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

Hypertensinogenic potency and other effects of acetate salts of aldosterone (ALA) and deoxycorticosterone (DOCA) were evaluated in 50-day-old mononephrectomized and saline-drinking Sprague-Dawley CD male rats. The steroids were administered by continuous subcutaneous infusion in a dose of 100 microgram/24 hrs by means of Alzet osmotic minipumps implanted subcutaneously. Within 3 weeks of steroid treatment, systolic blood pressure, measured in the tail of conscious animals by a photoelectric cell method at 27 degrees C environmental temperature, increased significantly in ALA rats as compared to that in DOCA rats, which was not different from controls. ALA rats exhibited marked polydipsia, decreased body weight, hypernatremia, hypokalemia, cardiomegaly, and kidney enlargement, whereas DOCA rats exhibited only cardiomegaly when compared with controls. The degree of cardiomegaly in ALA and DOCA rats was statistically much greater than the differences in their respective blood pressure levels when compared to controls. Under the conditions of this study, it is concluded that: 1) the hypertensinogenic potency of ALA is greater than that of DOCA; 2) ALA and DOCA may induce cardiomegaly, independent of their effect on blood pressure; 3) Alzet osmotic minipumps are effective tools for the administration of steroids by continuous infusion.
Hypertension
PMID:Hypertensinogenic potencies of aldosterone and deoxycorticosterone in the rat. 706 Nov 21

Both 19-nordeoxycorticosterone and 19-norprogesterone are potent hypertensogens. This particularly interesting in the latter case, since the parent steroid is antimineralocorticoid and antihypertensive. The present experiment compared the ability of testosterone and 19-nortestosterone to cause hypertension in rats. Both steriods caused adrenal atrophy, nephromegaly, relative hypoproteinemia and increased hematocrit, but only testosterone provoked saline polydipsia, hypernatremia, hypertension, cardiomegaly and vascular lesions. It is evident that demethylation of testosterone at C10 completely destroys any effect on sodium metabolism or blood pressure, but leaves certain other pathophysiologic responses, including extreme adrenal atrophy, unimpaired. The hypertensogenic effect of testosterone has been attributed to its inhibitory effect on adrenal structure and function, the latter characterized by an induced enzymatic defect leading to increased secretion of deoxycorticosterone. This raises the intriguing question of whether, despite the comparable involution of the adrenal cortex, there are significant differences in adrenocortical enzymatic changes initiated by the respective androgens, which could account for their quiet different blood pressure effects.
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PMID:Similarities and differences between effects of testosterone and 19-nortestosterone in rats, with particular reference to hypertensogenic potency. 708 83

A series of experiments was designed to explore the mechanisms contributing to hypertension caused by an acute or chronic sodium load. Acute salt-loading in totally or subtotally nephrectomized animals caused hypertension mediated partly through stimulation of excessive vasopressin release and partly through adrenergic stimulation. Chronic high-salt diet in rats submitted to partial nephrectomy, mineralocorticoid excess or one-kidney-one-clip renovascular hypertension caused blood pressure elevation mediated through a central neurogenic mechanism that could be reversed by administration of an inhibitor of phenylethanolamine-N-methyltransferase, the enzyme catalyzing conversion of norepinephrine to epinephrine. Thus, two vasopressor mechanisms were stimulated by sodium excess: an acute, transient, partly vasopressin-mediated phase seemed to be followed by a chronic phase mediated through stimulation of central sympathetic neurons. In neither phase was blood pressure related to intravascular fluid volume expansion.
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PMID:Possible mechanisms of sodium-dependent hypertension: volume expansion or vasoconstriction? 710 37

