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

To examine potential mechanisms responsible for the greater prevalence of hypertension among relatives of hypertensives than among relatives of normotensives, we subjected 43 normotensive first-degree relatives of known essential hypertensives and 43 age-, race-, and sex-matched normal subjects with no family history of hypertension to sodium loading and depletion. The data show that the relatives had higher blood pressures than did controls. They also had higher PRA values before and after a 2 L intravenous saline infusion over 4 hr. In addition, the relatives excreted less (p less than 0.05) sodium on the day of the infusion than did the controls. PA values and UNe excretion in the two groups did not differ. In the relatives, age correlated with systolic and diastolic blood pressure. Age correlated inversely with the 24 h urine sodium excretion on the sodium loading day. These correlations were not observed in controls. Normotensive first-degree relatives of hypertensives differ from relatives of nonhypertensives in that they have higher PRA values and a blunted natriuretic response to a saline load. These features may predispose them to the development of hypertension.
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PMID:Effects of sodium loading and depletion in normotensive first-degree relatives of essential hypertensives. 50 Dec 3

In two-kidney Goldblatt hypertensive, spontaneously hypertensive, and normotensive control rats the activity of the renin-angiotensin system was tested during variation of sodium balance. Acute, exactly calculable and selective changes of total body sodium were achieved by hemodialyzing the conscious rats using dialysate with either high or low sodium content. The activity of the RAS was evaluated by blood pressure response to AT II blockade (saralasin bolus injection; 25 micrograms/kg b.w., i.v.) and the plasma-renin activity. During sodium depletion blood pressure maintenance became renin-dependent; sodium loading caused a decrease of renin-angiotensin activity in renovascular hypertension. A weak direct correlation between deprssor response to saralasin and the PRA could be established in the different sodium-depleted and -loaded states.
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PMID:Effects of acute hemodialysis-induced changes in sodium balance on the renin-angiotensin system in renovascular and spontaneously hypertensive rats. 52 96

Whether the same patient with essential hypertension (EH) has the same PRA profile at different occasions, is still uncertain. The validity of the classification of these patients into low or normal renin hypertension depends upon the reproducibility of this profile. A nomogram based on PRA and 24 hr urine sodium in normals, was constructed by computing the regression line with its tolerance limits of not less than 95%. In 30 patients with EH, the PRA and 24 hr urine sodium were determined in 2 separate occasions. Classification of patients showed a change of 30% when PRA was taken during at least 2 hours recumbency. However, when PRA following ambulation is considered, the change appeared only in 6/30 (20%). This change was not large. Thus good reproducibility of PRA is obtained on post-ambulation PRA and changes larger than the 95% tolerance limits, are considered.
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PMID:Reproducibility of plasma renin activity (PRA) profile in essential hypertension patients. 66 86

The renin-angiotensin system has been implicated in the genesis of pre-eclampsia. To avoid fetal toxicity, five women were studied who developed hypertension, proteinuria, and edema in the last trimester of pregnancy and whose BP elevation persisted immediately postpartum. At about 6 hours after delivery the CE enzyme inhibitor (SQ 20,881) was given in incremental doses ranging from 0.25 to 3.0 mg. per kilogram intravenously, before and after diuresis with furosemide, 40 mg. intravenously. BP was measure every 2 minutes and PRA and angiotensin II concentration before treatment, 30 minutes after 0.25 to 0.30 mg. per kilogram, and 30 minutes after 2.0 to 3.0 mg. per kilogram. Echocardiographic assessment of CI and PVR was performed before treatment and after a maximum dose in three patients. Before diuresis, CE blockade had no effect on heart rate, BP, CI, PVR, or PRA, regardless of whether the patient was in positive or negative fluid balance or was sodium loaded or restricted over the preceding 24 hours. Angiotensin II fell by 77 and 10 per cent, respectively, after 0.25 mg. per kilogram was given to two patients, but rose slightly in the other three patients, then fell an average of 46 per cent after 1.0 to 3.0 mg. per kilogram were given. After diuresis, 1.0 mg. per kilogram resulted in a 24 per cent fall in BP which persisted for 3 hours in two patients and a 14 per cent fall which lasted for 30 minutes after 1.0 or 3.0 mg. per kilogram in a third patient. It is concluded that the BP elevation which persists after delivery in certain patients with pre-eclampsia is not angiotensin II dependent.
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PMID:SQ 20,881: effect on eclamptic--pre-eclamptic women with postpartum hypertension. 68 62

Plasma volume [PV] and plasma renin activity [PRA] were measured in 51 men with untreated borderline and mild essential hypertension [I and II degree according to W.H.O. classification]. PV in low- and normal-renin hypertension was not significantly different from normal values. Groups of patients with low- and high-renin hypertension differed significatly from each other not only br PRA after stimulation, but also by PRA at rest, PV and age.
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PMID:Plasma volume in men with low-, normal- and high-renin essential hypertension. 68 56

