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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thoracic aortic histamine synthesis has been examined in rats rendered hypertensive for periods ranging from 1/4 to 8 days through ligation of abdominal aorta between origins of the renal arteries, in a preliminary attempt to establish whether activity of the aortic nonmast-cell histidine decarboxylase system is increased in experimental hypertension. Results indicate that aortic histamine synthesis is increased 66, 75, 96 and 55% at postsurgical intervals of 1/4, 1/2, 1 and 8 days. These data suggest at least one biochemical explanation for both increased arterial wall permeability and the arterial inflammation consistently associated with both clinical and experimental hypertension by resolving these into those associated with the prolonged inflammatory response.
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PMID:Rat aortic histamine synthesis during short-term hypertension. 124 95

The vasoconstrictor effect, the binding, and the response of inositol phosphates to endothelin-1 (ET-1) were investigated in blood vessels of deoxycorticosterone acetate (DOCA)-salt hypertensive rats within 2 weeks of development of hypertension and in uninephrectomized control rats. In DOCA-salt and uninephrectomized rats, plasma levels of endothelin were similar (1.2 +/- 0.1 fmol/ml). Thoracic aorta and mesenteric artery rings devoid of endothelium presented significantly decreased responses to increasing concentrations of ET-1. Binding of ET-1 to mesenteric artery membranes was significantly lower in DOCA-salt rats (106 +/- 22 fmol/mg protein) than in uninephrectomized rats (172 +/- 19 fmol/mg protein, p less than 0.05), whereas affinity was similar. Phosphoinositide metabolism was examined in aorta and mesenteric arteries after incubation with [3H]myoinositol. Inositol phosphates were separated by high-performance liquid chromatography. In response to 100 nmol/l ET-1, accumulation of inositol 1,4,5-trisphosphate after 20 seconds and of inositol monophosphate, inositol bisphosphate, and inositol 1,3,4-triphosphate after 30 minutes (in the presence of 25 mmol/l LiCl) were significantly lower in DOCA-salt hypertensive than in uninephrectomized control rats, in both aorta and mesenteric arteries. In conclusion, decreased density of ET-1 receptors in DOCA-salt hypertensive rats results in decreased activation of phospholipase C and, consequently, reduced vasoconstriction induced by ET-1. Because the decrease in vasoconstrictor effects of ET-1 is found in the absence of endothelium, it is likely that receptor downregulation rather than prior receptor occupancy underlies these findings.
Hypertension 1992 Feb
PMID:Endothelin vascular receptors and responses in deoxycorticosterone acetate-salt hypertensive rats. 131 Apr 86

Thoracic aortic cross-clamping causes proximal aortic hypertension. Theoretically, the method used to treat hypertension can influence spinal cord perfusion pressure and neurologic outcome. Phlebotomy was compared to sodium nitroprusside/isoflurane in terms of ability to treat increased proximal mean aortic pressure (MAPp) after thoracic aortic cross-clamping in dogs. Dogs were assigned randomly to one of three groups depending on the method used to treat hypertension after cross clamping: 1) phlebotomy (n = 10); 2) sodium nitroprusside/isoflurane (n = 11); and 3) control (no treatment) (n = 8). In each dog, anesthesia was maintained with isoflurane in oxygen, 1.4% end-tidal. The thoracic aorta was occluded 2.5 cm distal to the left subclavian artery for 50 min and then was released. Hemodynamics, cerebrospinal fluid pressure (CSFP), and regional blood flows by the radioactive microsphere technique, were measured at 1) baseline; 2) 2 min after aortic cross-clamping; 3) after treatment of proximal aortic hypertension; 4) 5 min after aortic unclamping; and 5) 30 min after resuscitation. At 24 h, a neurologic assessment was performed. Thoracic aortic cross-clamping increased MAPp, decreased distal MAP (MAPd), and reduced lumbar spinal cord perfusion pressure (SCPPl), [SCPPl = MAPd - CSFP], in all three groups. Control of increased MAPp necessitated removal of 36 +/- 9 ml/kg of blood in the phlebotomy group. In the sodium nitroprusside/isoflurane group, sodium nitroprusside (16 micrograms.kg-1.min-1) was infused and end-tidal isoflurane concentration increased to 2.5 +/- 0.7%, restoring MAPp to baseline level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Treatment of proximal aortic hypertension after thoracic aortic cross-clamping in dogs. Phlebotomy versus sodium nitroprusside/isoflurane. 164 54

