Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cross-clamping of the ascending aorta in dogs for 15 min produced severe neurological deficit, observed for up to 20 h. Immediately after restoration of the circulation, the intracranial pressure in the cisterna magna increased transiently to a mean peak of 22.8 Torr (SD +/- 1.7) because of a compensatory increase in systemic arterial pressure, without a fall in cerebral perfusion pressure. The intracranial pressure returned to control values 15-30 min after ischaemia and showed no secondary rise during the 8 h of observation. The electroencephalogram became isoelectric 34 +/- 6.5 s (mean +/-SD) after circulatory occlusion, and was abnormal when it reappeared 5 h 36 min (SD +/- 2 h 4 min) after the circulation was restored. The electrical impedance of the brain increased immediately after ischaemia and returned rapidly towards pre-ischaemic values during re-perfusion. The cerebral water had not increased measurably 4 h after ischaemia. After ischaemia, the lactate concentration in the cerebrospinal fluid increased to 4.7 mequiv./1(SEM +/-0.1) and the pH decreased to 7.17 (SEM +/-0.02); both returned to control values after 3.5 h. The cerebral glucose uptake was decreased 35 min after ischaemia, cerebral oxygen uptake remained unchanged but cerebral blood flow decreased (P less than 0.05 at 90 min). Immediately after cardiac arrest, recovery was impaired more by the presence of focal abnormal brain perfusion than by intracranial hypertension.
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PMID:Total brain ischaemia in dogs: cerebral physiological and metabolic changes after 15 minutes of circulatory arrest. 0 Jul 50

Twelve Shetland ponies were fed a high-starch ration. Seven ponies which had a transitory metabolic acidosis developed laminitis 56 hours (+/- 3.5, SEM) after overfeeding. These ponies also developed persistent hypokalemia, hyperthermia, and increased heart rate 24 hours before the onset of lameness. Serum sodium, serum chloride, hematocrit, plasma volume, and blood volume were unchanged. At the onset of clinical signs of laminitis, cardiac output and blood pressure increased, but total peripheral resistance was unchanged. None of the measured or calculated values predicted the onset of laminitis. Hypertension appeared to be a response to, rather than a cause of, lameness. Three of the remaining ponies apparently died of shock 29.3 +/- 2.7 hours after overfeeding. All 3 had severe metabolic acidosis; decreased cardiac output, systemic arterial pressure, and plasma volume; and increased hematocrit, total peripheral resistance, and pulmonary vascular resistance. The 11th pony was unaffected and the 12th pony was euthanatized.
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PMID:Cardiovascular, acid-base, electrolyte, and plasma volume changes in ponies developing alimentary laminitis. 3 30

Regional differences in cell size in the hearts of rats with and without cardiac hypertrophy were studied using isolated muscle cells. Isolated cardiac myocytes were prepared from left ventricular free wall inner and outer halves and the right ventricle of six male 12-week-old spontaneously hypertensive (SHR), Wistar-Kyoto (WKY) and Fischer-344 rats. In SHR, blood pressure was increased to 188 +/- 4 (SEM) mm Hg versus 143 +/- 2 and 133 +/- 10 for WKY and Fischer rats, respectively (p less than 0.001). Total heart weight was increased to 1103 +/- 29 mg in SHR compared to 824 +/- 21 in WKY and 951 +/- 23 in Fischer rats (p less than 0.001. Isolated cardiac myocytes were prepared by perfusion of isolated hearts with Ca++ free Hanks' solution containing EGTA followed by collagenase-containing media. Mean length, width and volume of 150 cells stained with hematoxylin and eosin from each site were measured with a sonic digitizer. Two nuclei were present in 85 to 87% of isolated cells from all strains and regions. There was no difference among strains in right ventricular cell length, width, or volume, nor between left ventricular inner and outer halves within each strain. Left ventricular cells were larger than right ventricular cells (p less than 0.05) in all strains. Left ventricular cells of SHR were larger than left ventricular cells of WKY of Fischer rats in proportion to the increase in total heart weight, indicating that cardiac enlargement in SHR is due to increased cell size rather than increased cell number.
Hypertension
PMID:Regional myocyte size in normotensive and spontaneously hypertensive rats. 16 52

