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

1. Infusion of sufficient renin to raise the blood pressure of normal rats to hypertensive levels resulted in increased renin in the arterial wall. 2. Arterial wall renin and renal venous renin were normal in younger spontaneously hypertensive rats, but in older spontaneously hypertensive rats arterial wall renin was significantly increased and renal venous renin was significantly decreased. 3. Arterial wall renin in rats with either acute or chronic two-kidney Goldblatt renal hypertension was significantly increased, whereas circulatory renin was elevated in the former, but depressed in the latter. 4. Arterial wall renin may play a role in the maintenance of acute and chronic renal hypertension and also perhaps of spontaneous hypertension of long duration in older rats.
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PMID:Arterial wall renin and renal venous renin in the hypertensive rat. 47 82

1. Pentolinium tartrate (a ganglionic blocker) was injected in conscious rats during the early and late phases of two-kidney renal hypertension produced by aortic ligation. 2. In the early phase ( 5 days after aortic ligation), ganglionic blockade resulted in a decrease in blood pressure equal to that obtained in normotensive rats. Later, at days 12 and 40, for equally severe hypertension, ganglion blockade resulted in a greater decrease in blood pressure. 3. A 30 min infusion of [Sar1, Ala8]angiotensin II during the pentolinium-induced nadir in blood pressure resulted in a further decrease in blood pressure at day 5. Later, at days 12 and 40, this effect was smaller. 4. A 300 min infusion of [Sar1, Ala8]angiotensin II normalized the blood pressure in hypertensive rats at day 40. This delay response may be secondary to a central effect of the antagonist, reducing neurogenic tone or peripheral antagonism of locally generated angiotensin II in the blood vessel walls. 5. At day 40, removal of the small left kidney resulted in a greater decrease in blood pressure. This suggests the presence of a renal factor other than renin in the chronic phase of this hypertension.
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PMID:Neurogenic activity--angiotensin II interaction during the development and maintenance of renal hypertension in the rat. 47 45

On 75 patients with chronic renal insufficiency the relations between renal hypertension due to volume expansion and findings of the fundus of the eye were investigated. In compensated renal insufficiency in 20 of 23 patients a hypertension appeared, hypertensively conditioned changes of the fundus were observed only in about one third of the cases. When the functional disturbances progressed into the stage of the chronic terminal renale insufficiency on the other hand in 27 of 38 patients retina findings conditioned by hypertension were stated. Among 38 haemodialysis patients by regulation of the fluid balance 11 times a normal fundus and 15 times an improvement of the findings of the fundus of the eye could be revealed. In 13 patients the findings of the fundus generally improved after successful renal transplantation. Also our examinations call the usual stage subdivisions after Thiel and Keith and co-workers, respectively, in question.
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PMID:[Eye fundus pathology in chronic terminal kidney failure]. 48 28

The role of central nervous system (CNS) catecholamines in the development of hypertension and the control of drinking behavior was assessed in rats by depleting these amines with 6-hydroxydopamine (6-OHDA). Intraventricular administration of 6-OHDA completely prevented the development of one-kidney renal hypertension and abolished the associated increase in water consumption. 6-OHDA-treated rats showed deficits in drinking behavior when challenged with subcutaneous injections of angiotensin II (AII) and hypertonic sodium chloride. The acute pressor responses produced by intraventricular injections of AII and carbachol were virtually abolished by central catecholamine depletion. However, drinking produced by central cholinergic stimulation remained intact while AII drinking was significantly reduced. These data demonstrate that the integrity of CNS catecholamines is required for the development of one-kidney renal hypertension and the increased drinking which accompanies it. In addition, destruction of central catecholamine-containing neurons allows for a specific dissociation of the pressor and drinking responses produced by central cholinergic but not AII stimulation.
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PMID:Role of central catecholamines in the control of blood pressure and drinking behavior. 49 58

Water and electrolyte excretion after a salt load, plasma natriuretic activity, and sensitivity of the kidneys to the natriuretic factor were studied in experiments on Wistar rats with renal hypertension and on SHR rats with spontaneous hypertension. The "exaggerated natriuresis" phenomenon is observed in animals with hypertension after a salt load. The plasma natriuretic activity in rats with experimental hypertension does not rise in response to an increse in the volume of extracellular fluid. The sensitivity of the kidneys to the natriuretic factor in animals with experimental hypertension is the same as that in the control animals. Consequently, the natriuretic factor has no decisive role in the "exaggerated natriuresis" phenomenon in these types of experimental hypertension.
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PMID:[Role of the natriuretic factor in the phenomenon of "exaggerated natriuresis" in experimental hypertension]. 59 2