Changes in inulin space, plasma and blood volume, exchangeable and "noninulin" sodium were studied during the prehypertensive, early and late hypertensive stages of deoxycorticosterone (DOC)-salt administration in the rat. The effect of an acute water load in previously nephrectomized animals was also studied. Hypertension developed after 1 to 2 weeks of the DOC-salt regimen and was always preceded by enlargement of the inulin space and increased plasma and blood volume. Expansion of extracellular fluids receded when blood pressure started to rise but reappeared after 4 to 6 weeks of treatment. Plasma sodium was high only in the hypertensive groups. An acute water load increased blood pressure of normal rats and decreased blood pressure of DOC-salt early hypertensive rats. These findings suggest that extracellular volume expansion inhibits a vasopressor mechanism that involves vasopressin and could be stimulated by hypernatremia.
Hypertension
PMID:Role of extracellular volume expansion in the development of DOC-salt hypertension in the rat. 710 34

An anteroventral third ventricle (AV3V) lesion in the brain prevents several forms of experimental hypertension. The present experiment was designed to determine whether the AV3V lesion prevents NaCl-induced hypertension in Dahl salt-sensitive (S) rats and whether attenuation of vasopressin release reported in lesioned rats contributes to the protective effect of the AV3V lesion against hypertension. After the AV3V lesion Dahl S rats received daily injections of either vasopressin (pitressin tannate, 500 mU/kg) or vehicle during 10 wk of 8% high-NaCl diet. Sham-lesioned rats served as controls. The blood pressure in sham-lesioned rats receiving vehicle was 189 mmHg after 10 wk of high-NaCl diet. Lesioned rats given vehicle showed a significantly smaller increase in blood pressure than sham-lesioned rats (P less than 0.001), the blood pressure averaging 161 mmHg at 10 wk. Lesioned rats given vasopressin also showed a smaller increase in blood pressure than sham-lesioned rats (P less than 0.05), but the final blood pressure averaged 176 mmHg and was significantly higher than that of lesioned rats given vehicle (P less than 0.025). Vasopressin injections corrected the hypernatremia in lesioned rats. In another experiment the effect of the AV3V lesion on the renal papillary plasma flow (RPPF) in Dahl S rats was studied. Dahl S rats have a lower RPPF than Dahl salt-resistant (R) rats even on a low-NaCl intake. The AV3V lesion increased the RPPF by 14% in S rats (P less than 0.025). These findings suggest that NaCl-induced hypertension in Dahl S rats requires the integrity of the AV3V region for its full expression, and the ability of the AV3V lesion to attenuate the NaCl-induced hypertension in Dahl S rats is partly related to the attenuation of vasopressin release. Moreover, the AV3V lesion partly corrected one of the characteristic features of Dahl S rats, the reduction in RPPF, when compared with Dahl R rats, with both strains on a low-NaCl intake.
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PMID:Effect of an anteroventral third ventricle lesion on NaCl hypertension in Dahl salt-sensitive rats. 712 69

Several abnormalities concerning sodium (Na+) transport in erythrocytes of essential hypertensive patients have been recently observed. An abnormal extrusion of an erythrocyte Na+ load was described in our laboratory. This defect appeared to be specific for essential hypertension since it was absent in the secondary forms of the disease. The present investigation was performed on 194 Caucasian subjects with essential hypertension or born of hypertensive parents, 86 normotensive controls, and 14 families (78 subjects) studied over two to three generations. The distribution pattern of the erythrocyte defect is compatible with the expression of a single gene transmitted according to an autosomic and dominant mode. To confirm the genetic association between the red blood cell abnormality and primary hypertension, genetically hypertensive rats were investigated in parallel to our clinical studies. A reduction in the net Na+ extrusion from red blood cells was found in two varieties of genetic hypertension (SHR and H-prone-Na+-sensitive Sabra rats). The abnormality could be detected before the development of a significant hypertension. When these various rat sub-strains were acutely or chronically loaded with Na+ (either intraperitoneally or orally), a significant increase in erythrocyte Na+ content was observed only in those substrains having a genetic propensity to develop hypertension. This finding, which appears to be a consequence of the reduction in net Na+ efflux, is of interest for several reasons. It confirms the existence of a close association between a genetic predisposition to develop high blood pressure and cell Na+ retention in the presence of an excess Na+ intake. It draws attention to the possible role of intracellular Na+ in the pathogenesis of primary hypertension. Of more practical importance, the abnormal Na+ handling in erythrocytes may be a genetic marker of primary hypertension.
Hypertension
PMID:Abnormal erythrocyte cation transport in primary hypertension. Clinical and experimental studies. 726 80

