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

Keeping in mind the vasodilator action of prostaglandins, the control that they exercise over the vascular supply of kidneys and the sympathetic activity, research was conducted in order to establish the effect of arachidonic acid, the precursor of PGE2, on experimental hypertension in the rat. The experimental hypertension was induced by unilateral nephrectomy, followed by the administration of DOCA and the elevated sodium diet. The treatment was short in one group, long in the other, and both groups were compared to a control hypertensive group which received no treatment at all. Arachidonic acid worsened the experimental hypertension by 37% in the long treatment, and by 25% in the short treatment. The administration of lysine-acetylsalicylate diminished this hypertension. A non-saturated acid, oleic acid, which is not involved in prostaglandin synthesis, has no action. The authors would like to emphasize that in one of the previous experiments, L-tyrosine, the precursor of catecholamines, diminished the experimental hypertension in the rat, and also that L-DOPA and IMAO (MAOI) have comparable effects. It seems, therefore, that the depression of the central catecholaminergic activity, which is supposed to be the action of arachidonic acid via an increase in the PGE2 synthesis, appears to increase hypertension. It is noteworthy that the medial forebrain bundle (MFB) is catecholaminergic and that the periventricular system (PVS) is cholinergic. Thus hypertension may represent the peripheral vascular response to anguish which results from the activation of PVS and from the depression of MFB.
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PMID:The action of arachidonic acid on experimental hypertension in the rat. 112 60

Contrasting with the hypertension resulting consistently after DOCA implantation, mature female rats given Enovid daily for 20 weeks had only slight and occasional increases in blood pressure. The pressure elevations remained infrequent and transient even when drinking water was replaced with isotonic saline solution but they became more pronounced when Enovid treatment was initiated at an earlier age. Despite the failure to cause sustained hypertension, the data indicate that Enovid affects blood pressure and that both mestranol and norethynodrel are essential for this effect. Pressor responses to norepinephrine or angiotensin were unaffected even after 20 weeks of pretreatment but those to electrical stimulation of the posterior hypothalamus were increased in rats pretreated with Enovid. Enhanced responsiveness to hypothalamic stimulation occurred only in the awake state and was not demonstratable after the central nervous system (CNS) had been depressed with urethane. These results can be explained by an increased sensitivity of hypothalamic pressor areas produced by Enovid prior to the development of hypertension and the mechanisms involved may be similar to those occurring in spontaneously-hypertensive rats. However, the possibility of hypersensitivity at other sites in the sympathetic vasomotor outflow cannot be ruled out.
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PMID:Potentiation of hypothalamic pressor responses in awake rats treated with contraceptive steroids. 115 1

Esterase and Acid phosphatase isozymes were examined in a number of organs, glands and tissues from Spontaneously Hypertensive Rats (SHR) and kidney and liver from DOCA hypertensive rats at various stages in comparison with those of normotensive rats (CR). In SHR, the abnormalities in the patterns of esterase isozyme were demonstrated in endocrine glands and respiratory tracts as well as in the kidney, liver and digestive tracts throughout the whole life span, and abnormalities in the patterns of acid phosphatase isozyme was also demonstrated in the liver after seven days of age. Moreover, in DOCA hypertensive Rats, minute alterations in esterase isozyme were demonstrated in the kidney and liver after seventh month of the duration of hypertension.
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PMID:Zymogram analyses of various organs, glands and tissues from spontaneously hypertensive rats (SHR) and DOCA hypertensive rats. 116 4

The goal of these studies was to determine whether the hypertension caused by excessive salt loading results from sodium-induced expansion of the extracellular fluid volume or whether the salt increases the pressure in some other way, such as by causing vascular constriction. In one group of sheep, a combination of total nephrectomy and hemodialysis was used to produce and maintain step increases in extracellular fluid volume for 1 wk without a significant change in sodium ion concentration. In a 2nd group, unilateral nephrectomy, dialysis, and DOCA administration were used to cause step increases in sodium ion concentration while the extracellular fluid volume was held as close to normal as possible. The results showed a 41% increase in arterial pressure in the high-volume sheep and only a 4% increase in pressure in the high-sodium sheep. In both instances the total exchangeable sodium increased almost equally--a 21% increase in the high-sodium sheep. The data support the concept that sodium retention causes hypertension almost entirely because of sodium-induced expansion of the extracellular fluid volume.
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PMID:Separate roles of sodium ion concentration and fluid volumes in salt-loading hypertension in sheep. 119 Mar 20

