wave changes have recently been verified and explained. He contributed to a number of other advances in medical care, including blood transfusion and appendectomy for appendicitis. He initiated the Collective Investigation Record for the British Medical Association; this organization collected data from physicians practicing outside the hospital setting and was the precursor of modern collaborative clinical trials. Mahomed died from typhoid fever, almost certainly contracted from one of his patients, at age 35 at the height of his career.
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PMID:Frederick Akbar Mahomed. 173 55

This article reports the first successful human orthotopic liver transplantation performed in Mexico. The recipient was a 41 year old white male, with a history of essential hypertension and hepatitis in 1975. The diagnosis of postnecrotic cirrhosis was made in 1985 by liver biopsy. The HBsAg was negative and the functional reserve of the liver was limited (Stage "C" of the Child-Pugh classification). A liver graft was obtained through the National Cadaver Organ Transplant Program on May 2, 1988 and an orthotopic liver transplantation was performed without incidents, using the portosystemic veno-venous bypass. Inmunosuppression was carried out with triple drug therapy, cyclosporine, azathioprine, and prednisone. His postoperative course was characterized by idiopathic cholestasis, one episode of acute rejerction, arterial hypertension, renal dysfunction, esophageal herpes and inguinal lymphocele, all of which resolved. Currently the patient is alive 22 months postransplantation with normal liver function and adequate quality of life.
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PMID:[Liver transplantation in Mexico. Report of the first successful case]. 206 9

Thirty-one Japanese with essential hypertension were divided into training (n = 21) and non-training (n = 10) groups. Physical training of 10 weeks was instituted after 4 or more weeks of observation, and changes in blood pressure and serum concentrations of taurine and other amino acids were investigated. The workload in physical training was predetermined by the submaximal multistage graded exercise test on a bicycle ergometer, and the blood lactate threshold which reflects approximately 40-60% of maximal oxygen uptake was chosen. The hypertensive patients underwent bicycle ergometer training for 60 minutes, three times a week for 10 weeks. Blood pressures were significantly decreased by 14.8/6.6 mmHg in systole/diastole in the training group, but not in the non-training group. Serum concentrations of taurine and cystine were increased significantly by 26% and 287%, in the training group. Increase in serum asparagine (11%), histidine (6%) and lysine (7%) concentrations was also significant, only in the training group. Plasma norepinephrine level and whole blood and plasma volumes were significantly reduced. The change in serum taurine level was significantly negatively correlated with the change in plasma norepinephrine. In addition there was a significant positive correlation between the change in plasma norepinephrine and the change in diastolic blood pressure in the training group. Based on these results, the increase in serum taurine which is known for its antihypertensive activity could contribute, at least in part through the reduction in plasma norepinephrine level, to the antihypertensive effect of exercise.
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PMID:Changes in serum concentrations of taurine and other amino acids in clinical antihypertensive exercise therapy. 256 73

Although renin was identified as playing a part in cardiovascular homeostasis by the experiments of Goldblatt in the 1930s, neither its physiological role in organs other than the kidney nor its contribution to the genesis of essential hypertension have been defined. It is difficult to interpret studies with converting enzyme inhibitors because of their multiple pharmacological effects. Specific inhibitors of renin appropriate for clinical investigation would help to resolve many questions. Four classes of compounds have been shown to be renin inhibitors of high potency: specific antibody, general peptide inhibitors of acid proteases, analogues of angiotensinogens and peptides that are related to the amino-terminal sequence of prorenin. Of these, it is likely that angiotensinogen analogues will be the first applied in human studies. The minimal substrate for renin has the sequence: His-Pro-Phe-His-Leu-Val-Tyr. Variants of this sequence have yielded competitive inhibitors. Remarkably active compounds have recently been synthesized by reducing the peptide bond that is cleaved by renin, or by incorporating the amino acid statine, found in pepstatin. These compounds have been shown to be effective in dogs, rats and monkeys and, most recently, preliminary studies have reported their efficacy in man. Recent studies with one of these inhibitors, RIP, raise questions concerning both its specificity and site of action.
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PMID:Will renin inhibitors influence decision-making in antihypertensive therapy? 300 3

Although renin was identified as playing a role in cardiovascular homeostasis by the experiments of Goldblatt in the 1930's, neither its physiologic role in organs other than the kidney nor its contribution to the genesis of essential hypertension has been defined as yet. It is difficult to interpret studies with converting enzyme inhibitors because of their multiple pharmacologic effects. Specific inhibitors of renin appropriate for clinical investigation would help resolve many questions. Four classes of compounds have been demonstrated to be renin inhibitors of high potency: specific antibody, general peptide inhibitors of acid proteases, analogs of angiotensinogens, and peptides that are related to the amino-terminal sequence of prorenin. Of these, it is likely that angiotensinogen analogs will be the first applied in human studies. The minimal substrate for renin has the sequence: His-Pro-Phe-His-Leu-Leu-Val-Tyr. Variants of this sequence have yielded competitive inhibitors. Recently, remarkably active compounds have been synthesized by reducing the peptide bond that is cleaved by renin, or by incorporating the amino acid statine, found in pepstatin. These compounds have been shown now to be effective in dogs, rats, and monkeys, and most recently, preliminary studies have reported their efficacy in humans. Recent studies with one of these inhibitors, RIP, raise questions concerning both its specificity and site of action.
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PMID:Defining the physiologic and pathophysiologic roles of renin: the role of specific inhibitors. 388 1