The mineralocorticoid potency of 19-nor-progesterone was evaluated by both its effect on electrolyte excretion in adrenalectomized animals and its ability to cause hypertension and electrolyte changes in mononephrectomized, salt-loaded rats. The mineralocorticoid activity, measured using an adrenalectomized rat bioassay, indicated that 19-nor-progesterone was 2.5% as potent as aldosterone but did not antagonize the effect of aldosterone when both were administered. In mononephrectomized rats, the daily administration of 1 mg/day quickly caused an enhanced consumption of 1% saline and induced severe hypertension within 3-4 weeks. Some severely hypertensive animals had marked anemia, but other did not; as a group they were found to have hypernatremia and hypokalemia. Hypertensive animals were found during life to display a relative hypothermia and, at necropsy, to have heart and kidney enlargement with severe and extensive vascular lesions in both organs, but not adrenal hypertrophy. It is concluded that 19-nor-progesterone has the characteristics of a potent mineralocorticoid and, as such, is capable of causing hypertension. It is not yet clear why this should be accompanied by hypothermia.
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PMID:Mineralocorticoid and hypertensive effects of 19-nor-progesterone. 728 65

In order to explore the impact of nephritis on the development of hypertension, rats with Heymann nephritis were given 0.9% NaCl to drink, in combination with or without DOCA injections, for up to 6 months. Combined nephritis-DOCA-NaCl resulted in severe hypertension and shortened life span, whereas nephritis-NaCl combination failed to induce hypertension or shorten life span. All immunized rats developed membranous glomerulonephritis but creatinine clearance did not decrease. DOCA-NaCl-treated nephritic rats had a heavier proteinuria and more marked renal lesions than NaCl-treated nephritis rats. Proliferative-sclerotic glomerular lesions were seen in the nephritis-DOCA-NaCl group only, correlating to the severity of hypertension. Other renal and extrarenal vascular lesions, increasing with time, also appeared related to the severity of hypertension. This suggests a secondary relationship of vascular damage to hypertension in this model. Appearance of proteinuria preceded the establishment of hypertension, suggesting that nephritis sensitized to the development of hypertension during DOCA-NaCl treatment. Sodium excess alone, however, did not induce hypertension in Heymann nephritic rats. The present Heymann nephritis-DOCA-NaCl hypertension model appears a useful model for the study of hypertension complicating glomerulonephritis.
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PMID:Heymann nephritis-DOCA-NaCl hypertension in the rat. Role of nephritis, DOCA, NaCl, and vascular lesions in the development of hypertension. 729 Feb 77

