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

Deendothelialized rings of rabbit aorta relax after exposure to UV light because of release of a relaxing factor that is similar if not identical to nitric oxide. We tested the hypothesis that production of the photo-induced relaxing factor is impaired in a rat model of genetic hypertension. Thoracic aortas were removed from adult Wistar-Kyoto rats and stroke-prone spontaneously hypertensive rats. The vessels were cut into rings, denuded of endothelium, and placed in a muscle bath for isometric force measurement. Rings were contracted with phenylephrine, and relaxation was measured after exposure to UV light. Aortic rings from stroke-prone spontaneously hypertensive rats relaxed to a greater extent after exposure to UV light than did rings from Wistar-Kyoto rats. An inhibitor of nitric oxide synthase (N omega-nitro-L-arginine) greatly potentiated the relaxation responses to light in both strains, and these enhanced relaxations were attenuated by tetraethylammonium chloride, potassium chloride, ouabain, or inhibitors of guanylate cyclase. These results suggest that UV irradiation induces relaxation in aortic smooth muscle that is greater in hypertensive than normotensive rats and is greatly enhanced after addition of inhibitors of nitric oxide production. Thus, the unidentified photo-induced relaxing factor is not solely nitric oxide but may also represent either a hyperpolarizing factor, because depolarization blocks the responses entirely, or possibly smooth muscle guanylate cyclase that might itself be photoactivable.
Hypertension 1994 Jun
PMID:A photoactivable source of relaxing factor in genetic hypertension. 820 24

Abnormal contractile responses of blood vessels are observed widely in several hypertension models and are assumed to play a role in the etiology of essential hypertension. Inconsistent reports also exist due to different animals, preparations, and experimental techniques employed. In this investigation, we compared vascular response of normotensive Wistar-Kyoto rat (WKY) with that of spontaneously hypertensive rat (SHR) employing two experimental methods. Thoracic aorta obtained from age-matched animals were contracted by norepinephrine (NE) with either--single-dose method or cumulative-dose method. Differences in both reactivity (maximal tension) and sensitivity (ED50) to NE were observed. Although no significant differences were found between WKY and SHR with either method, the choice of the method employed could affect the outcome. For aorta from WKY, the reactivity to NE was similar for both methods; however, for aorta from SHR, the reactivity obtained by cumulative-dose method was significantly higher. Furthermore, the cumulative-dose method yielded higher sensitivity in both WKY and SHR when compared with that obtained by single-dose method. Taken together, the cumulative-dose method appeared to be a more sensitive method to determine contractile response. Nevertheless, no significant difference in either reactivity or sensitivity to NE in aorta was detected between WKY and SHR when cumulative-dose method was employed. These data indicate that aorta do not exhibit abnormal response to NE in SHR, consistent with earlier findings that not all tissue preparations behave similarly.
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PMID:Vascular contractile properties in hypertension. I. A study of testing methods. 828 17

We retrospectively reviewed all patients with a final diagnosis of spontaneous thoracic aortic dissection treated at Linkou Chang Gung Memorial Hospital between January 1989 and December 1994. There were a total of 109 patients with a mean age of 55 +/- 11 years ranging from 19 to 88 years. The male-to-female ratio was 2 to 1 (73 to 36). There was a predilection to present during the colder months, with 69% seen between September 1 and February 28 and only 31% during the warmer half of the year. In most patients, hypertension (85%) was the major predisposing factor with another 7% having Marfan syndrome. The remaining 8% had no obvious underlying disease except for one patient who had an atrial septum defect. Presenting chief complaints in order of frequency included: anterior chest pain 58.7% (64/109), back pain 19.2% (21/109), abdominal pain 10.1% (11/109), consciousness change 3.7% (4/109), neck pain 2.7% (3/109), paraparesis 2.7% (3/109), dyspnea 1.8% (2/109), and hemoptysis 0.9% (1/109). The diagnostic breakdown revealed 46% to be type A (50/109) and 54% type B (59/109). A total of 26 (24%) patients died in hospital (16% were type A and 8% were type B). (Type A included all proximal dissections and those distal dissections that extend retrograde to involve the arch and ascending aorta; Type B refers to the other distal dissections without proximal extension; proposed by Daily et al.) Thoracic aortic dissection remains an important concern in patients with a history of hypertension. Patients seem particularly susceptible during cold weather months. The average age of our patients was only 55 years and 24% of them died during hospitalization. Earlier identification and more aggressive antihypertensive treatment is required.
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PMID:Aortic dissection in Taiwan. 855 68