In this study, the effects of angiotensin II (A II, Asn-Arg-Val-Tyr-Val-His-Pro-Phe) and angiotensin III (A III, Arg-Val-Tyr-Ile-His-Pro-Phe) on blood pressure (B.P.), pulse rate, several hormones [plasma renin activity (PRA), plasma aldosterone (PA), ACTH, plasma cortisol (PC), urinary catecholamines and urinary aldosterone] and urinary electrolytes were investigated in 9 male patients with essential hypertension [mean age 36.2 +/- 4.1 (S.E.) years]. A II and A III infusions (8 ng/kg/min, 60 min) were started from 0900 h and blood samples were drawn before, at 15, 30, 45, 60 min after the beginning of the infusions, and at 15 min after their cessation. Urinary samples were collected within 2 hrs before and after the infusions, respectively. A II significantly increased B.P.(p less than 0.01) during the infusions, whereas A III did not increase B.P.. PRA significantly decreased after the infusions of A II and A III (p less than 0.05), but the potency of A II was significantly greater than that of A III (p less than 0.01). PA was increased after both infusions, but in response to A III, a peak was observed at 30 min after the infusion and subsequently, the levels decreased gradually. Significant differences between both responses were found at 45 and 60 min (p less than 0.05) after the infusions. ACTH was unchanged during the infusions, but PC was equipotentially suppressed during the infusions, with the suppression of A II being similar to that of A III. In the responses of urinary catecholamines, noradrenaline and dopamine were equipotentially decreased after the infusions (p less than 0.05). The results of the present study clearly indicate that several differences exist between the biological activities of A II and those of A III. Further systematic experimental studies are needed to resolve the details.
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PMID:[Changes in responses of blood pressure and several hormones to infusions of angiotensin II and angiotensin III in patients with essential hypertension]. 609 61

The precise contribution of the renin-angiotensin system to the genesis of essential hypertension is difficult to discern from clinical studies with converting enzyme inhibitors because of their multiple pharmacological effects. Specific inhibitors of renin, appropriate for clinical investigation, would help to resolve this question. Four classes of compounds have been demonstrated to be renin inhibitors of high potency: specific antibodies, general peptide inhibitors of acid proteases, analogues of angiotensinogens, and peptides related to the amino-terminal sequence of prorenin. Of these, it is likely that angiotensinogen analogues will be the first to be applied in human studies. The minimal substrate for renin has the sequence: His-Pro-Phe-His-Leu-Leu-Val-Tyr. Variants of this sequence have yielded competitive inhibitors. Recently, remarkably active compounds have been synthesized by reducing the peptide bond cleaved by renin or by incorporating the amino acid statine, found in pepstatin. These compounds have now been shown to be effective in dogs, rats and monkeys, and, according to recent preliminary studies, in man.
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PMID:The first Sir George Pickering memorial lecture. Which inhibitors will give us true insight into what renin really does? 609 85

The widespread clinical study of converting-enzyme inhibitors has shown that they are effective antihypertensive drugs even in patients who may manifest either normal or decreased plasma renin activity. This suggests either that renin in a site other than plasma may play a contributory role in essential hypertension or that the hypotensive effect is caused by increased concentrations of kinins and prostaglandins, both demonstrated consequences of converting-enzyme inhibitor administration. Specific renin inhibitors appropriate for studies in humans would aid in the resolution of this question. Four classes of compounds have been demonstrated to be renin inhibitors of high potency: specific antibody, general peptide inhibitors of acid proteases, analogs of angiotensinogens, and peptides that are related to the amino-terminal sequence of prorenin. With the purification of renin, specific polyclonal or monoclonal antibodies have become available. The former have already been used extensively in physiologic studies in intact animals. Pepstatin is an inhibitor of many acid proteases. Its in vivo application has been retarded by its relative insolubility, but recent chemical modifications, particularly the addition of charged amino acids at the carboxy terminus, have rendered it more useful. The minimal substrate for renin is an octapeptide segment of the protein substrate: His-Pro-Phe-His-Leu-Leu-Val-Tyr. Variants of this sequence have resulted in competitive inhibitors that are useful in vivo. Recently, remarkably active inhibitors have been synthesized by reducing the peptide bond that is cleaved by renin, producing what may be a transition state inhibitor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Is renin a factor in the etiology of essential hypertension? 641 50

Pickering first showed that blood pressure distribution is unimodal and that the diagnosis of essential (primary) hypertension is an arbitrary quantitative trait. His family studies suggested that not 1, but many, perhaps 30 or more, gene variations are responsible for raising blood pressure. Two approaches have been used to address the genetics of essential hypertension. Candidate genes have been selected by virtue of their physiologic function, and case-control association studies have been performed. Numerous candidates have been evaluated, genes of the renin-angiotensin-aldosterone system, genes coding for adrenergic receptors, genes coding for proteins regulating endothelial function, and genes involved in signaling have been studied. True to Pickering's prediction, each gene tested thus far seems to exert, at best, a small effect and contradictory studies are common. Linkage studies have been performed to map the loci of genes regulating blood pressure or inducing hypertension. Studies of dizygotic twins and their parents have permitted an identity-by-decent linkage analysis. Studies of affected sibling pairs involve subjects whose parents are generally already dead. Identity-by-state analysis requires a far greater number of pairs for results. Nevertheless, some large linkage studies have now been performed including subjects from Framingham. Log odds (LOD) scores are far removed from actually cloning genes responsible for hypertension. Single nucleotide polymorphisms (SNPs) permit linkage dysequilibrium mapping, which may enable cloning new genes. Thus far, very few new genes have been cloned for any complex genetic disease. The task is daunting but not impossible.
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PMID:Hypertension as a complex genetic trait. 1189 5


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