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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of dietary sodium upon serum and urinary calcium and selected vitamin D metabolites were studied in two groups (n = 10 each) of age and gender matched, white normotensive subjects and patients with normal-renin hypertension. Isocaloric diets were consumed on a metabolic ward with sequential daily sodium intake of 109 meq for 5 days and 9 meq and 259 meq for 6 days each. Values for serum and urinary calcium, phosphorus, magnesium and electrolytes, creatinine clearance, plasma immunoreactive parathyroid hormone, and serum 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D were similar in both study groups on each diet. Measurements of plasma renin activity and serum aldosterone levels were higher in the hypertensive than in the normotensive group on each diet (p less than .05-.01). Serum 1,25-dihydroxyvitamin D and urinary calcium increased on the high sodium diet in the normotensive (p less than .05) and the hypertensive groups (p less than .01). When the data for normotensive subjects and hypertensive patients were pooled by gender, males had a 1 1/2 to 3 times the urinary calcium excretion than females, regardless of diet. The present study indicates that there are no differences in the selected components of calcium and vitamin D metabolism in response to sodium intake in patients with essential hypertension and normal plasma renin activity as compared to normal controls.
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PMID:Normal vitamin D and mineral metabolism in essential hypertension. 305 8

Because there is little published information on the effects of atrial peptides in hypertensive humans, 100 micrograms of alpha-human atrial natriuretic peptide was injected intravenously into six patients with essential hypertension in a double-blind, placebo-controlled study under standardized conditions of body posture and dietary sodium and potassium intake. The peptide increased urine sodium excretion sixfold in the first 30 minutes. Smaller increments occurred in urine volume and in calcium, magnesium, and phosphorus excretion; the rise in urine potassium concentration was not statistically significant. Most of these indices returned to time-matched placebo values within 1 hour, but urine sodium excretion remained high for 2 1/2 hours. Arterial pressure fell within 2 minutes of alpha-human atrial natriuretic peptide injection, then returned to matching placebo levels by 10 minutes. Conversely, heart rate increased rapidly and remained elevated for 3 hours. The peptide induced a prompt, brief rise in plasma norepinephrine concentration and a more sustained fall in epinephrine and aldosterone levels, but it did not affect plasma renin activity or cortisol concentration. Compared with normotensive volunteers studied previously under the same conditions, the hypertensive subjects had a greater response in urine volume and sodium, calcium, and magnesium excretion but a less sustained fall in arterial pressure.
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PMID:Effects of alpha-human atrial natriuretic peptide in essential hypertension. 316 25

The involvement of elements in the pathological process of primary hypertension has been established. The tissue distribution of 12 elements was studied in spontaneously hypertensive rats (SHR) and normotensive homologous rats (WKY). A multi-element analytical technique allowed simultaneous determination of sodium, potassium, calcium, magnesium, strontium, rubidium, manganese, copper, zinc, iron, sulphur and phosphorus in blood, plasma, brain, liver, kidney, skeletal muscle, heart and bone. Most elements were modified in SHR, except Ca, Rb and S. In plasma, an increase in Cu (+22%) and a decrease in K (-8%), Mg (-15%) and P (-11%) were observed. These variations, qualitatively similar to those found in man, suggest that the results in animal tissues could be extrapolated to man. Modifications were observed in all the tissues tested. Among them significant variations were noted in Na (+18%), Mn (+12%) and Cu (+29%) in kidney, and in K (+5%), Mg (+9%), Sr (-29%) and Zn (+14%) in heart. The role of these plasma and tissue variations in hypertension is discussed, as well as the possible involvement of the hypertensive process and/or hormones.
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PMID:Altered element concentrations in tissues of spontaneously hypertensive rats. 316 65