The role of the sympathetic nervous system in the development of deoxycorticosterone-sodium chloride (DOCA-saline) hypertension was investigated by measuring plasma levels of norepinephrine, total catecholamines, and dopamine-beta-hydroxylase activity at intervals after the initiation of the DOCA-saline regimen. Plasma norepinephrine was significantly higher in DOCA-saline-treated rats at 4 and 7 weeks and in rats treated with saline alone at 4 weeks compared with that in untreated controls. Total plasma catecholamine levels (epinephrine and norepinephrine) and dopamine-beta-hydroxylase activity were similar in hypertensive rats, untreated controls, and rats that received either DOCA or saline alone. The increases in plasma norepinephrine levels may have resulted from centrally mediated increases in peripheral sympathetic neuronal activity, since the destruction of central catecholaminergic neurons with intracerebroventricularly administered 6-hydroxydopamine (6-OHDA) prevented both the DOCA-saline-induced rise in blood pressure and the increases in plasma norepinephrine. Rats treated with 6-OHDA consistently drank less water or saline than did vehicle-treated controls. The actions of centrally administered 6-OHDA on blood pressure and plasma norepinephrine levels were not secondary to a reduction in salt intake, however, since intact rats given a similar reduced saline intake became hypertensive and demonstrated elevated plasma norepinephrine concentrations. Chronic salt loading may cause a centrally mediated increase in peripheral sympathetic neuronal activity with raised plasma concentrations of norepinephrine. The increased adrenergic activity in the presence of mineralocorticoid-induced sodium retention leads to the development of hypertension.
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PMID:Central and peripheral adrenergic mechanisms in the development of deoxycorticosterone-saline hypertension in rats. 119 56

The effects of various doses of 6-hydroxydopamine (6-OHDA) injected into the hypothalamus on DOCA-salt-induced hypertension were studied. The development of hypertension was prevented in the group treated with the highest dose of 6-OHDA, and the onset of hypertension was delayed in a dose-dependent fashion in the groups treated with the lower doses of 6-OHDA. Catecholamine histofluorescence observations showed that the cannula tips placed the drug lateral to the third ventricle. The most prominent change observed was a marked unilateral reduction in the fluorescence of the dopaminergic nerves of the caudate-putamen and in the number of cell bodies in the substantia nigra. These results suggest possible sites of central aminergic control of blood pressure.
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PMID:Central adrenergic neurons in DOCA-salt hypertension. 122 88

Deoxycorticosterone acetate (DOCA)-salt hypertension was induced in Brown Norway (BN) kininogen-deficient rats (BN-Ka) and normal rats from the same strain (BN-Ki) after nephrectomy. Systolic blood pressure, which was determined by the tail-cuff method, of BN-Ki increased gradually during this treatment. In contrast, the blood pressure of mutant BN-Ka increased rapidly 2 weeks after the onset of the treatment. Urinary excretion of active kallikrein and prokallikrein increased at the same degree in rats of both strains during this treatment. Significant increase in urinary sodium excretion was observed with a tendency to increase in urine volume during the treatment in normal BN-Ki rats, whereas both parameters were essentially not increased in mutant BN-Ka rats, which could not generate urinary kinin. Aprotinin infusion by osmotic minipump to normal BN-Ki rats during the DOCA-salt treatment resulted in significant further increase in the systolic blood pressure.
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PMID:Essential role of kallikrein-kinin system in suppression of blood pressure rise during the developmental stage of hypertension induced by deoxycorticosterone acetate-salt in rats. 128 79

