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)

A short and up-to-date review on the great advances made in the field of the atrial natriuretic factor (ANF) is presented. All the short active peptides (up to 33 AA) isolated after purification of atrial homogenates have the same core of 23 amino acids (Ser 103-ARG 125). The ANF liberated in the medium of cultures of rat atrial cardiocytes is the 26 amino acid Arg 101-Tyr 126. Cloning of the cDNA encoding for ANF and of the rat, mouse, and human ANF gene has been accomplished. ANF has a most potent and short-lasting diuretic and natriuretic effect that appears to be predominantly due to a significant increase in glomerular filtration rate. ANF inhibits the release of aldosterone both in vitro and in vivo. It produces a profound inhibition of vascular contraction induced by norepinephrine and angiotensin II. This vasorelaxation is followed by a prolonged refractory period. ANF administration corrects the hypertension in 2K-1C hypertensive rats and in spontaneously hypertensive rats. Specific high-density binding sites have been found in the brain, especially in the hypothalamus, subfornical organ, median eminence, area postrema, and nucleus tractus solitarius, all areas involved in the brain control of hypertension and in the regulation of salt and water. ANF has no effect on the known sodium transport mechanisms across cell membrane. It has a major effect on the stimulation of guanylate cyclase activity, especially in renal glomeruli. Specific radioimmunoassay procedures have been established and results of preliminary studies that establish clearly that ANF is a circulating hormone are presented.
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PMID:Atrial natriuretic factor. 294 45

The role of hypertension for the combined occurrence of incipient diabetic nephropathy and diabetic retinopathy (RP) was evaluated in 155 insulin-dependent diabetic patients (74 male/81 female); mean age 32.4 +/- 12.2 STD years; means diabetes duration 12.8 +/- 10 STD years). Albumin excretion rate (AER) was measured in 24 hours urine samples by RIA, retinal status was determined by both, fundoscopy and fluorescein angiography. Analysis of the data revealed a statistically significant correlation between the duration of disease and elevated AER (p less than 0.012), and the occurrence of retinopathy (p less than 0.0001). Although there was a close correlation between retinopathy and elevated AER (p less than 0.0001), it is remarkable that 31% of the patients with normal AER (less than 15 micrograms/min) showed signs of non proliferative RP. On the other hand 30% of patients without retinal changes showed an elevated AER (less than 15 micrograms/min). In the group of microalbuminuric patients (greater than 15 micrograms/min) systolic (p less than 0.004) and diastolic (p less than 0.04) blood pressures were significantly higher than in normoalbuminuric patients (less than 15 micrograms/min). Patients with proliferative retinopathy showed significantly higher systolic and diastolic (p less than 0.015) blood pressures compared to patients without retinal changes, though albumin excretion rates were not different in both groups of patients. In conclusion, our results show that diabetic nephropathy and diabetic retinopathy do not develop simultaneously in a representative number of insulin-dependent diabetic patients, but hypertension may be a major risk factor for the development of both microangiopathic complications.
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PMID:[Significance of arterial blood pressure for the development of microalbuminuria and retinopathy in type I diabetes mellitus]. 323 57

A lot of over 60 atherosclerotics with clinical manifestations of senile depressive illness was studied comparatively with a lot of subjects of the same age with essential arterial hypertension (EAH). As concerns the behaviour of the catecholamine content in CSF and blood, the total catecholamines are approxiately equal in the two lots, but with a clear difference of the catecholamine fractions. The CSF catecholamines behaviour in old atherosclerotics is characterized by the presence of increased values of noradrenaline (NA) and of adrenaline (A), with increased statistical significance, but without modifications of the adrenaline percentage (A %) from the total catecholamines, comparatively to the values found in normal subjects. The serotonin (5-HT) content of the CSF in men with atherosclerotic senile depressive illness was lower even than in subjects with coronary atherosclerosis. In atherosclerosis protides modifications precede the histologic changes. In CSF, GLU, ALA, TYR increase in old subjects. In blood, GLU, ALA, TYR, HIS, LEU, SER increase in the same subjects. ARG decreases with age. THR is higher in men than in women. In the urine of all the men as well as of all the women of more than 60 years, GLN and ALA have increased values. LYS increases with age. GLN and ARG are higher in men than in women.
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PMID:Pattern of the cerebrospinal fluid (CSF) and blood biogenic amines and of the CSF, blood and urine amino acids as pathogenetic ground of the senile depressive illness. 677 91

