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

1. The Carworth Long-Evans rat has been reported to develop adrenal-regeneration hypertension but not deoxycorticosterone acetate (DOCA) hypertension. Deficiency of a hypothalamic receptor for deoxycorticosterone which mediates saline polydipsia has been postulated to underlie this resistance. Since a mineralocorticoid etiology for adrenal-regeneration hypertension has been postulated and all mineralocorticoids are thought to act on common receptors, these previous reports are difficult to reconcile. 2. To determine if an absolute or relative resistance to mineralocorticoids is present, Charles River Long-Evans and Sprague-Dawley rats were given 40 mg (107 micromol) of DOCA pellets/rat or 250 microgrms (0.65 micromol) of 2 alpha-methyl-9-alpha-fluorocortisol/day subcutaneously. 3. Saline polydipsia occurred with both steroids with both rat strains, though significantly less with the Long-Evans rats. Both types of rats became hypertensive and developed cardiac and renal enlargement with both steroids. Hypertension developed more rapidly with 2 alpha-methyl-9 alpha-fluorocortisol. 4. Thus mineralocorticoid hypertension can be produced in the Charles River Long-Evans rat, and the development of adrenal-regeneration hypertension in this rat strain is not incompatible with a mineralocorticoid etiology for adrenal-regeneration hypertension.
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PMID:Hypertension with mineralocorticoid administration to the Long-Evans rat. 47 92

1. In rats with inherited diabetes insipidus, unilateral nephrectomy plus drinking of 0.6% NaCl solution (saline) did not influence blood pressure in adult rats. However, when these factors applied before puberty, they produced hypertension. 2. We therefore analysed whether saline administration before puberty or unilateral nephrectomy before puberty was more important for this hypertensive response. 3. Saline drinking was found to be necessary for the response because hypertension was elicited by unilateral nephrectomy in adult rats only if saline consumption began before puberty.
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PMID:Effect of age on hypertensive stimuli and the development of hypertension in Brattleboro rats. 47 60

Genetically hypertensive (GH) rats of the New Zealand strain and normotensive (N) rats were sympathectomized from birth with 6-hydroxydopamine (100 mg/kg,s.c, on alternate days, seven treatments). In adult treated rats from each strain (GHTr and NTr), blood pressure was lower than normal. Functional tests and electron microscopy showed that denervation was virtually complete in mesenteric and hindlimb arteries; the innervation of the renal artery was little affected. Ganglionic blockade still caused a large fall in blood pressure in treated rats. Vascular resistance was higher in blood-perfused hindlimbs and tails of GH rats than in those of N rats; in contrast, resistance was similar in limbs and tails of GHTr and NTr rats and was greater than that found in untreated N rats. Saline-perfused limb vessels had neither neurogenic nor myogenic tone and resistance was higher in GH limbs (whether these were from treated rats or not) than in untreated N limbs. In saline-perfused NTr limbs, there was a paradoxical structural adaptation (probably luminal narrowing) of the hindlimb blood vessels and resistance was higher than in untreated N rats. The resistance of saline-perfused GH and GHTr limbs was similar. A high peripheral resistance appears to be the main mechanism sustaining genetic hypertension, and the integrity of the vasomotor sympathetic nerves is necessary for the development of this form of experimental hypertension.
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PMID:Blood pressure and vascular resistance in genetically hypertensive rats treated at birth with 6-hydroxydopamine. 66 60

High plasma renin activity (PRA) was found in 16 of 42 randomly selected nonuremic systemic lupus erythematosus (SLE) patients. Mild hypertension was present in 3 of the 16.6 high-PRA and 10 normal-PRA patients were admitted to a metabolic ward. Salt restriction produced a disproportionate rise in both PRA and aldosterone, a decrease in glomerular filtration rate (GFR) and a slightly greater negative sodium balance in the group with high PRA. Potassium excretion was less than intake in both groups. Balance studies were performed in 6 additional high-PRA patients before and during indomethacin administration (150 mg/24 h). PRA and aldosterone were markedly suppressed by indomethacin. UnaV was significantly greater than in the control period despite of the 28% reduction in GFR. These results suggest that high PRA is secondary to impaired distal tubular sodium reabsorption. Such a defect could be responsible for the relatively low frequency of hypertension in lupus nephritis.
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PMID:Normotensive hyperreninemia in systemic lupus erythematosus. An indicator of tubular dysfunction. 74 33

