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

A report is given on a 47-year-old woman with periarteritis nodosa. A unilateral retinopathy with disseminated cotton-wool-spots surrounded by retinal haemorrhages and edema was observed. Fluoresceinangiography showed a multifocal constriction of the retinal capillaries. This lesion of the retinal vessels can be distinguished from those caused by hypertension. An acute immunological reaction has been suggested as the pathogenesis. Some authors have described this retinal lesion in collagen diseases as a "toxic" retinopathy. We prefer the term acute immunological microangiopathy (AIM).
 ...
PMID:[Early neuro-ophthalmological symptoms of periarteritis nodosa. A case report (author's transl)]. 1 63

The activity of lysyl oxidase which catalyzes the initial step of cross-linking of collagen and elastin polypeptides was measured in blood vessels of the hypertensive rat. The enzyme activity was increased in the aorta and mesenteric artery when hypertension was induced in 8-week-old rats with administration of deoxycorticosterone acetate (DOCA) and 1% saline. Reserpine diminished this increase in vascular lysyl oxidase activity concomitant with reduction in blood pressure. When beta-aminopropionitrile, a specific inhibitor of lysyl oxidase, was administered before the onset of DOCA-salt hypertension, the aortic collagen content was reduced markedly. Concomitant with reduction in the aortic collagen content, the development of hypertension and arteriosclerotic changes in the kidney was partially prevented. These results would indicate that hypertension increases the amount and the degree of cross-linking of vascular collagen and that the deposition of excess collagen in the vascular wall contributes to the development of hypertension and arteriosclerosis.
 ...
PMID:Increased lysyl oxidase activity in blood vessels of hypertensive rats and effect of beta-aminopropionitrile on arteriosclerosis. 2 27

There is a definite need for replacement estrogen therapy in menopausal women exhibiting vasomotor symptoms or osteoporosis, particularly if the woman has had bilateral oophorectomy. There is a less clearly defined need in women complaining of emotional symptoms. Atrophic vaginitis and trigonitis is usually best treated with topical application of estrogen, which does not have systemic side effects if used weekly; more frequent use can lead to vascular absorption. Some of the problems associated with estrogen replacement are dose-related and can be eliminated by using smaller dosages. Uterine bleeding can usually be controlled by administering cyclically with progesterine. Hypertension, thrombosis, and adenocarcinoma are problems associated with administration of exogenous estrogens; use should be undertaken with great care in women exhibiting these conditions and patients should be followed closely to make sure such conditions are not developing. Other conditions which may worsen with estrogen therapy are diabetes mellitus, seizure disorders, migraine, multiple sclerosis, collagen diseases, cholelithiasis, and hyperlipidemia. None except hyperlipidemia is an absolute contraindication but risk/benefit ratios must be considered carefully in these cases.
 ...
PMID:Estrogens for the menopause. Maximizing benefits, minimizing risks. 19 9

In two models of hypertension in rats, it was shown that collagen synthesis and deposition are increased in arteries where blood pressure is elevated. By contrast, there were no alterations in any of the markers of collagen synthesis in veins, where blood pressure was only slightly elevated. It would appear that the stimulus for vascular collagen synthesis is provided by a direct effect of the increased pressure on the arterial cells rather than by a humoral factor released into the general circulation.
 ...
PMID:Hypertension: increase of collagen biosynthesis in arteries but not in veins. 19 77

An immunohistochemical method and light microscopy were utilized to determine localization of prolyl hydroxylase in the cardiovascular tissues of hypertensive rats. The blood vessels and renal glomerulus from these animals demonstrated an enhanced immunoreaction for prolyl hydroxylase. As the most prominent staining was observed in medial smooth muscle cells of blood vessels, these are probably the major collagen-producing cells in arteriosclerotic lesions induced by hypertension. In the glomerulus, endothelial cells and probably mesangial cells are mainly responsible for the collagen formation. An intense immunoreaction was also found in the fibroblasts which proliferated in the area of myocardial fibrosis in hypertensive rats, while there was no specific staining in myocardial cells in either hypertensive or normotensive rats.
 ...
PMID:Localization of prolyl hydroxylase by the immunoperoxidase method in cardiovascular tissues of hypertensive rats. 21 94

Platelet aggregability was measured using platelet rich plasma (PRP) collected from 197 clinical cases including 52 healthy volunteers. In 31 patients of acute stage of thrombosis (within 2 weeks from the onset), a significant enhancement of platelet aggregation measured 5 min after an addition of 3 and 10 muM ADP or 0.1 and 1 mug/ml of adrenaline to PRP (p less than 0.05, compared to the healthy group). Also a significant enhancement of secondary aggregation induced by adrenaline was observed (p less than 0.05). The enhancement was especially marked in the response induced by adrenaline. Such an enhancement was not observed in patients in the recovery stage of thrombosis, hypertension, angina pectoris and other miscellaneous diseases. There was no difference in the parameters related to the velocity of aggregation or intensity of primary aggregation between the diseased and the healthy group. In response induced by collagen (bovine achilles tendon, 0.3 and 1 mg/ml) any difference in the aggregation curve was not observed between the diseased and the healthy group. Such findings suggest a presence of an enhancement of ADP-release mechanism of platelets in acute thrombosis. Aslo a significance of adrenaline-induced platelet aggregation was proposed to detect platelet functions for analysis of mechanism of thromboembolic disorders.
 ...
PMID:Hyperaggregability of platelets in thromboembolic disorders. 24 93

