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

The antihypertensive effect of clonidine has been attributed to acute inhibition of sympathetic outflow from the central nervous system. This conclusion is derived from experiments with single doses of clonidine. The mechanism of the long-term blood pressure-lowering effect of clonidine has been less well characterized. Antihypertensive therapy may alter renal hemodynamics and these changes may ultimately affect systemic blood pressure. We studied the effect of long-term clonidine therapy on intrarenal hemodynamics, the renin-angiotensin system, and selected indices of sympathetic nervous system activity in 13 patients with essential hypertension to further elucidate its action. Long-term clonidine therapy resulted in decreased MAP and RVR associated with the suppression of supine but not upright PRA. RPF, RBF, FF, and WBV did not change. UKA, on index of the the putative vasodilating renal kallikrein-kinin system, was also not changed. Our findings suggest a role for PRA in modulating RVR during long-term clonidine therapy. This was associated with the reduction observed in MAP.
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PMID:Reduced renovascular resistance by clonidine. 49 99

The antihypertensive effect on the selective beta-1-adrenoceptor blocking agent, atenolol, given in doses of 100 and 200 mg once daily, was evaluated in 37 patients with primary hypertension. The drug induced an efficient reduction of BP, and in the whole patient series there was no difference in BP on either dosage. Exercise tests, performed in 10 patients, showed the same degree of partial beta-blockade 24 hours after intake of 100 and 200 mg atenolol. PRA decreased during treatment with atenolol but there was no correlation between the stimulated pretreatment renin level and the antihypertensive effect of atenolol. Side-effects were few and 35 out of 37 patients continued on atenolol treatment. Central nervous side-effects were not seen.
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PMID:Atenolol administered once daily in primary hypertension. Effects on blood pressure in relation to pre-treatment plasma renin activity. 50 2

Measurement of the integrated concentration is most suited for the study of blood components that fluctuate rapidly. The integrated concentration of plasma aldosterone (IC-ALDO) and plasma renin activity (IC-PRA) were measured in 24 patients with essential hypertension and in 10 normal adult subjects, using a non-thrombogenic 24-hour constant blood withdrawal system. The integrated concentration of plasma aldosterone in the control subjects was 7.7 +/- 1.8 ng/100 ml (mean +/- 1 SD). Eight hypertensive patients had IC-ALDOs that were more than 3 standard deviations above the mean. Although the mean IC-PRA of the hypertensive patients was lower than the mean of controls (0.6 +/- 0.6 and 0.9 +/- 0.6, respectively), the difference was not significant. However, high integrated concentration of plasma aldosterone was mostly associated with low integrated concentration of plasma renin activity. Consequently, the ratio of IC-ALDO to IC-PRA in the hypertensive patients was significantly higher (p less than 0.001). In six hypertensive patients the ratio was more than 4 standard deviations above the mean for the normal control subjects (12.2 +/- 7.6). Individuals with inappropriately high integrated concentrations of plasma aldosterone can therefore be identified by the simultaneous determination of IC-ALDO and IC-PRA.
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PMID:The integrated concentration of plasma renin activity and aldosterone in essential hypertension. 62 94

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

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

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

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 and 15 minutes after intravenous administration of oxoprenolol (mg 2). Contemporarely we have taken up arterious pression levels in each class of subjects of these studies. Postural changes produces significant rise of PRA in subjects affected with essential hypertension, that is significantly inhibited by pharmacologic interference produced by beta-blocking agents. This occurrence is independent of arterial pressure changes.
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PMID:[Oxoprenolol and plasmatic renin activity in essential hypertension: preliminary data]. 75 62

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

Body fluid volumes, cardiac output, PRA and pressor responses to angiotensin II (AT) and norepinephrine (NE) were compared between untreated patients with essential hypertension aged younger than 35 (EH-I) and those aged older than 36 years (EH-II). Men blood volume, total body water and extracellular volume were not significantly different between the patients with essential hypertension and normotensive subjects. There were no difinite differences in each volume between the EH-I and EH-II patients either. However, the distribution of blood volume was significantly larger in the essential hypertensive patients than in the normotensive subjects, suggesting that the changes in blood volume might not be homogenous in essential hypertension. In addition, blood volume was noted to have a significant inverse correlation with PRA. Cardiac output at rest was slightly but not significantly less in the EH-I and EH-II groups than in the normotensive group. A decline in blood pressure following 'bed-rest' was accompanied by a decrease in total peripheral resistance index (TPRI). Thus, elevated peripheral vascular resistance seems to be responsible for the mild to moderate hypertension even in the younger patients. PRA and its increases in response to standing or furosemide were normal in the EH-I patients, while they were markedly suppressed in the EH-II patients as compared to the age-matched normotensive subjects. In addition, PRA had a significant inverse correlation with the blood pressure and the scores of the severity of hypertension in the patients with essential hypertension. Thus, it seems likely that low renin in essential hypertension is secondary to long-lasting hypertension. Pressor response to AT significantly correlated with mean blood pressure and that to NE did so with 24 hours' urinary sodium excretion in essential hypertensive patients. The influence of aging on the pressor responses were obscure: the relationships of the pressore responses to blood pressure or to urinary sodium excretion were not different between the EH-I and EH-II groups. The examinations were repeated in 16 patients with essential hypertension (16 to 48 year-old) in 11 to 30 days after the initial study. Twelve of the 16 patients had declines in blood pressure and TPRI at the second study. In 7 of the patients whose blood pressure declined following 'bed-rest', there were significant decreases in pressor response to AT and in blood volume and a significant increase in PRA (group A). The other 5 patients showed a significant decrease in PRA and an enhanced pressor response to NE (group B). The blood volume in the group A was significantly larger than that in the group B at the initial study. It is suggested that the cause of essential hypertension is not homogeneous in that the increased vascular resistance may have been attributed to sodium excess in some patients and to an increased sympathetic activity in others. Some additional factors remain to be taken into account to clarify the complicated aspects of essential hypertension.
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PMID:Comparisons of body fluid volumes, plasma renin activity, hemodynamics and pressor responsiveness between juvenile and aged patients with essential hypertension. 87 Jul 21


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