PRA was simultaneously measured in both renal veins and in a peripheral vein of patients with essential (6) and renovascular (37) hypertension. In renovascular patients suppression or renin secretion from the contralateral kidney was always observed: otherwise in patients with essential hypertension both kidneys contribute to peripheral PRA. The suppression of renin secretion from the ischemic kidney either by nephrectomy or by revascularization, joins with normalization either of peripheral PRA or of blood pressure. This finding points to the role of the renin-angiotensin system in the genesis of human renovascular hypertension.
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PMID:Plasma renin activity in renal veins of renovascular patients. 69 83

PG A1, B1, E2, F1,2alpha and PRA have been measured in 8 hypertensive patients with unilateral renal arterial stenosis, 7 hypertensive patients with unilateral renal atrophy and 20 control normotensive subjects. PRA and PGA1 were significantly increased in patients with renovascular hypertension but not in patients with atrophy. PGE2 and PGF1,2alpha were increased in both groups of patients, especially on the stenotic or atrophic side. The increase of PGA1 and PGE2, represents a secondary antihypertensive, diuretic and natriuretic mechanism, the increase of PGF1,2alpha a direct hypertensive mechanism.
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PMID:Prostaglandins in renovascular and renal hypertension. 69 90

The effects of pretreatment with l, H, and a combination, Hl, were assessed in rats made hypertensive by LRA. SBP, PRA, and urinary sodium and potassium excretion were measured 7 days and 1 day before LRA and 2 and 7 days after LRA on a fixed sodium diet. SBP increased 2 days after LRA in C rats, l- and Hl-treated rats but not in H-treated rats. The elevation of SBP was higher in the l group than in the C group. Hl showed a greater increase than H but less than C. PRA levels did not correlate with changes in SBP. PRA first increased 7 days after LRA. A highly significant decrease in sodium and potassium excretion was observed 7 days after LRA in C and l-treated rats. The data suggest that hydralazine may control blood pressure in this model by preventing sodium retention or, alternatively, that it may reduce blood pressure by direct peripheral vasodilation. Since natriuresis and vasodilation are two well-known effects of PGs, the results are compatible with the possibility that l exerted its noxious effect by inhibiting the synthesis of these compounds. It is also suggested by these studies that the renin angiotensin system does not play a central role in the acceleration of hypertension after l administration.
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PMID:Modification of experimental renal hypertension in the rat by indomethacin and hydralazine. 71 91

We have studied PRA levels in 10 healthy subjects compared with 10 patients affected with essential hypertension (with low PRA) on venous blood samples collected after 8 hours of rest and after 15-20 minutes of slow plain walk. Contemporarely we have taken up arterious pression levels in each class of subjects of these studies. No significant differences of PRA are demonstrable in healthy subjects and in patients affected with essential hypertension. Postural changes in hypertension produces significant rise of PRA, not related to arterial pressure.
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PMID:[Plasma renin activity in hypertensive patients under basal conditions and in various postures: preliminary data]. 75 61

The basal levels of plasma norepinephrine have been measured in 113 carefully characterized patients with essential hypertension, and the results have been correlated with the PRA sub-grouping and the levels of blood pressure, plasma aldosterone, plasma 18-hydroxy-deoxycorticosterone, and plasma volume. In addition, the influence of furosemide on plasma norepinephrine concentration has been assessed. Essential hypertensives, when considered as a whole, did not exhibit any significant abnormality in basal plasma norepinephrine concentration, but interesting alterations were observed in certain specific sub-groups. High renin patients had significantly elevated levels of basal plasma norepinephrine. In addition, a sub-group of the low renin population who were relatively young had reduced plasma norepinephrine conentration. In these individuals with both reduced PRA and plasma norepinephrine, the levels of both increased concomitantly to the normal range with marked salt depletion. Furosemide administration induced increases in plasma norepinephrine in all PRA sub-groups. Plasma norepinephrine correlated significantly with blood pressure in normal and low renin hypertensives, but the relationships were confined only to male subjects. Significant correlations were also observed between plasma norepinephrine and plasma aldosterine in males with normal PRA but not in the other sub-categories. No significant relationships between plasma volume and either plasma norepinephrine or blood pressure could be detected. Plasma 18-hydroxy-deoxycorticosterone was greater in males as compared with females and appeared elevated above control levels in normal and high renin essential hypertensives. Significant positive correlations between plasma aldosterone and plasma 18-hydroxy-deoxycorticosterone were observed in both males and females with normal renin hypertension. These studies have demonstrated abnormalities in basal plasma norepinephrine concentration in certain patients with essential hypertension. They also suggest that the levels of blood pressure and plasma aldosterone may be related to peripheral sympathetic activity in essential hypertension.
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PMID:Relationship of basal plasma norepinephrine to blood pressure, plasma renin activity, mineralocorticoids, and plasma volume in essential hypertension. 75 99


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