Forty patients (34 males and 6 females) with neurological complaints/manifestations and with a past history of multiple sexual partners attending the Government Rajaji Hospital, Madurai, India between April 1992 and October 1992 were investigated for neurosyphilis. Metabolic disorders, hypertension, ischaemic heart disease, arrhythmias and trauma were excluded. Seven males (17.5%) were found to have neurosyphilis. The youngest was 26 years old and the oldest was 47. All were married and of low socioeconomic background. Meningovascular syphilis was the predominant presentation (6:1). Associated cardiovascular involvement was noticed in one of the cases. There was no associated HIV infection in these cases. The incidence is higher than previous reports from this centre.
Int J STD AIDS
PMID:Prevalence of neurosyphilis at Government Rajaji Hospital, Madurai, India. 794 62

Increased elastin production and accumulation is a rapid and sensitive response to elevated vascular wall stress in both systemic and pulmonary hypertension. While initially protecting the vessel wall, these structural changes may in the longer term result in reinforcement of the hypertensive state and contribute to the persistence of the pathology of hypertension. Rapid responses apparently uncorrelated with increased elastin mRNA, at least in the case of systemic vessels, suggest novel mechanisms perhaps including increased efficiency of message translation or matrix accumulation of the protein. Investigations using in vitro organ and cell culture models have indicated a role for phospholipases and protein kinases, including protein kinase C, in stretch-induced elastin synthesis. In addition, tyrosine phosphorylation of membrane/sub-membrane/cytoskeletal sensors, including focal adhesion kinase and members of the lipocortin family, have been shown to be important in this transduction mechanism. Because its turnover is normally very slow, additional vascular elastin accumulated during hypertensive episodes, together with its consequences for the physical properties of the vessel wall, may persist long after blood pressure is restored to normal levels. Thus, recent interest has been drawn to the possibility of achieving regression of accumulated matrix elastin by promoting turnover of this protein through activation of endogenous vascular elastase and collagenase activities.
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PMID:Elastin in systemic and pulmonary hypertension. 857 61

Angiotensin II (AII), acting via its G-protein linked receptor, is an important regulator of cardiac, vascular, and renal function. Following injection of AII into rats, we find that there is also a rapid tyrosine phosphorylation of the major insulin receptor substrates 1 and 2 (IRS-1 and IRS-2) in the heart. This phenomenon appears to involve JAK2 tyrosine kinase, which associates with the AT1 receptor and IRS-1/IRS-2 after AII stimulation. AII-induced phosphorylation leads to binding of phosphatidylinositol 3-kinase (PI 3-kinase) to IRS-1 and IRS-2; however, in contrast to other ligands, AII injection results in an acute inhibition of both basal and insulin-stimulated PI 3-kinase activity. The latter occurs without any reduction in insulin receptor or IRS phosphorylation or in the interaction of the p85 and p110 subunits of PI 3-kinase with each other or with IRS-1/IRS-2. These effects of AII are inhibited by AT1 receptor antagonists. Thus, there is direct cross-talk between insulin and AII signaling pathways at the level of both tyrosine phosphorylation and PI 3-kinase activation. These interactions may play an important role in the association of insulin resistance, hypertension, and cardiovascular disease.
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PMID:Cross-talk between the insulin and angiotensin signaling systems. 890 9

