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

Information defining the renin-angiotension-aldosterone axis as a control system concurrently regulating salt balance and blood pressure has been applied to reexamine the role of renin in experimental and clinical forms of renovascular and renal hypertension, and thence to develop criteria for differentiating these entities. Experimentally, there are two models of renovascular hypertension; one is characterized by excess renin with reduced sodium (vasoconstrictor form) and the other by excess sodium with reduced renin (volume form). But with sodium depletion, the volume form converts to a vasoconstrictor form illustrating how the two factors coordinate to maintain blood pressure. In man, renovascular and renal hypertensions appear to be sustained by the same two mechanisms. Studies in man show that, in the absence of unilateral disease, the supine renal venous renin level in each kidney is consistently 24 percent higher than the peripheral level. Because of this constant relationship, the peripheral renin level is a measure of the renal secretion rate. Our studies indicate the curable unilateral renovascular hypertension is, in fact, renin-dependent vasoconstrictor hypertension. Three criteria, derived from four renin measurements, identify this situation: (1) Hypersecretion of renin is reflected by a high peripheral level when indexed against sodium excretion. (2) Lateralization of renin secretion with contralateral suppression rules out occult bilateral disease. It is indicated by V-A equal 0 from the uninvolved kidney. (3) (V-A)/A greater than 48 per cent from the ipsilateral kidney supports unilateralization. With data derived from patients with essential hypertension as a reference, the degree to which (V-A)/A is greater than 0.48 can be used to estimate the degree of renal ischemia, using Fick's principle. Corroborative evidence to support these three criteria can be developed from the blood pressure response to angiotensin blocking drugs or to antirenin therapy with propranolol. Clinical analysis validates these criteria to identify curable hypertension from unilateral renovascular or parenchymal disease. In patients with either occult or overt bilateral renal disease, the volume factor often predominates and is expressed by some suppression of plasma renin levels. Continued
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PMID:The renin axis and vasoconstriction volume analysis for understanding and treating renovascular and renal hypertension. 23 77

Changes in the fractional distribution of cardiac output (FF), organ blood flow, and regional vascular resistance were measured by the isotope dilution technique of Sapirstein using 86Rb as indicator in unanesthetized rats during acute arterial hypertension produced by bilateral lesions of the nucleus tractus solitarii (NTS). After NTS lesions, the FF was significantly reduced in skin, muscle, and colon, increased in ventricular myocardium, spleen, and adrenal glands, and was unchanged elsewhere. Because of a marked reduction in cardiac output (CO) during hypertension, the absolute organ blood flow (FF X CO) was reduced in lesioned rats to 30-40% of control in skin, muscle, and colon and between 60% and 75% of control in most of the remainder of the gastrointestinal tract and renal cortex; it was unchanged in myocardium and endocrine glands. Resistance was substantially increased (4- to 6-fold) in skin, muscle and colon but was only moderately increased (1.5- to 2.5-fold) in the remaining organs. The results indicate that, while NTS lesions will increase resistance in most vascular beds, the response is unequally distributed, influencing skin, muscle, and colon disproportionately to other tissues. Because of an interaction between a reduction in CO and little autoregulation, blood flow is reduced primarily in skin, muscle, and colon. The pattern of redistribution of CO was consistent with the interpretation that NTS hypertension results from interrupting baroreceptor reflexes centrally. The pattern of redistribution of blood flow in rats with NTS lesions differs from that produced by deoxycorticosterone acetate-salt and renal ischemia.
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PMID:Regional distribution of blood flow during arterial hypertension produced by lesions of the nucleus tractus solitarii in rats. 33 95

The synthesis and deposition of collagen and other proteins has been measured in the aorta of the rat by radiolabeling in short term organ culture. Under these conditions, the synthesis of collagen and other proteins is linear for at least five hours. Autoradiography demonstrates a labeling in all cell layers and protein deposition in the extracellular matrix. Hypertension was induced by renal ischemia using Goldblatt's technique. The synthesis and deposition of collagen was stimulated in aorta from the first week of hypertension and in pregnancy, and was even more increased in hypertensive pregnant animals. Reserpine suppresses the rise in blood pressure in operated animals and prevents these modifications.
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PMID:Aortic collagen biosynthesis during renal hypertension, pregnancy and hypertension during pregnancy in the rat. 36 58

Partial ligation of the aorta between the renal arteries in the rat induces malignant hypertension, metaplasia of smooth-muscle cells of arterioles and arteries into juxtaglomerular cells, and a complex series of events in tubular cells at all levels of the ischemic kidney. The tubular cells of the outer cortex, particularly the proximal convoluted cells, show a very rapid and progressive simple atrophy. In contrast, necrosis of individual cells is followed by mitotic activity in atrophic tubular cells of the inner cortex, medulla, and papilla. Subsequently, polyploidy and hyperplasia occur in the inner cortex. At the same time, hypertrophy of the protein-synthesizing apparatus and an increase in protein, DNA, and RNA, followed by a decrease in the protein content, are seen in the tubular cells of the inner cortex. In the medulla and papilla, necrosis of individual cells proceeds side by side with waves of mitotic activity. These events take place, albeit to a lesser degree, even in cases of very mild renal ischemia. While they may by unrelated to hypertension, these changes are probably involved in the increase in hydrolytic enzyme activity characteristic of the ischemic renal cortex.
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PMID:Metaplastic and mitotic activity of the ischemic (endocrine) kidney in experimental renal hypertension. 47 9

