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

The chronic administration of prindolol in patients with essential hypertension resulted in the following: 1) a significant decrease in blood pressure and heart rate (with only the exception of the unchanged diastolic blood pressure after the stimulus of the seven-minute standing period), 2) a significant decrease of plasma noradrenaline concentrativn at rest and under orthostatic conditions, 3) a significant decrease of PRC at rest and an even more pronounced suppression of PRA after the stimulus of upright posture, 4)a significant decrease in total exchangeable sodium and 5) a concomitant significant increase in total body potassium even with an increase in body weight. These findings are not subject to easy interpretation. In particular, we cannot conclude which of the changed parameters plays the initial role in lowering blood pressure. A working hypothesis might presume that beta blocking agents inhibit central and/or peripheral sympathetic nervous activity. The results reduction in plasma renin concentration would in turn lead to a drop in aldosterone secretion rate indicated by the increase in potassium and decrease in sodiummour data would support such a sequence of events.
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PMID:The effect of prindolol on plasma noradrenaline, plasma renin and sodium-potassium metabolism in patients with essential hypertension. 103 72

CI, TPRI, PV, ECFV, Nae, PRA and a pressor response to NA and AT was measured before and after 1) sodium restriction and 2) spontaneous blood pressure fall (spontaneous fall) in the patients with essential hypertension and the following results were obtained. 1) CI did not change during sodium restriction and increased after spontaneous fall. TPRI was reduced and the degree of this reduction was positively correlated with that of blood pressure reduction under these two conditions. 2) Sodium restriction caused the decrease of PV, ECFV and Nae and the increase of PRA. The degree of the reduction of PV and Nae was positively correlated with that of blood pressure fall. After spontaneous fall, PV, ECFV and NAe was increased and PRA did not change significantly. 3) A pressor response to NA and AT was depressed after one week of sodium restriction, and after 4 weeks the former returned to the basal response, while the latter was still reduced. NA response was correlated positively with basal Nae, ECFV and interstitielle fluid volume and negatively with basal PRA. AT response was negatively correlated with PRA before and during sodium restriction. No correlation was observed, however, between the degree of reduction of blood pressure and that of the change in pressor response to NA or AT. After spontaneous fall, the response to NA was not reduced but increased. These results suggested that, although the fall in blood pressure under these experimental conditions was mediated by the reduction of TPRI, the changes in pressor response to NA and AT did not affect primarily the reduction of blood pressure.
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PMID:Studies on etiology of essential hypertension. Hemodynamics, water-sodium balance and response to pressor substances during long-term sodium restriction and after spontaneous blood pressure fall--. 115 91

Elevated blood pressure (160/120 mm Hg) was found in an 8 1/2-year old body and remained unchanged during the following 3 years. The only abnormal findings were undetectable plasma renin activity (PRA less 0.16 ng/ml-3 h) even after sodium restriction and upright posture and a slight tendency for hypokalemia (3.7 mEq/1, lowest value 3.3 mEq/1). Plasma aldosterone (PA) and plasma cortisol (PC) were normal. Administration of dexamethasone and spironolactone resulted in only a minimal decrease of blood pressure whereas hydrochlorothiazide was slightly more effective. The circadian rhythm of PRA, PA and PC was studied by otaining frequent blood specimens during one night. The diurnal variation of PA and PC was normal despite undetectable PRA (less than 0.16 ng/ml-3 h). Primary aldosteronism and other conditions associated with mineralocorticoid excess were excluded. The patient seems to represent an example of low renin essential hypertension. This is the second recorded case of this syndrome in childhood.
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PMID:Low renin essential hypertension in a child. 124 35

Plasma renin activity, arterial and venous angiotensin II (A II), plasma aldosterone, and sodium excretion were measured in a group of 101 patients with mild essential hypertension. For the total hour; arterial A II was 5.2 +/- 1.0 pg/ml; venous A II was 4.2 +/- 0.6 pg/ml; and plasma aldosterone was 5.0 +/- 0.45 ng/100 ml. All values were lower corresponding values for normal subjects on a high salt intake despite the fact that salt intake in the normal subjects exceeded that for the hypertensive group more than 3-fold. Moreover, when the range of diastolic blood pressure up to 114 mm Hg was divided into three successive class intervals of increasing severity, there was a negative correlation between diastolic blood pressure and both PRA and plasma aldosterone. Arterial A II showed an anomalous increase in the class interval 105-114 mm Hg, despite the fact that this group exhibited the lowest level of PRA. At diastolic blood pressures above 114 mm Hg, the PRA appears to rise again. The anomalous increase in arterial A II in the presence of marked suppression of PRA is consistent with the presence of a renin activator or accelerator factor in hypertensive plasma as postulated by others. It also identifies a possible mechanism whereby even small increases in PRA could exert an adverse effect on the hypertensive state.
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PMID:Relation between plasma renin activity, angiotensin, and aldosterone and blood pressure in mild untreated hypertension. 126 97

