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

The role of brain catecholaminergic neurones in the pathogenesis of DOCA-salt hypertension in the rat was investigated by selective depletion of central catecholamines using intraventricular or intracisternal administration of 6-hydroxydopamine (6-OHDA). Only the intraventricular injections prevented the development of hypertension. In addition, intraventricular 6-OHDA reversed the hypertension produced by two weeks but not six weeks of DOCA-salt treatment. The ability of intraventricular injections of 6-OHDA to prevent or reverse DOCA-salt hypertension while intracisternal injections do not, appears to be related to the greater depletion of brain catecholamines produced by the intraventricular injections. Only in the spinal cord and in the locus coeruleus were the norepinephrine contents depleted equally by either injection route. These findings suggest that central catecholaminergic neurones other than those originating in the locus coeruleus or descending in the spinal cord are important in the initiation, but not in the long term maintenance, of DOCA-salt hypertension. The influence of the central catecholamine neurons involved in the development of DOCA-salt hypertension might be mediated neurally via nonadrenergic pathways or hormonally via the brain-pituitary-endocrine system.
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PMID:6-hydroxydopamine destruction of central adrenergic neurones prevents or reverses developing DOCA-salt hypertension in rats. 32 22

Partial infarction of one kidney and contralateral nephrectomy was followed by a similar initial increase in blood pressure in athymic (nude) and normal mice of the C57/BL/6J strain. The chronic phase of the hypertension was, however, thymus dependent, since the athymic mice failed to maintain an increased blood pressure, in contrast to the normal mice. A response of thymus transplantation in athymic mice was the ability to maintain the blood pressure high in the chronic phase of the hypertension, whereas cyclophosphamide treatment to the normal hypertensive mice decreased the blood pressure in the chronic phase of the hypertension, but not in the early (acute) phase. Some perivascular round cell infiltrations were found in the uninfarcted part of the kidney in normal and thymus-transplanted nude mice after 80 days of hypertension, but the degree of cellular reaction was less than previously observed in the NMRI-strain of mice. Substantial perivascular cellular infiltrations, which appeared to be thymus-dependent, occurred in the ischemic border-zone of the infarcted area. Athymic mice of the NMRI-strain were able to develop the initial blood pressure elevation of DOCA/salt hypertension during the chronic phase of loomis hypertension, in which phase the arterial pressure otherwise would be declining towards normal values.
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PMID:The importance of thymus in the pathogenesis of the chronic phase of hypertension in mice following partial infarction of the kidney. 33 61

1. The pressor response to angiotensin II was reduced in rats with early (less than 6 weeks) and chronic (greater than 4 months) Goldblatt two-kidney, one-clip hypertension and enhanced in DOCA-salt hypertension. 2. Converting enzyme inhibition with captopril brought the angiotensin pressor response curves into closer proximity although the DOCA hypertensive rats were minimally hyper-responsive and rats with early and chronic renovascular hypertension showed slightly reduced responsiveness. 3. After bilateral nephrectomy the pressor responses to angiotensin were similar. 4. The pressor response to angiotensin II in these animals was inversely related to plasma renin concentration and therefore largely dependent upon receptor occupancy by endogenous angiotensin II. There is no evidence for enhanced pressor responsiveness to angiotensin in either renovascular or DOCA hypertension.
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PMID:Pressor responsiveness to angiotensin in renovascular and steroid hypertension. 39 91

A case characterized by a dark pigmentation of the skin with an initial hypotension and a lung tuberculosis in the remote anamnesis is described. The skin pigment was formed by lipofuscin and emosiderin, but only the former was found in the liver biopsy. Anyway, the pigment was not melanine and the surrenalic function of the patient was completely normal; therefore, an Addisonism syndrome is excluded. The patient was treated for a very long time with DOCA: this caused hypertension, probably supported by the hypervolemia triggered by the DOCA depending retenction of sodium and water. A sure diagnosis of the case was not made, but an Addisonism syndrome was certainly excluded.
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PMID:[A case of melanoderma erroneously considered to be addisonian]. 43 70

Uninephrectomized, saline-fed male Sprague-Dawley rats were given DOCA 5 mg per week alone or together with progesterone 20 mg per week for 6 weeks (phase I). Subsequently, the doses of DOCA and progesterone were doubled and the rats were studied for an additional 6 wk (phase II). Progesterone prevented DOCA-induced hypertension during phase I. Phase II blood pressures were higher in DOCA-progesterone-treated animals than in controls, but remained lower than in animals treated with DOCA alone. At the end of phase II the animals were killed, and blood samples and skeletal muscle samples were taken for analysis of electrolyte content. DOCA-treated animals were found to have an increased rate of potassium excretion, an increase in muscle sodium concentration, and a decrease in muscle potassium concentration compared to the controls. Progesterone treatment significantly blunted the DOCA-induced changes in muscle electrolyte concentrations and increased the rate of sodium excretion. No hypotensive effect was observed when progesterone in doses similar to those of phase I was administered to spontaneously hypertensive rats. Thus, in experimental mineralocorticoid hypertension, the hypotensive effect of progesterone appears to correlate closely with its mineralocorticoid antagonistic properties.
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PMID:Antihypertensive effect of progesterone in rats with mineralocorticoid-induced hypertension. 43 99

