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)

1. Sar1-Ala8-Angiotensin II (an angiotensin antagonist) was infused in rats during the development and maintenance of renal hypertension produced by aortic ligation between renal arteries. 2. In the early phase (5 and 12 days after ligation), infusion of the antagonist markedly decreased blood pressure although it did not reach normal pressures. Later (day 40) only a modest decrease in blood pressure was noted. 3. Removal of the small left kidney always decreased the blood pressure to normal pressures. 4. It is concluded that the renin-angiotensin system is the major pressor component in the initiation of this hypertension. Later, other factors of renal origin assume a pressor function.
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PMID:Effect of administration of Sar1-Ala8-angiotensin II during the development and maintenance of renal hypertension in the rat. 65 33

1. Structural changes in the thymus during the evolution experimental renal hypertension were investigated to determine their possible role in the genesis of hypertensive vascular disease. 2. The thymus, adrenal glands and the progression of hypertensive vascular lesions were investigated in rats during the first 30 days after occlusion of the aorta between the two renal arteries. 3. Hypertension was initially accompanied by marked atrophy of the thymus, most pronounced 9 days after operation. During this time, the adrenal glands doubled in size and the heart became enlarged. 4. After 21 days the thymus regenerated and became hypertrophic. Histological features of hyperactivity accompanied by infiltration of plasma cells were evident, while the adrenal glands remained enlarged. 5. The observed structural changes of the regenerated thymus in the presence of sustained adrenal hypertrophy indicate that the thymus may contribute to the production of hypertensive vascular disease.
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PMID:Biphasic changes in thymus structure during evolving renal hypertension. 67 25

We isolated and perfused both the "clipped" and "contralateral" kidneys from Goldblatt renal hypertensive and sham-operated control rats, 1--104 days postoperatively. Responses to renal nerve stimulation were depressed in clipped kidneys from hypertensive rats (1 day postoperative), and these kidneys were supersensitive to exogenous norepinephrine (1--31 day) when compared with the contralateral organ of the same animal. Similar alterations were found between clipped and contralateral kidneys from sham-operated control rats. There was no difference in responses to renal nerve stimulation of norepinephrine between clipped kidneys from hypertensive and control rats, but clipped kidneys from hypertensive rats were supersensitive to angiotensin II (17 and 31 days). Comparison of contralateral kidneys from hypertensive and control rats revealed no change in norepinephrine sensitivity or in responses to renal nerve stimulation, but there was a reduction in the slope of the dose-response curve to norepinephrine and of the maximal effect of the catecholamine (104 days) and a pronounced supersensitivity to angiotensin II (17--104 days) in the hypertensive rats. These results indicate that (1) renal nerve function and norepinephrine sensitivity of the isolated renal vasculature are unchanged in renal hypertension, but clipping partially denervates the kidney causing depressed nerve function and unilateral norepinephrine supersensitivity, unrelated to hypertension; (2) the prolonged high pressure load on the contralateral kidney may impair the function of the vascular smooth muscle; and (3) bilateral supersensitivity to angiotensin II is associated with hypertension but is not solely a consequence of the high pressure.
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PMID:Increased renal vascular reactivity to angiotensin II but not to nerve stimulation or exogenous norepinephrine in renal hypertensive rats. 68 57

Histological studies including electron microscopy were performed on the carotid sinuses of dogs with renal hypertension of 17 to 82 days duration or hypertension of two years secondary to aortic coarctation. Physiological abnormalities in the baroreceptors including resetting had been demonstrated before death. Histologically there were no qualitative or quantitative differences in the intrasinus nerve fibers of the hypertensive animals compared tp controls with normal blood pressures, and there was no evidence that baroreceptor degeneration occurred as a consequence of the hypertension. Structural lesions confined to the intima were evident in the sinus walls of some of the renal hypertensive animals whereas the dogs with coarctation showed more advanced sinus wall changes including medial calcification and enlargement of the vascular lumen.
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PMID:Histology and ultrastructure of the carotid sinus in experimental hypertension. 69 Feb 67

Three types of renal hypertension in the rat have been compared with respect to blood pressure increase, activity of the RAS, and secretion of aldosterone and corticosterone: type I - unilateral stenosis of the renal artery in the presence of an intact contralateral kidney; type II - unilateral stenosis of the renal artery after contralateral nephrectomy; type III - bilateral stenosis of the renal arteries. Blood pressure rose more rapidly and reached higher values in type II and type III hypertension than in type I hypertension. In the latter group, the activity of the RAS was more stimulated than in types II and III. The marked stimulation of the RAS in type I hypertension is ascribed to the negative fluid and sodium balance, which is the consequence of a pressure-induced diuresis of the unclamped contralateral kidney. Suppression of the activity of the RAS by a 4-week pretreatment with DOC-TMA and saline or by the administration of DOCA and saline as from the induction of renal artery stenosis did not prevent the development of hypertension caused by the clamping of one renal artery (type I). In spontaneously hypertensive rats of the stroke-prone substrain, high dietary salt intake caused higher blood pressure values and a higher incidence of cerebral lesions than normal dietary salt intake. Low salt intake was followed by a marked stimulation of the RAS, but blood pressure rose only slightly and no symptoms of cerebrovascular lesions were observed. It is concluded that neither in hypertension induced by renal artery stenosis nor in spontaneously hypertensive rats, the RAS contributes significantly to the increase in blood pressure nor does it play a major part in the pathogenesis of vascular lesions. These seem to be related to the retention of sodium, which may be obtained by renal artery stenosis, by excessive salt intake, or by the administration of a mineralocorticoid and salt.
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PMID:What makes the renin-angiotensin system a pathogenic factor? 69 4