Aldosterone receptors from rat kidney slices were utilized in a competitive binding technique to analyze the contribution of various steroids to plasma "mineralocorticoid" activity and to assess their possible role in hypertension. To consider simultaneously the plasma binding, steroids were incubated with slices in undiluted plasma; competitor activities for [3H]aldosterone binding were aldosterone, 100%; deoxycorticosterone, 16.2%; cortisol, 0.4%; and 18-hydroxy-deoxy-corticosterone and d18-hydroxy-corticosterone, 0.1%. These steroids were more active in buffer than plasma, suggesting that they bind to plasma and that this reduces their receptor binding. Analysis of the competition data suggests that at normal plasma concentrations, aldosterone occupies the receptors to a major extent, cortisol occupies some of the receptors, and deoxycorticosterone and 8-hydroxydeoxycorticosterone contribute little to receptor occupancy. Two steroids implicated in low-renin essential hypertension, 16beta-hydroxy-dehydro-epiandrosterone and 16-oxoandrostenediol, did not have significant competitor activity. Competitor activity in plasmas from normal subjects taken at 12 noon (upright) was greater than that in those taken at 8 a.m. (supine). Since the 12 noon samples had higher aldosterone and lower cortisol levels than the 8 a.m. samples, the competitor activity under these physiological circumstances reflects aldosterone more than cortisol. The competitor activities of plasmas from patients relative to normal subjects (100+/-12.1%; mean+/-SEM) were: normal renin "essential" hypertension, 117+/-14%; low-renin essential hypertension, 101+/-6.6%; and primary aldosteronism, 176+/-14.3%. Thus a significant increase in activity of steroids that interact with mineralocorticoid receptors was detected in primary aldosteronism (P LESS THAN 0.01) BUT WAS NOT DETECTED IN LOW-RENIN OR NORMAL-RENIN ESSENTIAL HYPERTENSION.
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PMID:Aldosterone receptors and the evaluation of plasma mineralocorticoid activity in normal and hypertensive states. 18 23

Primary hyperparathyroidism was the most likely diagnosis in sixty-eight non-thiazide treated patients with hypercalcaemia detected in a health screening. The group included fifty-five females and thirteen males with a mean +/- SEM age of 55.0 +/- 0.7 years. On a pair basis, these patients were compared with a series of sixty-eight age- and sex-matched normocalcaemic subjects selected from the health screening register. Five subjects in each group were receiving medication for hypertension. Systolic and diastolic blood pressures were significantly higher in the hypercalcaemic subjects in the remaining fifty-eight pairs (P less than 0.001). This difference was unrelated to impaired renal filtration and many other factors associated with hypertension. It is concluded that hypercalcaemia and/or other effects of deranged parathyroid function per se may result in a blood pressure elevation on which need not necessarily attain the level of hypertension.
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PMID:Blood pressure in subjects with hypercalcaemia and primary hyperparathyroidism detected in a health screening programme. 40 55

To compare angiographically-determined coronary artery disease in diabetic patients with controls, 1,653 patients coming to cardiac catheterization were reviewed retrospectively to find 37 diabetic and 79 control patients matched for sex, age (+/- 3 years), and risk factors (hypertension, hyperlipidemia, and smoking). The severity of coronary artery disease was assessed using an angiographic grading system. The following results were obtained: 16 of 37 diabetic patients (43%) had three-vessel disease compared to 20 of 79 controls (25%). Seventy-six of 111 (68%) diabetic vessels were diseased compared to 110 of 237 control vessels (46%) (P less than 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 +/- (SEM) compared to 594 for controls (mean 7.5 +/- 0.7, (P less than 0.01). Diabetic patients had a statistically similar number of diffusely diseased vessels as controls (28% vs 22%). There were only three of 76 diabetic vessels (4%) considered inoperable compared to seven of 110 (6%) control vessels. We conclude that diabetic patients with chest pain have more coronary artery disease than nondiabetics, but no more diffuse or inoperable disease.
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PMID:Diffuse coronary artery disease in diabetic patients: fact or fiction? 61 80