This study examined the calcium dependency of contractions in arteries from rats made hypertensive by aortic coarctation and in rats with genetic hypertensive (stroke-prone spontaneously hypertensive rats). Mesenteric artery and aortic strips were suspended in tissue baths for isometric force recording and contractions to two drugs were characterized: 1) a phorbol ester, TPA (12-O-tetrade-canoylphorbol-13-acetate), and 2) the calcium channel agonist, Bay K 8644. Thoracic aortae and mesenteric arteries from hypertensive rats were more sensitive to the contractile properties of the protein kinase C activator TPA than comparable arteries from normotensive rats. In thoracic aortae from coarcted rats, the contractile activity of Bay K 8644 was potentiated compared to normotensive values. In the presence of 19.2 mmol/L KCl, responses to Bay K 8644 in thoracic aortae from normotensive rats were potentiated and did not differ from coarcted values. In contrast, contractions to Bay K 8644 and TPA in abdominal aortae obtained below the coarctation were not different from normotensive values. Upon exposure to 26.2 mmol/L KCl, contractions to Bay K 8644 in abdominal aortae were potentiated and those in aortae from coarcted rats did not differ from sham values. Contractile responses to both drugs were blocked by nifedipine and verapamil and responses were attenuated in calcium-free solution. We conclude that calcium channel function and its regulation by protein kinase C contribute to altered vascular reactivity in hypertension. Further, these abnormalities have a pressure dependency, because they did not occur in abdominal aortae from coarcted rats.
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PMID:Calcium and contractile responses to phorbol esters and the calcium channel agonist, Bay K 8644, in arteries from hypertensive rats. 169 54

Recent data from this laboratory indicate that insulin resistant obese Zucker rats exhibit hypertension associated with exaggerated in vitro vascular reactivity to phenylephrine, serotonin, and KCl, and we have found insulin to attenuate vascular reactivity responses to these agonists. Accordingly, in the present study we evaluated the possibility that exaggerated vascular reactivity responses in obese Zucker rats may result from insulin resistance and a consequent failure of insulin to attenuate vasoactive responses. Thoracic aortae were isolated from male 16 week old lean and obese Zucker rats, and replicate helical strips from each animal were suspended in a muscle bath under a resting tension of 1.4 g in the presence or absence of insulin (0.1 mU/mL) for 1 h. The insulin was then washed out, and vascular reactivity responses to phenylephrine were determined. The obese rats exhibited greater reactivity to phenylephrine (ED50:1.10 +/- 90 X 10(-8) v 7.57 +/- 0.88 X 10(-10) mol/L in lean and obese rats, respectively, P less than .025). Insulin caused a significant attenuation of the contractile response in both the lean and obese aortae. However, lean rats exhibited a markedly greater attenuation than the obese rats (46.0 +/- 17.0 v 17.8 +/- 7.5% attenuation in the lean and obese rats, respectively, P less than .01). These data suggest that increased vascular reactivity responses in obese Zucker rats may result from their insulin resistant state and, consequently, a diminished ability of insulin to attenuate vasoconstrictor responses.
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PMID:Insulin attenuation of vasoconstrictor responses to phenylephrine in Zucker lean and obese rats. 187 6

Recent studies suggest that serotonergic receptor activation is coupled to phospholipase C-mediated phosphoinositide hydrolysis, which results in the release of intracellular second messengers. The purpose of this study was to determine whether altered phosphoinositide metabolism is the basis for augmented vascular responsiveness to serotonin in genetic hypertension. Thoracic aortic segments isolated from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive rats (WKY) were labeled with myo-[3H]inositol and stimulated with serotonin in the presence of LiCl. Accumulation of [3H]inositol phosphates was then quantitated by column chromatography. Basal inositol phosphate accumulation and basal incorporation of myo-[3H]inositol into aortic cell membranes from SHRSP was not significantly different from WKY values. At 2.6 x 10(-7) to 2.6 x 10(-4) M serotonin, phosphoinositide metabolism was significantly augmented in aortae from SHRSP compared with WKY. Depolarization (100 mM KCl) did not increase phosphoinositide hydrolysis above basal levels in SHRSP or WKY. 2-Nitro-4-carboxyphenyl-N,N-diphenyl carbamate (NCDC), an inhibitor of phospholipase C, prevented the serotonin-induced phosphoinositide metabolism. NCDC also partially inhibited phasic contractions (responses in calcium-free solution) to serotonin in aortas from SHRSP and WKY. In conclusion, abnormal phosphoinositide metabolism may be one mechanism responsible for the characteristic increase in vascular reactivity to serotonin in hypertension.
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PMID:Augmented phosphoinositide metabolism in aortas from genetically hypertensive rats. 215 30