Deoxycorticosterone-salt (DOCA-salt) hypertension is characterized by elevated vasoconstriction to agonists that stimulate G protein-mediated activation of phospholipase C. However, the mechanisms responsible for the augmented responsiveness are unknown. This study tested the hypothesis that this augmented vascular responsiveness is due to elevated content of G(alpha)q, the G protein alpha-subunit that activates phospholipase C. Thoracic aortae from DOCA-salt hypertensive rats (systolic blood pressure 183 +/- 7 mm Hg) and normotensive controls (systolic blood pressure 115 +/- 2 mm Hg) were homogenized and G protein content determined. Western analysis revealed that G(alpha)i content was decreased in DOCA compared with control rats (1364 +/- 196 versus 2343 +/- 188 densitometry units, P < or = .05) with no differences observed for G(alpha)q or G(alpha)s. In addition, contractile responses in denuded femoral artery strips revealed a significant decrease in EC50 values in DOCA arteries to all of the agonists examined: aluminum fluoride (DOCA = 1.42, control = 2.34 mmol/L), mastoparan (DOCA = 0.51, control = 35 micromol/L), phenylephrine (DOCA = 0.08, control = 0.53 micromol/L), and serotonin (DOCA = 0.014, control = 0.04 micromol/L, EC20 values). Finally, arteries from DOCA rats contracted with aluminum fluoride had increased sensitivity to G protein antagonists but not to a phospholipase C inhibitor. The enhanced contractile responsiveness in the DOCA arteries may be mediated in part through decreased G(alpha)i levels. However, it is not caused by increased concentrations of G(alpha)q in the cell membrane or by increased phospholipase C sensitivity, and the increased constrictor response to G protein stimulators of phospholipase C appears to depend primarily on increased G protein sensitivity.
Hypertension 1996 Mar
PMID:Increased responsiveness and decreased expression of G proteins in deoxycorticosterone hypertension. 861 34

We tested the hypothesis as to whether elevated arterial pressure in hypertension alters cGMP, or cAMP, mediated vasorelaxation. Relaxation to nitroglycerin and isoproterenol was determined in isolated aortic rings from one-kidney, one clip hypertensive (1K1C), coarctation hypertensive (CH) and normotensive control (C) rats. Thoracic aortas from 1K1C and CH rats, as well as abdominal aortas from 1K1C rats, but not abdominal aortas from CH rats were exposed chronically (4-6 weeks) to elevated arterial pressure. Sensitivity of rings with and without endothelium to nitroglycerin was suppressed significantly only in vessels exposed chronically to high arterial pressure. Impaired sensitivity to nitroglycerin in abdominal rings from 1K1C rats could not be abolished by exposure to 100 uM L-arginine, the substrate for production of NO by endothelial nitric oxide synthase, or 100 uM L-cysteine, the source of thiol groups required for the production of nitric oxide from nitroglycerin. Maximum relaxation to isoproterenol was impaired significantly in thoracic and abdominal rings, with and without endothelium, from 1K1C and CH rats. Relaxation to 8-bromo-cGMP and dibutyryl cAMP was similar in abdominal rings from all groups. We conclude that impaired vasorelaxation to nitroglycerin and isoproterenol in hypertension involves mechanisms prior to activation of vascular smooth muscle cGMP-dependent and cAMP-dependent protein kinase, respectively. Impaired cGMP, but not cAMP, mediated relaxation of aortas appears to result from their exposure to high arterial pressure per se. This effect does not appear to involve the vascular endothelium or vascular sources of thiols, but rather may reflect an effect of high arterial pressure to impair the ability of the artery to respond to nitric oxide derived from nitroglycerin.
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PMID:Selective effect of high arterial pressure in hypertension upon inhibition of cGMP versus cAMP mediated vascular relaxation. 884 63