Salt resistant rats (R-strain of Dahl) accumulate large amounts of colloid in the pituitary cleft. Such colloid is largely absent in pituitaries of salt susceptible rats (S-strain of Dahl). Polyacrylamide gel electrophoresis of pituitary cleft colloid from R rats shows 4 proteins, designated R1, R2, R3 and R4 in order of decreasing electrophoretic mobility. These proteins have apparent molecular weights of 52,000, 63,000, 130,000 and greater than 235,000, respectively. Their apparent isoelectric points as determined by preparative isoelectric focusing are 4.82, 5.02, 5.54 and 4.35, respectively. Ferguson plots for R1, R2 and rat albumin suggest that R1 and R2 are size isomers of albumin. The molecular weights of R2, R3 and R4 suggest that R2 may polymerize to form a dimer and tetramer. Chronic feeding of 8% NaCl diet for 6 weeks does not influence pituitary accumulation of R1 protein in either R or S rats. Pituitary R1 accumulation does, however, segregate with resistance to salt-induced hypertension in genetic experiments. This strongly suggests that the accumulation of R proteins in the pituitary cleft reflects some genetically controlled change concerned with control of sodium metabolism.
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PMID:Characteristics of pituitary colloid proteins and their correlation with blood pressure in the rat. 86 65

Salt consumption was compared in two strains of rats, selected for their disparate proneness (strain "H") or resistance (strain "N") to Doca-salt hypertension. NaCl intake was similar in "H" and "N" rats prior to an following administration of Doca, while their respective blood pressures at the end of this experiment was 178 +/- 5mm Hg vs. 134 +/- 3 mm Hg. Thus, disparate responses of the blood pressure to Doca in the two strains cannot be ascribed to differences in salt intake. In another study, salt preference was tested in "H" and "N" rats by two-bottle self-selecting technique. Before Doca, saline preference in "H" rats averaged 60.3 +/- 5.8% of total daily fluid consumption, vs 18 +/- 4.2% in "N" rats. Following Doca treatment for 3 weeks the respective values were 96 +/- 1.7% vs 67 +/- 6.6%. Thus Doca treatment enhanced salt appetite in both strains, but salt preference remained significantly higher in the "H" rats. The increased susceptibility to hypertension and enhanced salt appetite in the "H" rat, corroborates similar reports in the Okamoto "SH" rat. In the Brookhaven "S" rat, however, susceptibility to hypertension is associated with salt avoidance. The conflicting data do not support a unified concept of a genetically determined link between salt appetite and proneness to hypertension.
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PMID:Sodium chloride preference in hypertensive (H) and normotensive (N) rats. 94 89

The hemodynamic pattern of response to bilateral nephrectomy was studied in 29 patients with end-stage renal disease on maintenance hemodialysis. Four patterns of hemodynamic response were seen. In 12 patients with nonmalignant hypertension, bilateral nephrectomy reduced blood pressure and total peripheral resistance with no effects on cardiac output. In 5 patients with malignant hypertension, bilateral nephrectomy reduced blood pressure, increased cardiac index, and reduced total peripheral resistance more markedly. In these two groups, at equivalent levels of total exchangeable sodium, before and after bilateral nephrectomy, mean arterial pressure and total peripheral resistance were invaribly lower in the absence of renal tissue. In 3 additional patients with nonmalignant hypertension, the decrease in blood pressure after bilateral nephrectomy was delayed from 3 to 12 weeks. When this occurred spontaneously, it was accompanied by a decrease in total peripheral resistance. The fourth hemodynamic pattern was seen in 6 normotensive patients with end-stage renal disease. After bilateral nephrectomy, there were no significant changes in mean arterial pressure, total peripheral resistance, or cardiac output. Salt and water loading failed to elevate blood pressure significantly. Renal transplantation was performed in 3 hypertensive patients before removal of the end-stage kidney. The functioning renal homograft did not result in normal blood pressure as long as the end-stage kidneys remained in place. Removal of the end-stage kidneys significantly decreased mean arterial pressure and total peripheral resistance. In the anephric state, a sharp difference was seen in blood pressure response to salt and water loading between previously normotensive and previously hypertensive patients. Previously hypertensive patients responded with a progressive increase in blood pressure that reached hypertensive levels. Previously normotensive patients failed to elevate their blood pressure significantly. It is concluded that the vasopressor function of the kidney is the most important factor in the pathophysiology of hypertension of end-state renal disease. Expansion of body fluid plays a role, but elevates the blood pressure only in patients who were previously hypertensive. The antihypertensive function of the kidney does not appear to be a major factor in the regulation of blood pressure in end-stage renal disease.
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PMID:Blood pressure regulation in end-stage renal disease and anephric man. 109 52