In order to clarify the relationship and the pathophysiological role of renal dopamine, kallikrein-kinin and prostaglandin systems in essential hypertensives, the effects of dopamine on these systems and renal sodium handling were investigated. Basal levels of kallikrein, kinin and prostaglandin E2 in essential hypertensives were significantly lower than those in normotensives. Those of kallikrein and kinin were obviously more suppressed in the low renin group than in the normal renin group, but no significant difference in prostaglandin E2 was found in either subgroup. Urinary dopamine excretion was significantly lower in the low renin essential hypertensives, while no significant difference was found between normotensives and normal renin essential hypertensives. Kallikrein activity and prostaglandin E2 were significantly increased in essential hypertensives by dopamine infusion, and no significant difference was found in kallikrein-quantity and kinin between normotensives and essential hypertensives after the infusion. These increases of kallikrein and kinin were significantly higher in the low renin group than in normal renin group, but those of prostaglandin E2 were not. Urine volume, urinary sodium excretion and fractional excretions of sodium and inorganic phosphorus were all increased in both normotensives and essential hypertensives after dopamine infusion. The increases of these were significantly greater in essential hypertensives than in normotensives, and greater in the low renin group than the normal renin group. From these results, it was suggested that the dopamine, kallikrein-kinin and prostaglandin E2 system have a close relationship with each other, and the suppression of these systems may contribute to the pathophysiology of essential hypertension, especially in the low renin group.
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PMID:The pathophysiological role of renal dopamine, kallikrein kinin and prostaglandin systems in essential hypertension. 332 11

In a randomized, double-blind parallel group study the 24-hour hypotensive effect of piretanide and its influence on biochemical variables were compared with those of placebo in patients with mild to moderate essential hypertension. Sixty patients entered the study, all of whom met the inclusion criteria (RRdiast between 95 and 120 mmHg). There was no drop-out during the study, so that the results of all 60 patients were statistically analysed. Piretanide produced a significant reduction of both systolic and diastolic blood pressure over 24 hours which was evident at four weeks and was maintained and further enhanced over the ensuing trial period. A mean maximal fall (at 12 weeks) of 10.7% (BPdiast supine) was observed. Placebo tablets did not produce any clinically relevant changes in systolic blood pressure, whereas a slight decrease was seen in diastolic blood pressure. This blood pressure reduction was significantly less in the placebo group than in the piretanide group at the end of the study (weeks 10 and 12). Dose doubling was needed in 13 of the 30 patients in the piretanide group, whereas as many as 20 out of 30 patients needed dose doubling in the placebo group. Pulse rate did not change relevantly during the trial in either group. A slight reduction in body weight was observed in the piretanide group. The mean values of serum potassium and sodium showed a slight decrease but remained within the normal range during the study period. A small increase in serum phosphorus was noted. None of these changes required any specific measures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Piretanide in the treatment of essential hypertension. A double-blind comparison versus placebo. 352 59

In order to clarify the significance of the renal kallikrein(KAL)-kinin(KIN) system and prostaglandins (PG) in exaggerated natriuresis in essential hypertensives, the effect of acute sodium load on urinary KAL, KIN, PG, and renal water and sodium handling were investigated in normotensives (NT) and patients with essential hypertension (EHT). Nine NT and seven EHT were studied following acute physiological saline infusion (1000 ml/2 hrs). Urine volume (UV), urinary sodium excretion (UNaV), fractional excretion of sodium (FENa), and fractional excretion of inorganic phosphorus (FEP) were measured by the clearance method. Urinary KAL and KIN were determined by direct-RIA. Urinary kininase (total, I and II) activities were measured by the kinin destroying capacity. Urinary PGE was measured by RIA. Following saline infusion, UV, UNaV, FEP, KAL, KIN and PGE significantly increased in both NT and EHT. The increases of UV, UNaV, FENa, FEP and KAL were remarkably greater in EHT than each in NT, while no significant difference was found in the increment of PGE between NT and EHT. Significantly positive correlations were observed between PGE and KAL or KIN in NT (r = 0.889, p less than 0.005; r = 0.574, p less than 0.05, respectively), but not in EHT. From these results, it was concluded that the exaggerated natriuresis observed in EHT following infusion may be significantly related to the augmentation of renal KAL-KIN system, but was not directly related to PGE.
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PMID:The role of renal kallikrein-kinin system and prostaglandins in diuresis and natriuresis following saline infusion in normotensives and essential hypertensives. 364 30