In order to investigate relationship between regional cerebral blood flow (rCBF) and the white matter lesions on MRI in silent cerebral infarction, we quantitatively measured rCBF by 123I-IMP autoradiography method (IMP ARG method) and single photon emission tomography (SPECT) in 36 patients with silent cerebral infarction (SCI group), 22 patients with multi-infarct dementia (MID group), and 16 control subjects without periventricular hyperintensity (PVH) and lacunar infarction on MRI (CL group). Regions of interest (ROIs) on rCBF images were set in the frontal (F), temporal (T), parietal (P), occipital (O) cortex, and the cerebral white matter (W). The severity of PVH on MRI T2-weighted image was divided into four grades (grade 0-3). Our results: 1) Though the frequency of hypertension was significantly higher in SCI group and MID group compared with CL group, no significant difference was seen in the mean age among these three groups. 2) rCBF in the white matter and cerebral cortices except the occipital cortex in SCI group was significantly low compared with CL group (gamma CBFSCI/gamma CBFCL: W 0.87, F 0.87, P 0.88, O 0.92). 3) rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex, in MID group was significantly low compared with SCI group (gamma CBFMID/gamma CBFCL: W 0.69, F 0.71, T 0.74, P 0.75, O 0.81). 4) The mean grade of PVH in MID group was significantly higher that that in SCI group (SCI 1.1 vs MID 2.5). 5) The severity of PVH was significantly correlated with each rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex. Our findings suggest that the quantitative measurement of rCBF by IMP ARG method is useful for the follow-up study in the patients with silent cerebral infarction as well as the evaluation of the severity of PVH on MRI.
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PMID:[Regional cerebral blood flow and periventricular hyperintensity in silent cerebral infarction--comparison with multi-infarct dementia]. 893 95

In this review, the role of tyrosine kinases in angiotensin II-mediated signal transduction pathways in vascular smooth muscle is discussed. Angiotensin II was isolated by virtue of its vasoconstrictor abilities and has long been thought to play a critical role in hypertension. However, recent studies indicate important roles for angiotensin II in inflammation, atherosclerosis, and congestive heart failure. The expanding role of angiotensin II indicates that multiple signal transduction pathways are likely to be activated in a tissue-specific manner. Exciting recent data show that angiotensin II directly stimulates tyrosine kinases, including pp60(c-src) kinase (c-Src), focal adhesion kinase (FAK), and Janus kinases (JAK2 and TYK2). Angiotensin II may activate receptor tyrosine kinases, such as Axl and platelet-derived growth factor, by as-yet-undefined autocrine mechanisms. Finally, unknown tyrosine kinases may mediate tyrosine phosphorylation of Shc, Raf, and phospholipase C-gamma after angiotensin II stimulation. These angiotensin II-regulated tyrosine kinases appear to be required for angiotensin II effects, such as vasoconstriction, proto-oncogene expression, and protein synthesis, on the basis of studies with tyrosine kinase inhibitors. Thus, understanding angiotensin II-stimulated signaling events, especially those related to tyrosine kinase activity, may form the basis for the development of new therapies for cardiovascular diseases.
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PMID:Angiotensin II signal transduction in vascular smooth muscle: role of tyrosine kinases. 913 Apr 41

Originally known to be a vasoconstrictor and thought to play a critical role in hypertension, angiotensin II has recently emerged to be important in inflammation, atherosclerosis and congestive heart failure. The expanding role of angiotensin II implies that multiple signal transduction pathways are likely to be activated in a tissue-specific manner. Recent data show that angiotensin II stimulates not only cytoplasmic tyrosine kinases including c-Src, focal adhesion kinase (FAK), and Janus kinases (JAK2 and TYK2), but also may transactivate receptor tyrosine kinases such as Axl and PDGF by as yet undefined autocrine/paracrine mechanisms. Finally, tyrosine kinases, which mediate tyrosine phosphorylation of key signal mediators such as Shc, Raf, and phospholipase C-gamma following angiotensin II stimulation, remain to be defined. These tyrosine kinases, activated by angiotensin II, appear to be required for angiotensin II effects such as vasoconstriction, proto-oncogene expression, protein synthesis, and cell proliferation. Thus, it is important to understand angiotensin II-mediated signaling events, especially those related to tyrosine kinase activity, to develop new therapies for cardiovascular diseases.
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PMID:Angiotensin II signal transduction in vascular smooth muscle cells: role of tyrosine kinases. 921 88

We have presented here are a long list of conditions associated with an increased incidence of fetal growth restriction. Missing from much of the literature on FGR are data that would allow more informed counseling of patients in terms of predicting their risk of carrying a pregnancy complicated by FGR. For example, very little has been published on the chances of having an infant with FGR in a woman suffering from SLE or chronic hypertension. Future studies of FGR should address these issues so that clinicians may counsel their patients properly.
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PMID:Etiologies of fetal growth restriction. 942 86


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