The effects of intraventricular and intraspinal administration of 6-hydroxydopamine (6-OH-DA) on the development and maintenance of DOCA-saline hypertension in rats have been investigated. Intraventricular administration of 6-OH-DA prevented the development of DOCA-saline hypertension in rats, but was ineffective in developed DOCA-saline hypertension. Treatment with intraventricular 6-OH-DA on rise in blood pressure was not secondary to a reduction in salt intake, however, since vehicle-treated rats given a similar reduced salt intake became fully hypertensive. The development of DOCA-saline hypertension was unaffected by pretreatment with intraspinal administration of 6-OH-DA, which produced a virtually complete loss of noradrenaline only in the spinal cord. It is suggested that brain adrenergic neurones may participate in the production of DOCA-saline hypertension but the noradrenergic projections in the spinal cords are not essential for this process.
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PMID:Effects of intraventricular and intraspinal 6-hydroxydopamine on blood pressure of DOCA-saline hypertensive rats. 48 4

The effects of d,l-alpha-tocopheryl nicotinate (EN) on model hypertension in rats were studied in comparison with d,l-alpha-tocopheryl acetate (EA). The progress of hypertension in young SHR during the 9th to 15th weeks after birth was markedly accelerated by replacing their driking water with 1% saline. The highly-developed hypertension in old SHR (9 months of age) was further advanced by salt-loading. Oral administration of 20 or 100 mg/kg of EN or 88 mg/kg of EA, once a day, delayed the progress of hypertension in young SHR and reduced advanced hypertension in old SHR. An antihypertensive effect of tocopheryl esters was also found in DOCA-salt hypertensive rats. The treatment with EN or EA definitely reduced the incidence of pathological changes accompanying model hypertension such as suppressed weight gain, pulmonary edema, myocardial fibrosis, cerebral hemorrhage and protected the animals from death. In antihypertensive effect, EN was about 5 times more active than EA in molecular base, and the effects of EN protecting from pathological changes associated with model hypertension were more definite than those of EA. The treatment with EN or EA reduced water and sodium retention in the DOCA-salt hypertensive animals. This fact may suggest the implication of a mechanism through electrolyte metabolism in the antihypertensive action of these tocopheryl esters.
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PMID:Antihypertensive action of d,l-alpha-tocopheryl nicotinate in rats. 50 48

Plasma catecholamine levels have been used experiemtally and clinically as the indices of the sympathetic nerve activity. We measured plasma catecholamines using high pressure liquid chromatography in rats to assess the significance of plasma catecholamines as an index of the sympathetic nerve activity and its role in hypertension. Pentobarbital anesthesia depressed plasma catecholamine levels, especially plasma adrenaline. Sodium loading for 5 weeks suppressed plasma noradrenaline, while administration of furosemide (1 mg/kg) produced the elevation of plasma noradrenaline. Experimental hypertension, one-kidney and two-kidney types of Goldblatt hypertension and DOCA-salt hypertension, raised plasma noradrenalines both in acute and chronic phases. The infusion of pressor doses of angiotensin II suppressed plasma noradrenaline by the reflex mechanism. Sar1, Ile8-angiotensin II and SQ 14,225 did not suppress plasma cathecholamine elevation due to hemorrhage. L-Hydroxyldopamine produced elevation of plasma catecholamines in experimental nypertension and controls in rats. After adrenal demedullation, plasma noradrenaline was decreased by the administration of 6-hydroxy-dopamine. Acute reduction of circulating blood volume and blood pressure fall produced the elevation of plasma catecholamine, especially plasma adrenaline. In rats, the adrenal medulla plays an important role in the regulation of blood pressure.
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PMID:Plasma catecholamines determination using high pressure liquid chromatography and their roles in blood pressure regulation and experimental hypertension in rats. 50 4

The activity of the adrenaline-forming enzyme, phenylethanolamine-N-methyltransferase (PNMT) and the levels of the catecholamines dopamine, noradrenaline and adrenaline were determined during the development of the DOCA-salt hypertension in selective areas of the rat brain stem and hypothalamus. Increases in PNMT activity were restricted to the A1 area and locus coeruleus after 2 weeks of DOCA-salt treatment and were extended to the A2 area after 9 weeks of treatment. Adrenaline concentrations were higher in these areas only after 9 weeks of treatment. Noradrenaline levels did not change, except in the nucleus tractus commissuralis. Dopamine levels were unchanged at all times and in all structures studied. These results implicate brain stem adrenaline neurons in the central response which occurs during the DOCA-salt experimental hypertension.
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PMID:Brain catecholamines during development of DOCA-salt hypertension in rats. 50 25

The onset of DOCA-salt hypertension in male Sprague-Dawley rats was prevented during 11 weeks of oral treatment with indapamide (0.5, or 10.0 mg/kg) or propranolol (60 mg/kg) administered in the diet. The body weights of the indapamide treated groups were significantly (P < 0.01) greater, at weeks 4, 5, 6, 7 and 11, while the body weights and food intake of the propranolol treated group were significantly (P < 0.05) lower at week 11, than the control group. A significant reduction in heart wet weight (P < 0.001) was measured in the indapamide treated animals only. No significant diuresis nor natriuresis was measured in any group during week 11 of treatment. When all groups were subjected to an increased salt load, four weeks after cessation of drug treatment only the indapamide (10 mg/kg) treated animals failed to show an increased blood pressure. Vascular reactivity studies carried out six weeks after termination of drug treatment, indicated a significant (P < 0.01) reduction in pressor activity elicited by electrical stimulation of the entire sympathetic outflow in indapamide (10 mg/kg) treated pithed rats. No significant difference in the pressor activity elicited by noradrenaline (5 x 10(-8) - 5 x 10(-6) g/kg, i.v.) or tyramine (10(-5) - 5 x 10(-5) g/kg i.v.) was observed in any treatment group. In conclusion, chronic oral treatment with indapamide or propranolol, prevented the onset of DOCA-salt hypertension in rats. A long lasting antihypertensive action of indapamide involving the sympathetic nervous system is also indicated.
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PMID:The effects of long term oral treatment with indapamide on the development of DOCA-salt hypertension in rats: vascular reactivity studies. 55 96


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