We studied a 59-year-old man with transient paroxysms of hypertension, tachycardia, and flushing in whom pheochromocytoma was excluded. Although catecholamine excretion was normal, plasma catecholamine levels rose from normal basal levels (282 +/- 14 pg/ml) to increased levels (585 +/- 67 pg/ml; x +/- SEM; n = 4) at the peak of spells. Other hormones or substrates expected to rise with nonspecific "stress" did not increase after paroxysms. Therapy with clonidine (0.2 to 0.4 mg/day) suppressed basal catecholamines to undetectable levels and markedly reduced peak levels during spells (80 pg/ml). An epileptic pathogenesis was suggested by stereotypic olfactory and epigastric prodromata before spells, and abolition of paroxysms with the anticonvulsant carbamazepine. This patient represents a rare case of autonomic epilepsy with the seizure focus in the temporal lobe.
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PMID:Autonomic epilepsy: clonidine blockade of paroxysmal catecholamine release and flushing. 62 48

Because pulmonary hypertension and systemic hypertension occur during sleep-induced obstructive apnea, six patients underwent overnight hemodynamic monitoring before and after tracheostomy. Variables studied included heart rate, pulmonary artery pressure, femoral artery pressure, and arterial oxygen tension (Po2). After tracheostomy, significant reductions were noted during sleep in mean pulmonary artery pressure from 45 +/- 6 mm Hg (mean +/- SEM) to 22 +/- 2 mm Hg (P less than 0.05) and in mean femoral artery pressure from 137 +/- 6 mm Hg to 97 +/- 3 mm Hg (P less than 0.005). There was also a significant increase for the group in arterial Po2 recorded during the apneic episodes from 38 +/- 3 mm Hg before tracheostomy to 71 +/- 2 mm Hg (P less than 0.001) after tracheostomy. We conclude that tracheostomy improves the hemodynamic abnormalities and hypoxemia that occur during sleep in patients with sleep-induced obstructive apnea.
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PMID:Tracheostomy and hemodynamic changes in sleep-inducing apnea. 69 23

Minoxidil-induced sequential changes in plasma renin activity, urinary aldosterone and norepinephrine excretion were assessed in 11 patients with severe hypertension receiving propranolol or oxprenolol, chlorthalidone and spironolactone. Blood pressure with this treatment alone averaged 175 +/- 7/114+/-4 mm Hg (mean +/- SEM). Addition of minoxidil in a dose of 5 to 35 mg/day (mean 16 mg/day) reduced blood pressure within one week to 125+/-5/87+/-3 mm Hg. Plasma renin, urinary aldosterone and norepinephrine increased two- to threefold initially, but returned to baseline within two weeks and remained unchanged during a mean follow-up of 6.8 months. In 6 patients beta-blocking drugs were then progressively reduced and withdrawn without adverse effects, though blood pressure and heart rate increased slightly in 5 patients who required readministration of minimal doses of beta-blockers. Neither renin nor urinary aldosterone or norepinephrine excretion changed significantly after discontinuation of beta-blockade. Thus, the stimulating effect of minoxidil on renin, aldosterone and norepinephrine secretion lasts less than 3 weeks. With long-term minoxidil treatment the need for beta-blockade is markedly reduced, and these drugs may even become unnecessary in some patients.
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PMID:[Long-term minoxidil therapy: renin, aldosterone, noradrenaline and the need for beta blockers]. 71 7

Diazoxide was administered to sixteen pediatric patients (ages 10 months to 13 years) with secondary forms of hypertension. Admission BP was 178+/-8/130+/-5 mm Hg (mean +/- SEM). Diazoxide was administered rapidly intravenously in doses ranging from 2 to 7.5 mg/kg. A significant (P less than 0.001), linear log dose-response relation was obtained which showed that a 3 mg/kg dose of diazoxide lowered diastolic BP by an average of 30 mm Hg. In five patients reduction of idastolic BP by a single injection of diazoxide was no different than when the same total dose was given as two or three small injections repeated at fifteen to twenty minute intervals. It is concluded that 1) many hypertensive children respons significantly to doses of diazoxide smaller than the usually recommended 5 mg/kg; 2) diazoxide has a significant dose-response relation in hypertensive pediatric patients; and 3) the desired blood pressure response in hypertensive children can be titrated using repeated small injections of diazoxide.
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PMID:Dose-response relation of diazoxide in children with hypertension. 92 46


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