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

In patients with renovascular hypertension, a significant decrease in glomerular filtration rate (GFR) and in renal plasma flow (RPF) in the stenotic kidney was accompanied by a significant homolateral decrease in extraction of PAH(EPAH) and in net tubular reabsorption of sodium (RNa). There was a highly significant correlation between differences in RNa and differences in either GFR or RPF, while no correlation between differences in RNa and in EPAH was noted. It is suggested that the nature of the relationship between GFR and RNa is essentially the same in unilateral renal artery stenosis in man, as in acute constriction of the renal artery or the aorta in the experimental animal.
Nephron 1977
PMID:Relationship between glomerular filtration rate and tubular reabsorption of sodium in patients with unilateral renal artery stenosis. The role of the renal prostaglandins. 84 24

Catecholamines and catecholamine-synthesizing enzymes have been studied quantitatively in specific brain areas of spontaneously (genetically) hypertensive rats by means of a combination of sensitive enzymatic-isotopic methods and a microdissecting technique. Changes in catecholamine metabolism were found to be localized to regions of the brain implicated in the regulation of blood pressure. Noradrenaline levels were decreased in specific nuclei of the anterior hypothalamus and in the nucleus interstitialis striae terminalis ventralis. The activity of the adrenaline-forming enzyme, phenyl-ethanolamine-N-methyl transferase, was increased in the A1 and A2 areas of the brain stem. These results implicate catecholamine-forming neurons in the hypothalamus and brain stem in the development of spontaneous hypertension in rats.
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PMID:Biochemical and morphologic study of catecholamine metabolism in spontaneously hypertensive rats. 86 35

Hypertension in spontaneously hypertensive rats (SHR) develops initially without any obvious organic lesions, and mainly with hemodynamic alteration due to increased peripheral vascular resistance. It is then followed later by various cardiovascular complications such as stroke. These facts indicate that this spontaneous hypertension is very similar to essential hypertension in man. Studies on the pathogenic mechanisms of spontaneous hypertension up to the present have revealed the following points. (1) This hypertension is genetically transmitted to the offspring in an additive mode by a relatively small number of major genes; (2) Environmental factors such as stress and salt-loading accelerate the hypertension; (3) Parabiosis between SHR and normotensive rats offered no positive evidence indicating the involvement of any strong humoral factors; (4) Assays on adrenal and thyroid hormones have suggested that this hypertension is not a simple endocrine hypertension; (5) The destruction of the central nervous system or sympathectomy on blood pressure or peripheral vascular resistance, as well as the recording of spontaneous sympathetic discharge, etc. have indicated the positive involvement of the autonomic nervous system in the development of this hypertension; (6) Changes in the enzyme activities of the central nervous system and in the central responses to various candidates of central neurotransmitters suggested that 'noradrenergic inhibitory mechanisms for blood pressure regulation in the brainstem' (Yamori, Lovenberg and Sjoerdsma, 1970) might be insufficient and result in the initial enhancement of peripheral vasomotor tone causing labile hypertension; (7) Noradrenalin turnover study of the heart and hindlimb perfusion experiments indicated that the neural factor was mainly involved in the development or the early stage of hypertension; this finding was further supported by the increased noradrenalin level or dopamine-beta-hydroxylase activity in the blood; (8) Histometrical studies indicated that the structural component of the peripheral vascular resistance stabilized the hypertension; (9) The initial neurogenic factors and successive involvement of nonneurogenic factors are relayed by the acceleration of protein metabolism of the vascular wall ('adaptive metabolic change', Yamori, 1974). This acceleration is commonly detected by amino acid incorporation study in both spontaneous and other experimental hypertension; (10) Increased lysine incorporation into the noncollagenous protein of the mesenteric arteries detected in the prehypertensive SHR was experimentally confirmed to be influenced by neural innervation. This confirmation indicated the importance of such a trophic effect of the nervous system on the structural alteration of blood vessels in the development of hypertension (neurovascular linkage, Yamori, 1975)...
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PMID:Pathogenesis of spontaneous hypertension as a model for essential hypertension. 87 Jul 22

Nephronophthisis (previously described as familial juvenile nephronophthisis and medullary cystic disease) is characterized by insidious renal failure, its main features being increased urinary sodium loss, pitressin-resistant hypotomic polyuria, polydipsia, normal urine sediment and absence of hypertension. Renal function and histologic studies were performed in a family in which two siblings had this disorder, while the parents and two other siblings appeared clinically normal. Both parents demonstrated a moderate impairment of maximum urinary concentration. The values for tubular free water reabsorption (TcH2O) were relativley normal in the parents and the healthy siblings. One of the index patients showed only minimal sodium wasting even though he had hyposthenuria, thus suggesting an involvement of the collecting ducts in the early stage of neophronophthisis. No evidence of proximal tubular dysfunction was found. Although the light-microscopic examination of renal biopsies from the parents and the healthy siblings was unremarkable, electron microscopy revealed probable abnormalities in all four. An autosomal recessive mode of inheritance is, therefore, suggested in this family. The etiology of nephronophthisis is obscure but a likely possibility is that the renal damage results from an inborn metabolic error.
Nephron 1977
PMID:Nephronophthisis. Renal function and histologic studies in a family. 88 91

Juxtaglomerular cell count (JGCC) and juxtaglomerular activity (JA) on the fragments of the ischemic kidney and plasma renin activity (PRA) in peripheral venous blood were studied in 26 renovascular patients. In 11 cases PRA was also measured in renal venous blood. JGCC and JA values were always above normal range and both were significantly related to the PRA values in peripheral venous blood, while only JA was related to the PRA values in renal venous blood. These data indicate that in human renovascular hypertension the juxtaglomerular apparatus is hyperplastic and hypergranulated: the correlation between its morphological appearance and PRA seems to indicate that the renin-angiotensin system may be in some way involved in the genesis of hypertension.
Nephron 1977
PMID:Relationship between juxtaglomerular apparatus and plasma renin activity in human reno-vascular hypertension. 91 69