To clarify the hemodynamic and endocrine mechanisms of the hypotensive effect of amosulalol, an alpha- and beta-adrenoceptor antagonist, 19 patients with essential hypertension received amosulalol (20-80 mg/day; average 48.4 mg/day) for 16 weeks. Mean blood pressure (MBP) was significantly decreased (105 +/- 1 vs. 120 +/- 1 mm Hg, p less than 0.001), associated with a decrement in heart rate (HR). Although both cardiac index (CI, 3.68 +/- 0.09 vs. 3.91 +/- 0.09 L/min/m2, p less than 0.001) and total peripheral resistance index (TPRI, 2,271 +/- 78 vs. 2,441 +/- 79 dynes.s.cm-5.m2, p less than 0.001) were reduced, changes in TPRI positively correlated with those of MBP (r = 0.9155, p less than 0.001) but the change in CI did not (r = 0.3568, NS). Plasma renin activity (PRA, 0.55 +/- 0.09 vs. 0.95 +/- 0.14 ng/ml/h, p less than 0.05) and aldosterone concentration (4.6 +/- 0.4 vs. 8.6 +/- 0.5 ng/dl, p less than 0.001) were also decreased with amosulalol. Thus, the hypotensive effect of amosulalol may be due mainly to vasodilation by alpha 1-blocking action. In addition, this hypotensive effect may be facilitated by either beta-blocking action such as decreased cardiac output (CO), with suppression of reflex tachycardia or of the renin-angiotensin-aldosterone system.
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PMID:Hemodynamic and endocrine changes associated with hypotensive action of amosulalol in essential hypertension. 138 33

The subgroup of patients with nonmodulating hypertension demonstrates a number of abnormalities of the renin-angiotensin-aldosterone axis. We previously identified abnormalities in plasma and urinary dopamine in nonmodulators and posited that this may be in part due to a generalized defect in sympathetic nervous system activity. In the present study we assessed the state of activation of the renin-angiotensin system and the sympathetic nervous system in normal subjects and patients with modulating, nonmodulating, and low renin essential hypertension during sodium depletion and change from supine to upright posture. Levels of plasma norepinephrine were higher in non-modulators during the posture study (P < 0.05). PRA rose with upright posture in all groups, but low renin subjects had a blunted response. Nonmodulators and low renin subjects had lower aldosterone levels both supine (P< 0.05) and upright (P< 0.01). However, the aldosterone/PRA increment ratio was increased in low renin subjects (P< 0.01), whereas it was decreased in nonmodulators. Twenty-four-hour urine collections for catecholamine determinations were obtained in a subgroup of the subjects, with nonmodulators showing higher levels of norepinephrine excretion which approached significance (P = 0.08). In vitro experiments using rat and human adrenal glomerulosa cells showed that norepinephrine does not affect aldosterone secretion per se. These observations extend the series of abnormalities observed in nonmodulating hypertension. However, it is likely that the alterations in norepinephrine levels during sodium depetion and upright posture are a secondary event and not linked to the altered aldosterone production in these patients.
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PMID:Abnormal norepinephrine and aldosterone responses to upright posture in nonmodulating hypertension. 140 Aug 65

The behavior of plasma atrial natriuretic factor (ANF) and digoxin-like substance (DLS), and the daily urinary excretion of kallikrein (uKK) were evaluated in young hypertensives and in young normotensives with or without a family history of essential hypertension. Each group was also evaluated, separating those with low plasma renin activity from the total sample. The sample group was made up of 75 young males; 31 hypertensives (mean age 22.7 +/- 2.5 years), 28 normotensives with hypertensive heredity (normotensives F+) (mean age 22.2 +/- 1.9 years) and 16 normotensives (mean age 22.0 +/- 2.1 years). An inverse correlation between ANF and PRA was shown in all groups. In hypertensives, ANF was inversely correlated with uKK (r = -0.664, P less than .0001). Plasma ANF (P less than .012) and DLS (P less than .0001) were higher in hypertensives than in normotensives, while uKK excretion was lower (P less than .0001). Plasma levels of DLS were higher in F+ normotensives than in normotensives (P less than .003). Low renin hypertensives showed the lowest uKK excretion (P less than .0001 v normal-high renin hypertensives). Furthermore, low renin hypertensives showed the highest plasma levels of ANF (P less than .0001 v normal high renin hypertensives) and DLS (P less than .012 v normal-high renin hypertensives). Plasma ANF (P less than .0001) was higher, while uKK was lower (P less than .045) in low renin F+ normotensives than in normal-high renin ones. In conclusion, our data indicate that plasma ANF and DLS are elevated since the early phase of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Natriuretic hormones in young hypertensives and in young normotensives with or without a family history of hypertension. 141 48