Washout urography was used as a screening test for 100 hypertensive patients. Eleven patients had renal hypertension. These were 4 cases of unilateral renal artery stenosis, 6 cases of unilateral pyelonephritis and one case of bilateral pyelonephritis with atherosclerosis of the right renal artery. The increase in size of the affected kidneys after Lasix injection was much restricted relatvie to the normal contralateral kidneys. The test proved valuable for screening cases of renovascular hypertension and unilateral pyelonephritis.
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PMID:Washout urography in the diagnosis of renal hypertension. 70 Sep 44

The lipolysis in the adipose tissue obtained from adrenalectomized and intact rats with spontaneous and renal hypertension and from rats of corresponding control groups was studied. Lypolysis under the effect of epinephrine and without it was evaluated by the concentration of nonesterified fatty acids in the tissue and by glycerine release into the incubation medium (in vitro). Reaction of the adipose tissue in response to epinephrine was the same in hypertensive and control rats when the adrenal glands were intact. Preliminary adrenalectomy which eliminated the corticosteroid action reduced the epinephrine lypolysis in the adipose tissue in control normotensive rats, but not in hypertensive rats ("facilitation" of catecholamine action on the lypolysis mechanism). This phenomenon is regarded by the authors as the alteration of plasmatic membranes adipocytes function in hypertensive animals. The adrenal cortex hypertrophy and the enhanced corticosteroid secretion in the types of hypertension studied are therefore considered as the measure for compensation of disturbances of the cell plasmatic membranes function in the internal environment tissues.
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PMID:[Adrenaline lipolysis in the adipose tissue of rats with spontaneous and renal hypertension]. 72 4

The morphological findings in spontaneously hypertensive rats (SHR) were compared with the findings after experimental renal hypertension. In addition the effect of an arteriosclerogenic diet was investigated. Cardiac hypertrophy occurred in all types of hypertension. During the course of renal hypertension there was also hypertrophy of the tunica media of the arterial vessels of the heart, kidneys, mesenterium, and orta. Degenerative changes in the vascular walls occurred when nephrectomized rats were given a diet containing 2% cholesterol and 1% cholic acid. This produced intima lipoidosis after seven to eleven weeks. The intensity seemed to be dependent on the degree of hypertension and the duration of the experiment.
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PMID:Morphological findings in spontaneously hypertensive rats in comparison with findings after experimental renal hypertension. 74 8

The development of hypertension was studied in rats after neonatal sympathectomy by s.c. injection of 6-hydroxydopamine HCl. Three different types of hypertension were investigated: renal hypertension in the two-kidney Goldblatt model, steroid hypertension produced by deoxycorticosterone (DOCA) implantation and saline as drinking fluid, and genetic hypertension in the spontaneous hypertensive rat (SHR). Blood pressure was measured directly in conscious animals via the iliac artery. Mean blood pressure of conscious sympathectomized (SX) normotensive rats was not significantly different from that of normotensive controls. Renal hypertension reached the same level in controls and SX rats four weeks after application of a renal artery clip. DOCA-salt hypertension developed faster and to a higher level in SX rats than in control rats. The hypertension in SX DOCA-salt hypertensive rats was accompanied by a marked tachycardia. In contrast hypertension did not develop in SX SHR. Up to 12 months of age mean blood pressure was markedly lower than that of control SHR, but slightly higher than that of SX normotensive Wistar Kyoto rats. These differential effects of neonatal sympathectomy on the development of hypertension in the rat may point to differences in the pathophysiological mechanisms. It is concluded that an intact sympathetic nervous system is essential for the development of hypertension in SHR. In DOCA-salt hypertension the intact sympathetic nervous system appears to protect against a rapid rise in blood pressure.
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PMID:Differential development of renal, DOCA-salt, and spontaneous hypertension in the rat after neonatal sympathectomy. 75 48

Ablation of tissue surrounding anteroventral third ventricle (AV3V) was studied in three models of hypertensive rats. Lesions were placed in the AV3V at one and six weeks following the initiation of one kidney Grollman renal hypertension. At one week the rise in blood pressure was arrested and water intake was reduced; at six weeks arterial pressure returned to prehypertensive levels in animals surviving the post-lesion hydrational crisis. In two kidney (one clip) Goldblatt animals lesioned two weeks post-clip, arterial pressure was significantly reduced but did not become fully normotensive. Finally, the AV3V was also lesioned in spontaneously hypertensive rats (SHR-Okamoto strain) with established hypertension. The lesion did not reduce arterial pressure in adult SHR although characteristic initial adipsia and weight loss occurred. Ablation of the AV3V thus altered the course of maintenance of renal hypertension; however, the arterial pressure of SHR was not affected.
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PMID:Interruption of the maintenance phase of established hypertension by ablation of the anteroventral third ventricle (AV3V) in rats. 75 72


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