1. Propranolol was administered to groups of mature rats before and during the development of renal hypertension induced by ligation of the aorta between the renal arteries. 2. At a dose 10 mumol (3 mg) of propranolol/kg, administered by intraperitoneal injection, the onset and severity of hypertension were not affected, although plasma renin concentration was significantly lower than in the untreated hypertensive rats in the first 5 days after the operation. 3. With 200 mumol (60 mg) of propranolol/kg, administered in the drinking water, peak blood pressure 5 days after aortic ligation was lower than in the untreated control rats, but plasma renin concentration was no lower than with the smaller dose. 4. The development of severe hypertension despite reduction in plasma renin concentration on the low dose of propranolol suggests the participation of renal vasopressor factors other than renin in this model. 5. A higher dose of propranolol reduced the rise in plasma concentration to an equal extent but the rise of blood pressure at 5 days was also reduced, which supports this concept.
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PMID:Effect of propranolol on blood pressure and renin in renal hypertension in the rat. 60 59

Renal-vein renin was determined in 55 children with renovascular or renal hypertension, 33 of whom being treated surgically. The overall cure rate after surgery was 87.9%. Of 23 patients having a renal-vein renin ratio greater than 1.5, 20 were operated successfully, but 9 of 10 operated patients with a ratio of less than 1.5 also benefited from surgery. Taking into account the frequency of "false-negative ratios" (27.3%) and the potential risks of catheterization, it is suggested that renal-vein renin measurements are not useful as a routine procedure for investigation of a child with renovascular hypertension.
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PMID:Predictive value of renal-vein renin measurements in children with various forms of renal hypertension. An international study. 61 63

Using the radioactive microsphere technique, cerebral blood flow (CBF) was measured in six conscious dogs before intervention and again on the 3rd-5th days after inducing hypertension by the one-kidney Goldblatt (1-KGH) procedure. Sham-operated controls were also studied. The normal temporal variability of CBF, as well as the precision of the microsphere technique in measuring CBF were also determined in other normal dogs. A left atrial catheter was used for the microsphere injections (15 micrometer diam spheres) and an aortic catheter was used for cardiac output and blood pressure measurements. On the 3rd-5th days after 1-KGH, mean aortic pressure increased from a control value of 94 +/- 7 mmHg to 135 +/- 20 mmHg (P less than 0.005). CBF did not change significantly from the control flow of 57.1 +/- 7.9 ml/100 g per min. Calculated cerebral vascular resistance increased by 47 percent (P less than 0.025) above the control value. Hence, the early phase of experimental renal hypertension is associated with adequate autoregulation of cerebral blood flow.
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PMID:Autoregulation of cerebral blood flow during early experimental renal hypertension in the conscious dog. 62 73

On the basis of the conception of renal hypertension, worked out by the authors, the new interpretation of the cause of 'essential' renal haemorrhages is discussed. Special attention is drawn to secondary 'arterial' venous hypertension in the kidney, which happens in cases when there are no obvious reasons for the distortion of the outflow through the renal vein. In a case of renal haematuria, the origin of which is not connected with the distortion of the venous blood outflow from the kidney, it is necessary to bear in mind the relationship between the venous pressure in the kidney and the systemic arterial pressure. In arterial hypertension the contralateral kidney may become the source of haematuria. The rarity of isolating a calycovenous canal as a separate definite cause is discussed.
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PMID:Essential renal haemorrhages. 63 Nov 52

The angiotensin II (AII) antagonist [Sar1-Ala8]AII (Saralasin) was injected into the brain ventricles (IVT) and intravenously (IV) in five different types of hypertensive unanesthetized rats. Renal hypertension was studied 16-22 days after kidney clipping. Intravenous infusions of cumulative doses (0.1-100 microgram/kg per min) and IVT injections (5-40 microgram) of Saralasin did not change mean arterial pressure (MAP) in controls and in one-clip, one-kidney Goldblatt hypertension, whereas MAP decreased in one-clip, two-kidney Goldblatt hypertension following IV and IVT Saralasin. In two-clip, two kidney hypertensive rats, IVT Saralasin decreased MAP but was ineffective when infused IV. Both IV and IVT Saralasin increased MAP in DOC hypertension. In spontaneously hypertensive (SH) rats, IV Saralasin increased MAP; IVT injection decreased MAP. The effect of IVT Saralasin in SH rats persisted 15-20 h after nephrectomy. We conclude that plasma AII may contribute to peripheral and central mechanisms of blood pressure regulation. The dissociation of the effects of IV and IVT Saralasin and the persistance of blood pressure decrease in nephrectomized SH rats following IVT Saralasin further support a role for locally formed brain angiotensin.
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PMID:Effects of central and peripheral angiotensin blockade in hypertensive rats. 64 31


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