Plasma renin reactivity (PRR) is the in vitro rate of angiotensin generation after addition of exogenous renin to plasma. The purpose of the present study is to compare measurements of PRR in venous effluent from the involved and uninvolved kidneys in both experimental and clinical renovascular hypertension. A two-kidney model of experimental hypertension was created by placing an ameroid resin constrictor around one renal artery in each of seven dogs. Plasma renin activity (PRA) in venous plasma from the involved kidney increased (p less than 0.001); comparing PRA in venous effluent from the stenotic and nonstenotic kidneys, the PRA ratio also increased ( p less than 0.005). Renal venous PRR did not change on either side after occlusion of the renal artery (p greater than 0.1), and the renal venous PRR ratio did not differ from the mean control ratio of 1.0 +/- 1 SE (p greater than 0.1). Similarly, in 9 patients with renovascular hypertension, mean PRR in venous plasma from the two kidneys did not differ (p greater than 0.8). These results suggest that measurement of renal venous PRR is not helpful in confirming a diagnosis of renovascular hypertension.
Nephron 1977
PMID:Renal venous plasma renin reactivity in clinical and experimental renovascular hypertension: renin reactivity in renovascular hypertension. 91 70

112 cases of MPGN, whose diagnosis was made on light microscopy, were reviewed. Histological examination showed 66 cases of 'classical' MPGN, 33 of MPGN with a lobular pattern and 13 of MPGN with epithelial crescents. In 11 patients dense intramembranous deposits were observed. On immunofluorescence (95 cases) 62 patients showed deposits of C3 together with immunoglobulins, 20 had a predominant deposition of C3 and in 13 C3 alone was present. At the moment of biopsy 57 patients had nephrotic syndrome, 43 hypertension, 43 impaired renal function and 65 hypocomplementaemia. In 23 cases, one or more episodes of macroscopic haematuria occurred. The actuarial survival was 70% after 10 years and 50% after 20 years from onset. At last observation 25 patients were dead or on haemodialysis, 22 had impaired renal function, 62 had normal renal function and 2 were in complete remission. The histological variety with epithelial crescents had a significantly worse outcome. The presence of dense deposits or of any specific immunofluorescence pattern had no prognostic significance. Nephrotic syndrome, renal function impairment and hypertension indicated a poor prognosis: however, macroscopic hamaturia or hypocomplementaemia did not influence the outcome.
Nephron 1977
PMID:The prognostic value of some clinical and histological parameters in membranoproliferative glomerulonephritis (MPGN): report of 112 cases. 91 74

Renovascular hypertension in two sisters, aged 22 and 20, respectively, has been described. Renal artery stenoses were observed unilaterally in the elder patient and bilaterally in the younger one. In both patients, the functional significance of unilateral stenosis of the renal artery was documented by the renal vein renin ratio between the affected side and the contralateral or less affected side. High blood pressure and elevated plasma renin activity have been normalized with a unilateral revascularization in the elder patient, and with the treatment of propranolol in the younger one. The histological examination of the stenotic renal artery in the elder patient showed a finding comparable to the perimedial fibroplasia in Harrison and McCormack's classification of idiopathic fibromuscular stenosis.
Nephron 1976
PMID:Occurrence of renovascular hypertension in two sisters. 95 Oct 17

Abnormalities of renal handling of urate occur in a wide variety of physiological and pathological conditions and are mediated by factors including renal blood flow, glomerular filtration rate, urine flow rate, urinary constituents, metabolites, hormones and drugs. The determination of the aetiological factors in each abnormal situation is complex and the problem is discussed in relation to a variety of conditions including renal tubular disorders and mental intoxications, hypertension, toxaemia of pregnancy, glycogen storage disease, fructose administration, hereditary fructose intolerance, as well as obesity, regular alcohol consumption and hyperlipoproteinaemia. Apart from those diseases, usually genetically determined, which are associated with excessive production of urate, the most common causes of hyperuricaemia act at a renal level and result in a reduction in the net renal excretion of urate.
Nephron 1975
PMID:Abnormal renal urate homeostasis in systemic disorders. 105 88

The renal prostaglandins PGS2 and PGE2 possess potent antihypertensive and vasodepressor activity. The mechanism of blood pressure lowering effect is through peripheral arteriolar dilation with a fall in total peripheral resistance. PGA unlike PGE escape degradation by the lung and thus could circulate as antihypertensive hormones. Since plasma PGA levels rise in humans on a low sodium intake, it has been postulated that the beneficial effects of a low sodium diet in some hypertensives may be the result of an increase in peripheral vasodilating PGA. Support that plasma PGA may be a regulator of systemic blood pressure is also derived from the fact a PGA-secreting renal tumor was associated with a fall in blood pressure and a rise in plasma PGA in a previously hypertensive woman. The removal of the tumor resulted in a return of blood pressure to elevated levels and a concomitant fall in PGA. Recently, a number of human patients with essential hypertension have been infused with PGA1 and PGA2. It was observed that there was an initial increase in renal blood flow, sodium and water excretion which was associated with no change in the elevated blood pressure. When blood pressure ultimately fell, there was a return of renal blood flow, sodium and water excretion to preinfusion levels. It would appear that PGA compounds act as 'ideal' antihypertensive agents since they favorably effect renal resistance, sodium and water homeostasis, plasma volume, total peripheral resistance, blood pressure and indirectly cardiac output through baroreceptor stimulation, all factors known to be important in etiology in human hypertension.
Nephron 1975
PMID:Renal prostaglandins. 110 Oct 92


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