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

In a group of hypertensive patients it has been shown that moderate sodium chloride restriction has a hypotensive effect that is similar to that produced by thiazide diuretics. Blood pressure changed in relation to body weight in individual patients, and appeared to correlate with their sodium balance. The more a patient was depleted of sodium, the lower was the blood pressure. The serum potassium level fell with the use of thiazide diuretics, but in this group of patients there was little change in total body potassium content. The fall in serum potassium level appeared to relate to a shift into the cells due to the accompanying alkalosis. Potassium supplementation appeared to have had little effect and was unnecessary for most patients who were given diuretics for hypertension. Amiloride corrected the alkalosis and restored the serum potassium level to normal.
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PMID:Sodium restriction and thiazide diuretics in the treatment of hypertension. 115 72

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

In response to an acute saline load, many patients with essential hypertension exhibit an exaggerated natriuresis relative to normotensive controls. In the present study, the urinary responses of conscious,Okamoto-strain, spontaneously hypertensive rats (SHR), and Wistar-Kyoto strain normotensive rats (NTR) to an acute saline load were evaluated to determine if a similar exaggerated natruiresis exists in this form of hypertension. Twelve rats of each strain per group (12 weeks of age) were housed in metabolism cages for 1 week. Systolic blood pressures (tail cuff) were significantly different (206+/- 9 mm. Hg in SHR and 135 +/- 3 mm. Hg in NTR). After a 4-hour control urine collection, 6 ml. of 0.9 per cent sodium chloride were given by gavage. Urine was collected again for 2 hours. Control urinary excretions of sodium, potassium, and creatinine in SHR and NTR were 11.2 +/- 4.8 muEq per hour, 50.1 +/- 7.6 muEq per hour, and 39.9 +/- 5.5 mg. per hour in SHR, and 13.8 +/- 2.4 muEq per hour, 34.9 +/- 5.5 muEq per hour, and 37.5 +/- 7.1 mg. per hour in NTR, respectively. The respective control values for sodium, potassium, and creatinine excretion in the two groups were not significantly different. Following the saline load, sodium and creatinine excretion rates were significantly elevated in both groups of rats. However, the increase in sodium excretion in SHR (60.8 +/- 7.2 MUEq per hour) was more than double and significantly different from that of the NTR (26.6 +/- 3.7 muEq per hour). In contrast, the increments in creatinine excretion in the two groups of rats were not significantly different from each other. In the NTS, urinary potassium excretion was significantly elevated (59.0 +/- 7.9 muEq per hour) whereas in SHR it was not significantly altered (12.0 +/- 8.8 muEq per hour). The change in urinary creatinine excretion as an index of change in glomerular filtration rate suggests that the greater increase in sodium excretion by the SHR was the result of decreased fractional reabsorption of sodium and not the result of a greater increase in glomerular filtration rate. The exaggerated natriuretic response to salt loading in SHR resembles that in hypertensive man except that in SHR, a simultaneous kaliuretic response is absent.
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PMID:Exaggerated natriuresis in the conscious spontaneously hypertensive rat. 124 91

The adrenaline-forming enzyme (phenylethanolamine N-methyltransferase) was elevated in the A1 and A2 regions of the brainstem of 4-week-old spontaneously (genetic) hypertensive rats and in the A1 region of adult experimentally (deoxycorticosterone acetate and sodium chloride) hypertensive rats. The administration of a phenylethanolamine N-methyltransferase inhibitor to experimentally hypertensive animals caused a reduction of the elevated blood pressure to normal values. These results implicate adrenaline-containing neurons in the brainstem in the development of hypertension.
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PMID:Adrenaline-forming enzyme in brainstem: elevation in genetic and experimental hypertension. 124 33

The present study investigated the role of ouabain-dependent inhibition of the Na(+)-K+ pump and stimulation of the brain renin-angiotensin system by looking at 1) the short-term and long-term effects of ouabain on arterial blood pressure, and 2) the acute and chronic effects of angiotensin II (ANG II) intraventricularly (i.c.v.) on the release of an endogenous inhibitor of the Na(+)-K+ pump. Ouabain infused subcutaneously in a dose of 1.5 mg.kg-1. 24 h-1 for 7 days did not affect arterial blood pressure in rats, whereas increases in both blood pressure and weight were observed in rats infused with ouabain at the same dose for a 4-week period. Plasma supernate obtained from pentobarbital-anesthetized dogs acutely treated with ANG II (1 microgram i.c.v. every 30 min for 2 h) induced a 44% decrease in the ouabain-sensitive 86Rb uptake by the rat tail artery which was prevented by pretreatment with saralasin i.c.v. Plasma supernate obtained from dogs that were infused for 4 days with ANG II (20 ng/min i.c.v.) and received saline as the drinking fluid also reduced by 34% the ouabain-sensitive 86Rb uptake by the rat tail artery. The present study provides evidence that chronic inhibition of the Na(+)-K+ pump for 4 weeks leads to the development of hypertension and that the release of an endogenous inhibitor of the Na(+)-K+ pump is implicated in the hypertension resulting from chronic stimulation of the brain angiotensin-system and an increase in sodium chloride intake.
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PMID:The ouabain-dependent Na(+)-K+ pump and the brain renin-angiotensin system. 131 74