One-kidney, one-clip hypertension (1-K, 1-C HT) is initiated by increased preglomerular resistance which decreases nephron perfusion and causes several intrarenal changes that lead to increased mean arterial pressure (MAP). Elevated MAP serves to return nephron perfusion and sodium excretion to normal, so that fluid intake and output are balanced. Increased MAP usually occurs through volume homeostasis mechanisms that initially raise cardiac output and later elevate total peripheral vascular resistance via autoregulatory adjustments. However, if adequate volume is unavailable because of sodium restriction, sustained activation of the renin-angiotensin system increases blood pressure sufficiently to restore nephron perfusion. Thus, depending upon the availability of volume, renal perfusion and sodium balance can be restored either by volume retention or by increased angiotensin II (ANGII) formation and peripheral vasoconstriction. Similarities exist between 1-K, 1-C HT and low-renin essential hypertension (LRHT). In both cases, renal-pressure natriuresis is shifted to higher levels and there are marked increases in preglomerular resistance that necessitate increased MAP to maintain sodium balance. However, in 1-K, 1-C HT, there is a parallel shift of pressure natriuresis with little or no change in the slope of this curve, similar to that found in the normal-renin essential hypertension. In LRHT the slope of pressure natriuresis is decreased, indicating that blood pressure is much more salt sensitive than normal. Another difference is that PRA is low compared to normal PRA in 1-K, 1-C HT after compensatory increases in MAP. There is also no indication of glomerular membrane damage in 1-K, 1-C HT, whereas LRHT may have significant glomerulopathy, especially as hypertension progresses. These differences suggest that there may be additional factors besides preglomerular vasoconstriction involved in the etiology of LRHT. One possible factor is a reduction in nephron number in LRHT. Decreased functional nephrons would lead to glomerular hyperfiltration and increased distal tubular flow rate in the remaining nephrons, causing decreased PRA and eventually glomerular damage. Increased fractional sodium reabsorption, particularly in distal tubular segments, could also contribute to decreased PRA and cause blood pressure to be salt sensitive. These abnormalities, along with preglomerular vasoconstriction, may explain many of the characteristics of LRHT.
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PMID:Renal function in one-kidney, one-clip hypertension and low renin essential hypertension. 174 89

In 10 patients with moderate essential hypertension, the neurohumoral and hemodynamic effects of 4 days' treatment with 2 x 75 micrograms clonidine (C), 2 x 20 mg nifedipine retard (N), and a combination of the two (C/N) were studied and compared with baseline values. The heart rate decreased significantly from a mean of 79 to 67 bpm (p less than 0.05) under C, increased again to 73 bpm (p greater than 0.05) under N, and decreased once more to 68 bpm (p less than 0.05) under C/N. The systolic blood pressure decreased from a mean of 184 to 171 under C, 168 after N, and 161 (p less than 0.01) under C/N; significant decreases of diastolic blood pressure were also observed (from 113 to 104 under C, 107 under N, 100 mmHg under C/N (p less than 0.05). Norepinephrine decreased from 440 to 281 under C (p less than 0.01), increased to 391 (p greater than 0.05) after N, and measured 404 pg/ml (p less than 0.05) under C/N. PRA decreased significantly under C, increased under N, and remained unchanged under C/N. These findings demonstrate that combined treatment with lowdose nifedipine and clonidine leads to an additive reduction of blood pressure. The disadvantage of neurohumoral counterregulation of nifedipine are neutralized by clonidine.
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PMID:[Nifedipine-clonidine combination in essential hypertension. Hemodynamic and neurohumoral findings of the combination in comparison with the effect of the individual substances]. 176 35

The episodic secretion of aldosterone depends on the dietary sodium intake, alterations in posture and follows ACTH circadian rhythm. Aldosterone daily profiles have been studied in 23 supine essential hypertensive patients on normal sodium intake. Secretory pulses at a frequency of two to five pulses per 12 hr have occurred, independent of PRA levels. Among 13 patients with normal PRA two lost pulsatility when sodium was loaded (10 g/24 hr) and the same happened with two others on sodium restricted diet (2 g/24 hr). These results suggest a profound effect of dietary sodium intake on the pulsatile pattern of aldosterone secretion, particularly in normal PRA essential hypertension.
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PMID:Daily profiles of aldosterone levels during normal, high and low sodium intake in patients with essential hypertension. 177 97


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