A case of acromegaly associated with variegated spinal disorders was reported. The spinal disorders were multiple cervical disc herniations, spinal epidural cavernous angioma, multiple ossification of the spinal ligament and lumbar canal stenosis. A 51-year-old woman with acromegaly, complaining of disturbances of delicate hand movement and gate, consulted our department. Her past history included diabetes mellitus, hypertension and progressing enlargement of her extremities. Serum growth hormone level was 65.7 ng/ml and somatomedin-c level was 746 ng/ml. Brain MRI showed a pituitary tumor extending to the right cavernous sinus. Cervical MRI revealed disc herniations at C5/6 and C6/7. Thoracic MRI revealed osteoporosis, ossification of the posterior longitudinal ligament and multiple ossification of yellow ligament. Lumbar MRI disclosed ossification of yellow ligament and canal stenosis. Anterior fusion of C5-C7 and an intracapsular removal of the pituitary tumor were performed. Its pathology was that of eosinophilic adenoma. After 3 months, she suffered from paraparesis. On repeating MRI examination with Gd-DTPA, a spinal epidural mass was found at T4. Under laminectomy of Th3-5 and Th8-11, the epidural mass and ossified yellow ligament were removed. The epidural mass was cavernous angioma. She was able to walk without any assistance. An association of spinal canal stenosis with acromegaly is well known. But the association of disc herniation and with the ossification of spinal ligaments is rather rare in the literature. Spinal epidural cavernous angioma is very rare. We discussed the etiological aspects and the management of spinal disorders with acromegaly.
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PMID:[A case of acromegaly associated with variegated spinal disorders]. 891 52

Cyclosporine A (CsA) is an immunosuppressive agent that also causes hypertension. The effect of CsA on vascular responses was determined in Sprague-Dawley rats and isolated rat aortic rings. Male rats weighing 250 to 300 g were given either CsA (25 mg. kg-1. d-1) in olive oil or vehicle by intraperitoneal injection for 7 days. CsA administration produced a 42% increase (P<0.001) in mean arterial pressure (MAP) that reached a plateau after 3 days. Conversely, the levels of both nitrate/nitrite, metabolites of nitric oxide (NO), and cGMP, which mediates NO action, decreased by 50% (P<0.001) and 35% (P<0.001), respectively, in the urine. Thoracic aortic rings from rats treated with CsA and precontracted with endothelin (10(-9) mol/L) showed a 35% increase (P<0.001) in tension, whereas endothelium-dependent relaxation induced by acetylcholine (ACh, 10(-9) mol/L) was inhibited 65% (P<0.001) compared with that in untreated rats. This response was similar to that of endothelium-denuded aortic rings from untreated rats in which ACh-induced relaxation was completely abolished (P<0.001), but relaxation induced by S-nitroso-N-acetylpenicillamine (SNAP, 10(-8) mol/L) was unaffected (P<0.001). ACh-induced formation of both nitrate/nitrite and cGMP by both denuded and CsA-treated aortic rings was inhibited 95% (P<0.001) and 65% (P<0.001), respectively, compared with intact aortic rings. The effects of CsA were reversed both in vivo and in vitro by pretreatment with L-arginine (10 mg. kg-1. d-1 IP), the precursor of NO. There were no changes in MAP and tension in rats treated with L-arginine alone. In summary, CsA inhibits endothelial NO activity, with resulting increases in MAP and tension, and this inhibition can be overcome by parenteral administration of L-arginine.
Hypertension 1998 Nov
PMID:Role of nitric oxide in cyclosporine A-induced hypertension. 982 43

This study was designed to determine whether the antioxidants ascorbic acid, aminotriazole, and glutathione acutely reduce blood pressure (BP) by endothelium-independent or -dependent vasorelaxation in spontaneously hypertensive rats. Blood pressure of male Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) was measured before and 4 h after administration of antioxidants. Thoracic aortic rings with and without endothelium were suspended in organ chambers for isometric tension recordings. Each of the antioxidants, administered in vivo, significantly decreased blood pressure in SHR but had no significant effect on BP in WKY rats. The endothelium-dependent impaired relaxation of SHR aortic rings to acetylcholine (ACh) was improved by prior in vivo administration of each antioxidant. ACh-induced relaxations of aortic rings from WKY was not affected by prior antioxidant treatment. Addition of each antioxidant directly to the organ chamber containing SHR or WKY aortas produced dose- and endothelium-dependent relaxations. Moreover, antioxidant pretreatment of SHR aortic rings significantly potentiated ACh-induced relaxations in these aortas, suggesting that this effect was endothelium dependent. Relaxations induced by the antioxidants alone or by ACh in the presence of antioxidants were inhibited by addition of either xanthine plus xanthine oxidase or nitro-L-arginine. These findings suggest that either excess production of oxidants or a deficiency of antioxidant systems may contribute to the high blood pressure and the endothelium-dependent impairment of vascular relaxation in SHR.
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PMID:Antihypertensive and vasodilator actions of antioxidants in spontaneously hypertensive rats. 988 Jan 27