Thirty healthy parturients, having given informed consent, were randomly allocated in a double-blind study to receive an intramuscular injection of either 0.9% sodium chloride (control), ephedrine 25 mg, or ephedrine 50 mg, 30 minutes prior to general anaesthesia for caesarean section. Nine patients (90%) in the 50 mg group and five patients (50%) in the 25 mg group demonstrated reactive hypertension of 20% or greater from control. The mean maximum increase in the 50 mg group was 28.2% (range 4.4-38.3%). Maternal pH was significantly lower (P = 0.03) in the ephedrine 50 mg group. Neonatal acid base status was significantly impaired in the ephedrine 50 mg group with umbilical venous pH (P = 0.0001) and umbilical arterial pH (P = 0.001) being significantly lower than the control group. The associated increase in umbilical arterial base deficit suggests a metabolic component due to fetal asphyxia related to decreased uterine blood flow. We conclude that the prophylactic administration of intramuscular ephedrine prior to spinal anaesthesia is associated with an unacceptably high incidence of maternal hypertension, and should the spinal fail and general anaesthesia be required, also results in adverse neonatal biochemical changes. The technique is therefore not to be recommended.
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PMID:Prophylactic intramuscular ephedrine prior to caesarean section. 834 83

The borderline hypertensive rat is the first filial offspring of the spontaneously hypertensive rat and the Wistar-Kyoto rat. With increased dietary sodium chloride intake, the borderline hypertensive rat develops hypertension and exaggerated cardiovascular and renal responses to acute environmental stress, similar to those observed in the hypertensive spontaneously hypertensive rat parent. In other models of sodium chloride-sensitive hypertension with different genetic background (Dahl rat), dietary potassium chloride supplementation protects against the development of hypertension, increased sympathetic nervous system activity, and exaggerated responses to acute environmental stress. This investigation sought to determine whether the dietary sodium chloride-induced development of both the hypertension and the exaggerated responses to acute environmental stress could be reversed or prevented by increased dietary potassium chloride intake. Dietary potassium chloride intake was increased with a 1% potassium chloride drinking solution either after 12 wk of 8% sodium chloride intake (reversal) or concomitant with the onset of 12 wk of 8% sodium chloride intake (prevention). An increase in dietary potassium chloride intake did not reverse or prevent the development of either the hypertension or the exaggerated cardiovascular and renal responses to acute environmental stress in borderline hypertensive rats fed 8% sodium chloride. It is concluded that the difference in genetic background between borderline hypertensive rats and other models of sodium chloride-sensitive hypertension is an important determinant of the protective effect of dietary potassium chloride supplementation.
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PMID:Effect of dietary potassium chloride in borderline hypertensive rats. 139 19

Studies over the past 10 years suggest that the atrial natriuretic factor (ANF) plays an important role in salt and water homeostasis. Responding to atrial stretch, the atria releases ANF into the circulation. The several actions of this hormone tend to increase renal NaCl excretion resulting in reduced blood volume and blood pressure. ANF increases the glomerular filtration rate and reduces sodium chloride reabsorption in the distal nephron. It also inhibits secretion of aldosterone from the adrenal cortex. Therefore actions of ANF appear to be opposed to the renin-angiotensin-aldosterone system. Drugs that alter ANF metabolism may constitute a new mechanism of treatment for hypertension and heart failure.
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PMID:Role of atrial natriuretic factor in salt and water homeostasis. 140 80

The hormonal regulation of sodium and volume homeostasis was investigated in three patients (two related) with the syndrome of familial hyperkalemic acidosis and hypertension with normal glomerular filtration rate. Recumbent plasma renin activity was low during normal sodium intake (135 mmol daily), and the response to upright posture or to low sodium diet (10 mmol daily) was blunted. Recumbent plasma aldosterone levels were normal in two patients and high in one, and the standing values were elevated in one; responses to upright posture were brisk on low sodium diet. Angiotensin II infusion induced a marked increase in plasma aldosterone. Plasma atrial natriuretic peptide was at the upper limit of normal during normal sodium intake, decreased during diuretic therapy, and increased during sodium chloride infusion in one patient. Basal urinary prostaglandin E2, prostaglandin F2 alpha, and 6-ketoprostaglandin F1 alpha excretion rates were decreased, and thromboxane B2 was increased. Total blood and plasma volumes were subnormal, whereas extracellular fluid volume and exchangeable sodium values were close to or above (in one patient) the mean normal values. Chronic treatment with hydrochlorothiazide in two patients corrected the hyperkalemic acidosis and hypertension, but on its discontinuation (in one patient) all biochemical abnormalities promptly reappeared.
Hypertension 1992 Apr
PMID:Endocrine sodium and volume regulation in familial hyperkalemia with hypertension. 153 66

The effects on blood pressure and the development of cardiac hypertrophy of sodium chloride (regular salt) and a novel potassium-, magnesium-, and l-lysine-enriched salt alternative, which in a previous study prolonged the life span of hypertensive rats nearly threefold as compared with the animals receiving regular salt, were compared both in spontaneously hypertensive rats and their hypertension-resistant genetic controls. In particular, the possible protective effect of increased intakes of potassium, magnesium, and l-lysine during a high intake of sodium chloride was examined. Therefore, the salt alternative was added at 1.75 times higher levels to produce the same dietary levels of sodium chloride in the regular salt and the salt alternative groups. Regular salt produced a remarkable left ventricular hypertrophy in both rat strains, but as compared with the respective control groups, it induced an increase of blood pressure only in the spontaneously hypertensive rats. The salt alternative did not induce a rise in blood pressure in either of the rat strains, nor did it produce left ventricular hypertrophy in the hypertension-resistant rats and, in the spontaneously hypertensive animals, significantly less hypertrophy than regular salt. The salt alternative appeared to prevent the sodium chloride-induced volume load since plasma levels of atrial natriuretic peptide were increased in the regular salt groups but remained normal in the salt alternative groups. Therefore, potassium, magnesium, and/or l-lysine of the salt alternative produced a powerful protection against the harmful effects of sodium chloride.
Hypertension 1992 Jun
PMID:Beneficial effects of a potassium- and magnesium-enriched salt alternative. 153 13


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