Vascular endothelial cells produce various biologically active factors regulating blood pressure, coagulation, and possibly cell growth of the vascular wall. Of the factors, nitric oxide (NO) has been the object of attention because of its quite simple molecular structure and variety of biological functions. In the present review, we focused on the physiologic and pathologic aspects of NO in hypertension. In experimental animals, both acute and chronic inhibition of NO synthase (NOS) with arginine derivatives produce a significant rise in blood pressure, indicating that tonic production of NO regulates basal vascular tonus. The chronic hypertension caused by NOS inhibitor is associated with cardiac hypertrophy and renal insufficiency. Sodium retention, though transient, and the plasma and tissue renin/angiotensin system in addition to the reduced production of NO have been implicated in the development of hypertension. Hypertension and the associated target organ failure can be reversed by co-administration of L-arginine or blockades of the renin/angiotensin system. Studies in which L-arginine as the substrate of NO or NOS inhibitor was administered demonstrated an important role of NO in the regulation of tonic vascular tonus also in normal subjects. In hypertensive subjects, however, endothelium-dependent vasorelaxation and production of NO are impaired, possibly due to a deficiency of L-arginine and/or a disorder of its utilization. Recent advances in the methods of detecting NO enabled us to demonstrate its diminished production from endothelial cells of hypertensive rats in vitro, although no definite biochemical evidence has been obtained in hypertensive subjects. The endothelial dysfunction, however, is not a primary cause of hypertension but a secondary result since it is commonly observed in various types of hypertension and can be reversed by correcting the blood pressure. Other common diseases including atherosclerosis and diabetes mellitus are also associated with similar abnormalities of the endothelium. NO has anti-atherogenic actions: inhibition of platelet functions and proliferation of vascular smooth muscle cells. Therefore, potentiation of endogenous NO and/or supplement of exogenous NO donors could be novel therapeutic approaches for the treatment of hypertension and atherosclerosis, while potential adverse effects of NO including cytotoxicity, immunosuppressibility, and hypotensive shock should be taken into account.
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PMID:[Clinical significance of nitric oxide in hypertension]. 752 65

The study aimed at evaluating an incidence of hypo- and hypernatremia in the elderly and the results of therapy. Hyponatremia. The studies involved 18 patients aged 69.8 +/- 5.9 years with hyponatremia of 126.8 +/- 2.7 mmol/L. The main causes of hyponatremia were: diuretics, diarrhoea, and vomiting. Sodium deficit was calculated prior to the treatment in all patients. An analysis of hyponatremia incidence indicates that hyponatremia was diagnosed in 1.39% of patients over 60 years, hospitalized within 1989-1990. Sodium deficit in this group was 495.5 +/- 167.7 mmol. Sodium chloride solution was given intravenously to 12 patients, according to the "free correction" principle (a mean increase in serum sodium level was 0.17 +/- 0.07 mmol/L per hour). Mortality in such treated patients was 33%. Sodium chloride was not given to 6 out of examined patients. In 12 patients (66.6%) hyponatremia developed prior to hospitalization, in 6 patients (33.3%) during hospitalization. Mortality rate was 16.6% and 50%, respectively. This confirms higher mortality rate of the rapidly developing hyponatremia in the hospitalized elderly patients. In some cases hyponatremia may constitute iatrogenic complication, especially in the elderly given diuretics in an uncontrollable way. Own experience suggests that elderly patients with a risk of hyponatremia require close monitoring and early compensation of the electrolyte disorders. Hypernatremia. The studies involved 20 patients aged 71.4 +/- 7.7 years with hypernatremia of 155.6 +/- 8.4 mmol/L. A total water deficit (DH20) was calculated in this group. An analysis of hypernatremia incidence showed that this state was diagnosed in 1.55% of patients treated at the Department of Arterial Blood Hypertension within 1989-1990. Total water deficit was 3.9 +/- 1.9 L. A 5% glucose was given intravenously to 15 patients whereas oral fluid therapy was carried out in 5 patients. A mean corrected DH2O in the first day was 46.0 +/- 21.0%. Mortality rate in this group was 65%. It is worth mentioning that 37% of patients with chronic hypernatremia which developed prior to hospitalization died while in case of the acute hypernatremia developed in the hospital mortality rate was 83%. A significant effect on the results of therapy plays an early correction of hypernatremia. Mortality rate in case of DH2o supplementation below 30% during the first 24 hours is about 66%., if DH2o supplementation is 31-60%, a mortality rate is 63%, and in DH2o supplementation over 60% mortality rate is 100%. The obtained results suggest that hypernatremia in the elderly is related to the high mortality rate (65%). An early decrease of water deficit increases mortality rate in patients with hypernatremia.
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PMID:[Hyponatremia and hypernatremia in the elderly]. 786 86


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