Since the first successful replacement of the aortic arch with perfusion of the head, various methods have been employed to preserve cerebral function during aneurysm operations. Although deep hypothermia was used for surgery of the aortic arch, as early as 1963, the introduction of prolonged circulatory arrest has simplified replacements of the aortic arch. Between October 1990 and September 1993, 69 patients underwent aortic arch replacement for aneurysmal disease at the Dept. of Cardio-Thoracic Surg., University of Vienna. 52 patients had an acute dissection Type A, 17 patients were operated on electively. The patients age (48 male, 21 female) ranged between 16 and 81 years. Primary diagnosis was hypertension (n=44), marfan (n=14), unknown (n=10) and trauma (n=1). Total cardiopulmonary bypass was established via femoral artery cannulation. All patients received Cortison and Thiopental for added cerebral protection. Deep hypothermia (12 degrees C), confirmed by 0-EEG, and circulatory arrest were induced in all patients. The aneurysm was opened longitudinally and a full thickness single patch or "island" of aortic wall, containing the origins of the three arch vessels, was constructed and anastomosed in a continuous fashion to an albumin coated graft. 68 patients survived the operation (intraoperative mortality 1%). The 30-day mortality was 23% (n=16). Twelve patients died of multiorgan failure, two patients of a stroke and two due to myocardial infarction. The mean cerebral circulatory arrest time was 32 minutes (range 11-61 min.). Our experience with aortic arch replacements using profound hypothermia and circulatory arrest supports our contention, that it is the method of choice in this very difficult surgical field.
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PMID:Operative management of aortic arch aneurysm using profound hypothermia and circulatory arrest. 1006 52

We have tested the hypothesis that growth factor signaling pathways are augmented in hypertension, a disease associated with vascular smooth muscle cell growth. Thoracic aorta was dissected from deoxycorticosterone acetate-salt (DOCA-salt) and one kidney, one clip (1K, 1C) hypertensive rats and from sham normotensive rats for use in isolated tissue bath experiments. Systolic blood pressure was significantly higher in DOCA-salt and 1K, 1C than in normotensive sham rats: 192 +/- 7, 185 +/- 10, and 117 +/- 4 mmHg, respectively. Although virtually no contraction to epidermal growth factor (EGF) was observed in endothelium-denuded sham rat aorta [1 +/- 1% phenylephrine (PE) (10 micromol/l)-induced contraction], the maximal EGF-induced contraction was 45 +/- 7% in endothelium-denuded aorta from DOCA-salt hypertensive rats and 39 +/- 7% in aorta from 1K, 1C rats. Although slightly attenuated, a contraction to EGF was still observed in endothelium-intact aortic strips from 28-day DOCA-salt hypertensive rats. We also conducted concentration-response curves to EGF on days 1, 3, 5, 7, 14, and 21 of DOCA-salt therapy. A significant contraction to EGF in aorta from DOCA-salt rats was observed on day 14, when DOCA-salt rats had significantly higher blood pressure than sham rats: 188 +/- 6 and 122 +/- 3 mmHg, respectively. Transforming growth factor-alpha, an agonist of the EGF receptor, contracted DOCA-salt rat aorta (30 +/- 7% PE-induced contraction) but not sham aorta (3 +/- 3%). The EGF receptor tyrosine kinase inhibitor 4,5-dianilinophthalimide (10 micromol/l), the mitogen-activated protein kinase kinase inhibitor PD-098059 (10 micromol/l), and the L-type voltage-gated calcium channel inhibitor diltiazem (1 mol/l), but not the cyclooxygenase inhibitor indomethacin (10 micromol/l), virtually abolished EGF-induced contraction (85, 98, and 99% reduction, respectively). These data support a striking difference in EGF signaling between normotensive and hypertensive animals. Furthermore, they provide evidence that growth factors should be considered vasoconstrictors as well as growth modulators in hypertension.
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PMID:Epidermal growth factor: a potent vasoconstrictor in experimental hypertension. 1007 82


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