beta-Aminopropionitrile, a specific inhibitor of lysyl oxidase prevented the rise in blood pressure induced by deoxycorticosterone-salt in rats. In addition, after the onset of hypertension, administration of beta-aminopropionitrile lowered the blood pressure. Concomitant with the lowering of blood pressure, there was a reduction in the more highly crosslinked form of vascular collagen. These findings would indicate that increases in vascular connective tissue are not only sequelae of hypertension, but may also contribute to the maintenance of elevated blood pressure.
 ...
PMID:Reduction of blood pressure and vascular collagen in hypertensive rats by beta-aminopropionitrile. 26 88

1. Biosynthesis and deposition of collagen, as well as DNA and total proteins, are increased in aortae of rats after 1, 3 and 6 weeks of hypertension. 2. The maximal increase in the rate of synthesis of collagen is observed within one week of hypertension when the stress to the arterial wall is maximal. 3. Reserpine administration prevents hypertension and inhibits the increase of collagen metabolism. 4. At any time of evolution of the hypertension, a linear positive correlation is found between the collagen content in the aorta and the level of blood pressure. 5. These data suggest that synthesis of matrix components by the arterial smooth-muscle cells is controlled by variation in the blood pressure level and is not a direct consequence of circulating humoral factors liberated by the ischaemic kidney.
 ...
PMID:The relationship between blood pressure and aortic collagen metabolism in renal hypertensive rats. 28 65

Studies on the Kyoto (SHR) and the New Zealand (GHR) strains of genetically predisposed hypertensive rats have shown that in the SHR neurogenic influences, primarily of higher central origin, play an important role in the initiation of hypertension. Studies on human essential hypertension indicate that this may also be true for man, although it is far from being the sole explanation. Brookhaven hypertension-prone rats illustrate the interaction between genetic and exogenous factors since they require an overload of salt for the development of high blood pressure. The Milan hypertensive rats (MHS), on the other hand, illustrate a genetic deviation of renal function with imbalance between glomerular filtration and tubular resorption of sodium and water, which may simulate at least some variants of the relatively mild forms of low renin hypertension in man. Structural adaptive vascular changes have been demonstrated in SHR and GHR and in nongenetic renal hypertension in rats, and there are several indications of their presence in MHS. Thus, regardless of the nature of the initiating factors, these secondary but rapidly established changes occur and greatly contribute to the maintenance and acceleration of the hypertensive state. The vascular changes can even be regarded as a common denominator for chronic hypertension and serve as an element which, in fact, reinforces the initiating mechanisms. The progress of the vascular changes can be interfered with by reducing the pressure load. Lowering the blood pressure by pharmacologic treatment is most effective when the treatment is initiated as such an early age when the cardiovascular structural adaptation is still minimal. Treatment in later phases is less successful since the adaptive increases in cardiac and vessel wall thickness can then no longer be fully normalized by pressure reduction because of increased amounts of collagen and other connective tissue elements in the vessel wall, which regress poorly. An increased wall thickness of the resistance vessels implies a vascular hyperreactivity to constricting influences which, in turn, rapidly brings the blood pressure back to supranormal levels as soon as therapy is stopped.
 ...
PMID:Mechanisms of spontaneous hypertension in rats. 32

This communication describes the electron microscopy (EM) study of the small arterial vessels in renal biopsies from 32 patients with a variety of glomerular and tubulointerstitial diseases. With the possible exception of lipoid nephrosis, all types of glomerular and tubulointerstitial diseases were associated with abnormal arterial vessels. The vascular abnormalities included variable thickening and irregularity of the basement membranes (sclerosis), excessive elastic tissue and collagen fibers, atrophic or necrotic smooth muscle cells, and electron-dense deposits. The EM of glomeruli and tubules from the same biopsy specimens often revealed similar features, i.e., sclerosis, necrotic changes and electron-dense deposits. The pathogenesis of the arteriolopathies, like that in many glomerular and tubulointerstitial diseases, remains unclear. Hypertension was considered a factor, but only 15 percent of the patients were hypertensive. Furthermore, vascular lesions in patients with hypertension were no worse than those without it. Whatever may be the pathogenesis of these arteriolopathies, the similarities between the renal arteriolar and glomerular abnormalities and between arteriolar and tubular lesions suggest a common mechanism of inducement of the lesions.
 ...
PMID:Ultrastructural analysis of renal arteriolopathies in glomerular and tubulointerstitial diseases. 36 Sep 59


1 2 3 4 5 6 7 8 9 10 Next >>