Increased vascular sensitivity to catecholamines characterizes mineralocorticoid hypertension. The present study investigated three possible sites that may account for this abnormality: agonist affinity, Ca2+ release from intracellular stores, and Ca2+ sensitivity of the contractile proteins. Adult male Sprague-Dawley rats underwent uninephrectomy and were implanted subcutaneously with deoxycorticosterone acetate (DOCA; 200 mg/kg, 1% NaCl:0.2% KCl drinking water, 4-6 weeks). Control rats were sham treated. Helical strips of mesenteric arteries were placed in muscle baths for measurement of isometric force development. Although the ED50 for norepinephrine was significantly lower in arteries from DOCA rats (pD2, 8.21 +/- 0.15) than in those from sham controls (pD2, 7.24 +/- 0.11), agonist affinity, determined by partial blockade with phenoxybenzamine, did not differ between the two groups. In contrast, norepinephrine-stimulated 45Ca2+ efflux in the absence of extracellular Ca2+ was significantly greater in arteries from DOCA rats than in those from sham rats. In the presence of ryanodine to deplete intracellular Ca2+ stores, force development to Ca2+ was not different in saponin-permeabilized vessels from DOCA rats, indicating that the Ca2+ sensitivity of the contractile proteins was not altered in DOCA hypertension. We conclude that increased vascular sensitivity to norepinephrine in mineralocorticoid hypertension is related to increased release of Ca2+ from a subcellular store and not to changes in agonist affinity or to the contractile protein interaction. Based on previous reports, it is likely that this abnormality reflects a postreceptor change in signal transduction, but there is also evidence to suggest that an increase in the number of alpha-adrenergic receptors may be involved.
Hypertension 1992 Jun
PMID:Alpha-adrenergic receptors and 45Ca2+ efflux in arteries from deoxycorticosterone acetate hypertensive rats. 131 54

The effect of manidipine on cardiac hypertrophy, coronary circulation, left ventricular weight and maximal coronary flow in hypertension was measured in DOCA/salt treated systolic hypertensive rats with and without manidipine treatment. Normotensive rats were used as controls. After feeding with 0.05% manidipine-containing food, blood pressure was reduced only in DOCA/salt hypertensive rats, but not in control rats. After 3 weeks of treatment, sodium excretion was significantly increased in DOCA/salt-treated rats with or without manidipine treatment. Hearts were removed and perfused with modified Krebs-Henseleit solution with adenosine (5 x 10(-5) M) in a Langendorff apparatus. Maximal coronary flow (MCF) was significantly decreased only in DOCA/salt hypertensive rats without treatment, while manidipine treatment restored MCF. Left ventricular weight/body weight was also markedly greater in DOCA/salt-treated rats not given manidipine. Left ventricular weight in DOCA/salt-treated rats given manidipine was significantly reduced compared with DOCA/salt hypertensive rats without treatment, although it was heavier than in the control animals. Morphological examination showed that the increased wall/lumen ratio in DOCA/salt hypertensive rats was reduced by manidipine treatment. These findings suggest that treatment with manidipine in DOCA/salt hypertensive rats lowered high blood pressure and improved impaired coronary circulation with a reduction in left ventricular and vascular hypertrophy.
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PMID:Effect of manidipine on cardiac hypertrophy and coronary circulation in DOCA/salt hypertensive rats. 134 89

Antihypertensive drugs have differing effects on renal hemodynamics, tubular function, plasma electrolytes, and hormonal responses. Nonselective beta-blockers without intrinsic sympathomimetic activities, such as propranolol, have been reported to reduce renal blood flow and to cause a modest decrease in glomerular filtration rate. Carvedilol is a new multiple action agent displaying nonselective beta-blockade without intrinsic sympathicomimetic activity, alpha 1-adrenoceptor blockade (probably responsible for its vasodilator activity), and possibly also calcium antagonist properties. The presence of these different pharmacodynamic properties results in a different effect on the kidney as compared with, e.g., propranolol. In the dog, intrarenal infusion of carvedilol resulted in a renal vasodilator response with preservation of renal blood flow and without inducing sodium retention; in contrast, propranolol induced a renal vasoconstrictor response and sodium retention in this model. A renal vasodilator response to carvedilol was also reported in spontaneously hypertensive rats (SHR) and in DOCA-salt SHR. In contrast to labetalol, i.v. infusion of hypotensive doses of carvedilol in conscious SHR did not cause sodium retention. Carvedilol was effective in controlling hypertension and preserving renal function in a rat model of progressive hypertensive renal disease. In patients with essential hypertension, carvedilol was reported to reduce renal vascular resistance in the presence of reduced perfusion pressure, allowing for normal renal autoregulation of renal blood flow. Although a small reduction in glomerular filtration rate was seen after acute administration, renal function was preserved during chronic treatment. It is concluded from these studies that renal perfusion and renal function are well maintained during acute and chronic treatment with carvedilol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Carvedilol and the kidney. 135 Apr 79


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