The effect of propranolol therapy on the mean arterial pressure (MAP) and plasma renin activity (PRA) was studied in three groups of hypertensive patients who were also treated with saliuretics. Group A: In 14 patients with essential hypertension on chlorthalidone treatment, an additional daily dose of 640 mg propranolol for two months led to a significant reduction of the MAP (from 124 to 105 mm Hg) and PRA (from 5.3 to 2.0 ng AI/ml/hr standing). There was no correlation between MAP reduction and either the original levels or change in PRA. Group B: In 14 patients with essential hypertension and 5 with renal artery stenosis studied on a fixed salt intake, the plasma and extracellular volumes, PRA, and blood pressures were recorded before and after three days of diuretic induced salt depletion and, with maintenance of the depleted state, after three days of propranolol. Salt depletion resulted in a decrease in MAP from 132 to 128 mm Hg (NS), and PRA increased from 3.4 to 22.3 ng AI/ml/hr (P less than 0.01). There was no correlation between change in MAP and PRA control values, PRA change, or any of the volume parameters. Addition of propranolol was followed by a rapid MAP decrease to 111 mm Hg (P less than 0.01), and the PRA dropped to a mean of 8.5 (P less than 0.01). No correlation was found between change in MAP and change in PRA. The patients with renal artery stenosis did not differ in their reactions from those with essential hypertension. Group C: In five patients with moderate renal failure and normal to expanded 82-Br distribution volume, propranolol lowered MAP by 10% and lowered the PRA in all five. Salt depletion by furosemide to 82-Br volumes below normal resulted in a 10% decrease of MAP and a marked rise in PRA. In this state propranolol was followed by a further MAP reduction of 18% and a decrease in PRA. There was no quantitative relationship between MAP and PRA change during either of the treatment regimes. It is concluded that in various forms of hypertension, the blood pressure can be effectively lowered by combining diuretics and propranolol regardless of the pretreatment PRA level.
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PMID:Effect of salt depletion and propranolol on blood pressure and plasma renin activity in various forms of hypertension. 109 56

Female rats of 2 Sprague-Dawley sub-strains and of the Wistar and Fischer 344 strains were sensitized to the hypertensogenic effect of excess salt by removal of 1 kidney and by being given 1% NaCl solution as their sole drinking fluid. One of the Sprague-Dawley sub-strains (SPD) and the Wistar (CFEP) rats developed progressive saline polydipsia of equivalent degree, blood pressure rose, and about half of the members became hypertensive during treatment. Rats of the other Sprague-Dawley strain (CFNP) also showed a progressive saline intake; but although they drank substantially less saline, the incidence of hypertension among them was increased by 50%. Animals of the Fischer 344 strain displayed neither saline polydipsia--the intake remaining relatively constant at a very low level throughout the experiment--nor hypertension. Salt hypertension appears to be affected by genetic factors in at least 2 ways, one of which regulates the quantity of salt ingested (salt appetite), while the other controls the susceptibility to salt excess or perhaps to hypertension per se. Fischer 344 rats have the ability to restrict the volume consumption of saline; their resistance to enforced high salt intake has yet to be established.
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PMID:Genetic influence on saline consumption and salt hypertension as exhibited by the response of various rat strains and sub-strains. 123 Oct 46

In the past 30 years 238 cases have been published which describe the nephronophthisiscystic renal medulla complex. Of these, 110 are sufficiently adequate to permit detailed analyses. Both isolated and genetically transmitted cases are reported. The latter include the dominant and recessive modalities, both autosomal, and the former perhaps also X-linked. Renal disease also has been inherited as a recessive trait in association with retinal degeneration. Medullary cysts have been found in 73% of cases in which kidney tissue has been examined directly. Their presence seems to bear no relationship to the ability of involved kidneys to conserve sodium. Salt wasting is described in the presence and absence of medullary cysts. Techniques short of anatomic examination of the kidneys have rarely allowed cysts to be detected and diagnosis continues to rest on a high index of suspicion, aroused in turn by a positive family history for the disease. Arterial hypertension occurs in roughly one third of cases. Aminoaciduria is not a part of the syndrome. A defect in maximum urinary concentrating ability may be the best single early sign of involvement but data are scarce.
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PMID:Juvenile nephronophthisis and renal medullary cystic disease. 126 65


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