In order to investigate the pathophysiological role of the renal kallikrein-kinin system in renin subgroups of essential hypertension, the quantity and activity of urinary kallikrein, urinary kinin excretion, and correlations of kallikrein and kinin excretions with renal sodium handling in the renal tubules were studied in 17 normal subjects, 23 patients with normal renin and 12 patients with low renin essential hypertension. Urine samples were collected by the 2-hour clearance method in the early morning. The quantity and activity of urinary kallikrein, and the urinary excretion of kinin were significantly lower in both low and normal renin patients than in normal subjects. Comparing the normal renin and the low renin group, no significant difference was found in the quantity of urinary kallikrein, while the activity of urinary kallikrein and urinary kinin excretion were significantly lower in low renin patients than in normal renin ones. Fractional excretions of sodium (FENa) and inorganic phosphorus (FEP), which reflect renal tubular and proximal tubular sodium reabsorption, respectively, were significantly lower in the low renin patients than in the normal renin ones. A significantly positive correlation was observed between the urinary kallikrein activity or urinary kinin excretion and FENa or FEP in both normal subjects and normal renin patients, but not in low renin patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of the renal kallikrein-kinin system in sodium metabolism in normal and low renin essential hypertension. 635 50

The whole body content of sodium, potassium, chlorine, calcium, phosphorus and nitrogen was measured by neutron activation analysis in 13 patients with untreated primary hyperaldosteronism (Conn's syndrome; aldosterone-secreting adenoma). Concurrently, exchangeable sodium and potassium were estimated by isotope dilution. Results were compared with values in the same patients during treatment with potassium-conserving diuretics and again after removal of the adenoma; and also with those in a series of 30 patients having untreated essential hypertension. Both total body and exchangeable sodium were high in Conn's syndrome before treatment and were reduced by spironolactone or amiloride and by subsequent surgery. There was no evidence of alteration in the proportion of non-exchangeable sodium in this disease, in contrast to earlier reports. Total body and exchangeable potassium were low in untreated Conn's syndrome and increased to normal after therapy: the proportion of non-exchangeable potassium was similar before and after treatment, and also similar to that in essential hypertension. Total body chlorine was increased before treatment in Conn's syndrome and returned to normal with therapy; body calcium, phosphorus and nitrogen were normal throughout.
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PMID:Body elemental composition, with particular reference to total and exchangeable sodium and potassium and total chlorine, in untreated and treated primary hyperaldosteronism. 653 85

Calcium metabolism in otherwise uncomplicated term pregnancies associated with essential hypertension is characterized by significantly reduced levels of parathyroid hormone and ionized calcium, as well as significantly increased levels of phosphorus in both the mother and fetus. It is not possible at this time to delineate with certainty the precise pathophysiology of these changes.
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PMID:Calcium metabolism in the hypertensive mother, fetus, and newborn infant. 665 May 97

Muscle biopsy specimens form 22 patients with primary hypertension, 10 patients with chronic renal failure and 21 healthy normotensive controls were analyzed using a Kevex 0600 X-ray spectrometer. Muscle potassium (MK), calcium (MCa), sulphur (MS) and phosphorus (MP) were determined. In the patients with primary hypertension, MK was decreased compared to the controls (p less than 0.001), MCa was increased (p less than 0.05), MS was decreased (p less than 0.05) and no difference was seen in MP. In the patients with chronic renal failure, MK was decreased compared to the controls (p less than 0.001), MCa showed no difference compared to the controls, whereas both MP and MS were lower (p less than 0.05 and p less than 0.001). It was concluded that intracellular potassium is low both in primary hypertension and chronic renal failure. In chronic renal failure the potassium decrease is probably secondary to loss of cellular potassium capacity, whereas in primary hypertension an inhibition of the sodium, potassium, adenosine triphosphatase is suggested as the cause of the low potassium.
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PMID:Potassium in skeletal muscle in untreated primary hypertension and in chronic renal failure, studied by X-ray fluorescence technique. 673 Oct 36


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