A 63-year-old man of thoracoabdominal aortic aneurysm was transferred to our department. Thoracic and abdominal enhanced CT scan revealed a Crawford's type I A thoracoabdominal aortic aneurysm ruptured into the right extrapleural and retroperitoneal spaces. Without any more additional examination, graft replacement and reconstruction of a lower intercostal artery were performed with an aid of femoro-femoral bypass. Although the postoperative course was complicated by hypertension, hypoventilation and liver dysfunction, the patient recovered from the operation and 10 months later he is leading an almost normal life. Since emergency operation of thoracoabdominal aneurysm is the most courageous challenge because of the difficulties of exposure and visceral organ protection against ischemic, there have been only nine cases with successful surgery in Japan. Now we actively reconstruct lower intercostal and lumbar arteries to prevent spinal cord ischemia without ESCP monitoring in emergency cases.
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PMID:[A case of thoracoabdominal aortic aneurysm ruptured into the right extrapleural cavity]. 225 Apr 43

The hemodynamic modifications during anesthesia induction with etomidat or thiopentalum, with and without pretreatment with fentanyl, were studied in 60 ASA I-II patients. The patients were randomly divided into six subgroups, as a function of the induction agent (etomidat, 0.15 mg/kg, or thiopentalum, 3 mg/kg) and of the pretreatment used (fentanyl, 5 micrograms/kg, or 0.9% 1 ml/kg saline solution). Systolic, diastolic ATs and pulse were followed and measured during induction and after tracheal intubation. During induction the presence or absence of the thoracic rigidity, after fentanyl administration, and also the appearance of myoclonias and of local pain after etomidat injection were noted. Measurement of hemodynamic constants showed, in the control subgroups unprotected by fentanyl, that AT and pulse frequency increase following laryngoscopy and intubation irrespective of the induction agent used. Association of thiopentalum with fentanyl influenced partially tachycardia and postintubation hypertension. Administration of 5 micrograms/kg fentanyl prevented the SAT and pulse modifications but not the DAT variation. Association of 10 micrograms/kg fentanyl ensured a complete protective effect versus the tracheal intubation but, it led, first, to a SAT decrease by intensification of the myocardial depressing effect of the barbiturate. On the other hand, use of fentanyl as induction adjuvant with etomidat ensured the blockage of the pressure response to intubation, with hemodynamic stability during anesthesia induction, irrespective of the dose of fentanyl injected. Thoracic rigidity and the side effects generated by etomidate were absent.
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PMID:[The effect of fentanyl as an adjuvant to etomidate and thiopental on the hemodynamic response to the induction of anesthesia and endotracheal intubation]. 253 39

The authors studied 8 patients (4 males and 4 females) with Cushing's syndrome due to ectopic ACTH secretion. Chronological age ranged from 15 to 45 years and duration of the disease ranged from 3 to 48 months. All patients presented typical signs of Cushing's syndrome, blood hypertension, and four of them had hyperpigmentation of the skin. Five patients had fasting hyperglycemia and all patients but one had serum hypokalemia (serum K = 2.2 to 3.9mEq/l). The circadian rhythm of cortisol was absent in all patients and basal cortisol levels were elevated in all patients but one. Basal ACTH levels evaluated in 7 patients were elevated in 6 (29 to 1050 pg/ml-MRC). One patient presented normal depression of urinary 17-OH after two days of dexamethasone and normal increase of urinary 17-OH and serum 11-dexycortisol after methyrapone. Four patients had carcinoid tumor (3 thymic and 1 bronchial), two had pancreatic islets cell tumors, one had bilateral pheochromocytoma and medular carcinoma of the thyroid, and one had oat cell carcinoma of the lung and medular carcinoma of the thyroid. Thoracic X-rays identified the ectopic ACTH secretion tumor in four cases, all confirmed by CT scan. Abdominal CT showed a difuse enlargement of the adrenals in seven cases and bilateral nodules in one case (pheochromocytomas). Six patients died within 3 years of the diagnosis. The authors concluded that clinical and hormonal findings could mislead the findings of ACTH ectopic secretion and Cushing's disease, and suggest that thoracic X-rays and CT scans of the skull, thorax, and abdome should be done in all cases of Cushing's syndrome.
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PMID:[Cushing syndrome due to ectopic ACTH secretion]. 255 51

Weak or absent lower limb pulses and a thoracic systolic murmur in a fifty-seven-year-old woman with hypertension suggested coarctation. Thoracic X-Ray showed a narrowing of the thoracic aorta over 10 cm due to an intraluminal calcified aortic mass. The remaining aorta and its branches were normal. Histologic examination of the operative specimen found atherosclerotic lesions with thrombosis. This very unusual condition seems to represent an individual entity of which a few cases have been reported in the literature.
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PMID:[Pseudocoarctation caused by a calcified intra-aortic mass]. 631 44


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