The intrarenal arterial and arteriolar changes in the kidneys of 80 patients with chronic renal insufficiency maintained on hemodialysis were studied semiquantitatively by light microscopy and histochemistry. Intimal proliferation was common and accounted for thickening of vessel walls and luminal narrowing. Fibrocollagenous and fibroelastotic intimal changes were located predominantly in the interlobular and arcuate arteries, whereas the fibromucinous intimal lesion was found mainly in the interlobar arteries. Thickening of the media was encountered in 25 per cent, and adventitial fibrosis in 20 per cent of the kidneys. Necrotizing arterial of arteriolar lesions were not seen. The significance of these alterations as a possible cause of renal ischemia and their role in the perpetuation of hypertension are discussed.
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PMID:Intrarenal vascular alterations in hemodialysis patients. A semiquantitative light microscopic study. 52 65

Hypertension is a frequent complication of reflux nephropathy. The cause of this hypertension is unknown. Our study was undertaken to assess the possible role of the renin-angiotensin system in the hypertension associated with unilateral reflux nephropathy. We selected for study 17 normotensive and 12 hypertensive patients with strictly unilateral reflux nephropathy. There were 3 normotensive and 2 hypertensive patients with a renal vein renin ratio exceeding 1.5. Of these 3 normotensive patients 1 had evidence from divided renal function studies to suggest functional renal ischemia. No consistent evidence was obtained to support the concept that the renin-angiotensin system has a primary role in the non-malignant hypertension of unilateral reflux nephropathy.
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PMID:Renal vein renin concentration in the hypertension of unilateral reflux nephropathy. 67 98

Thirty-three patients with acute pyelonephritis were studied with regard to the changes in plasma renin activity (PRA) along the clinical course of the disease. 1) Abnormally high PRA was found in 64% of patients in the active stage of acute pyelonephritis; they showed a decrease in urinary output of sodium, a reduction in creatinine clearance, and high indices of inflammatory activity. 2) The changes of PRA in the course of acute pyelonephritis were negatively correlated to the urinary sodium excretion and creatinine clearance, but positively to the activity of inflammation, serum sodium concentration and the number of E. coli in the urine. PRA returned to normal with the improvement of pyelonephritis. 3) Concerning the mechanism of hyperreninemia in the active stage of the disease, the following three factors may be considered; renal ischemia, negative sodium balance in the body, and inflammation. Of these, the negative sodium balance seems to be the most important. The patients could not take enough foods to maintain their energy and sodium balance because of fever and pain. 4) The significance of resting PRA in acute pyelonephritis might be to reflect the sodium status in the body, but not to be related to hypertension.
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PMID:Elevated plasma renin activity in patients with acute pyelonephritis. 69 21

Renal prostaglandins have several potential functions in renal physiology. Perhaps their best documented role is the maintenance of renal blood flow during renal ischemia, although they are apparently not essential to blood flow autoregulation in the absence of ischemia. Alterations in sodium excretion parallel the hemodynamic changes induced by prostaglandin infusions and prostaglandin inhibition with indomethacin. A direct action on sodium balance is unproven. Numerous studies, in vivo and in vitro, have convincingly demonstrated that prostaglandins or their precursors stimulate renin release and prostaglandin inhibition blunts renin release independent of hemodynamic and electrolyte balance. These functions of prostaglandins have implicated them in the manifestations of Bartter's syndrome, the nephropathy of liver cirrhosis, renovascular hypertension, and other nephropathies.
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PMID:Prostaglandins: renin release and renal function. 72 86

In the current study a) cardiovascular reactivity (CR) to norepinephrine (NE) and b) the effect of a ganglionic blocker (pentolinium, P) during the early (2nd week) and a later period (10th week) of hypertension elicited by unilateral renal ischemia and contralateral nephrectomy in the rat have been described. Neither the threshold doses nor the dose-pressor response curves have shown a greater reactivity of the cardiovascular system to NE in this type of hypertension. An increase in the activity of the nervous system apparently contributes to hypertension in the early period but would disappear when the one-kidney renovascular hypertension is chronically established; in both phases some other still undefined factor/s are present for fuller development of high arterial pressure.
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PMID:Cardiovascular reactivity and neurogenic tone in hypertension derived from renal artery stenosis and contralateral nephrectomy in the rat. 75 6

Hypertension secondary to segmental renal ischemia caused by segmental renal artery stenosis has been relieved by nephrectomy, partial nephrectomy, excision of atrophic segments, or repair of the segmental vessels. This is a report of hypertension caused by stenosis of a segmental renal artery and cured by simple ligation of the stenotic artery.
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PMID:Correction of renal hypertension by ligation of stenotic segmental renal artery. 84 6


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