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

Plasma levels of atrial natriuretic peptide (ANP) in 106 patients with essential hypertension with a supine mean blood pressure (mean +/- SEM) of 128.9 +/- 1.6 mmHg and not on treatment were significantly higher than those in 47 normotensive subjects (supine mean blood pressure 93.9 +/- 1.2 mmHg) with mean values of 17.2 +/- 1.1 and 8.6 +/- 0.6 pg/ml, respectively (P less than 0.001). Similar results were found in a subgroup of 35 hypertensive patients identically matched in terms of age, sex, and race with 35 normotensive subjects. Plasma levels of ANP were correlated significantly with age in normotensive subjects and with age and blood pressure in the hypertensive patients. In 12 hypertensive patients studied on a low (10 mmol sodium/day), on their usual sodium intake (around 120 mmol sodium/24 hr) and on a high (350 mmol sodium/day) intake, plasma ANP increased approximately twofold by the fifth day of the high sodium intake, but there was no significant difference between the plasma levels on their usual sodium intake and those on the fifth day of the low sodium intake. Supine mean blood pressure on the patients' usual sodium intake was 119.3 +/- 2.7 mmHg and was reduced to 110.0 +/- 3 mmHg by the fifth day of the low sodium intake (P less than 0.005). However, there was no significant difference between the blood pressure levels on their usual and high sodium intake (118.3 +/- 3.0 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma atrial natriuretic peptide in essential hypertension. Comparison with normotensive subjects and effects of changes in dietary sodium intake. 296 39

In order to investigate the role of cardiac hypertrophy in atrial natriuretic peptide (ANP) secretion in patients with essential hypertension, plasma levels of ANP were measured after overnight rest in 36 patients with untreated hypertension and in 31 normotensive controls. In the hypertensive subjects, plasma levels were correlated with left ventricular (LV) and left atrial abnormalities detected by chest X-ray, electrocardiogram (ECG) and M-mode echocardiography. Plasma ANP levels in patients with hypertension averaged 146 +/- 27 pg/ml compared to 46 +/- 7 pg/ml in the normotensive subjects (P less than 0.001). In patients with hypertension a significant correlation was found between ANP and supine systolic blood pressure (r = 0.54, P less than 0.001) and between ANP and diastolic blood pressure (r = 0.38, P less than 0.05). Furthermore, plasma ANP levels were correlated with total heart volume (r = 0.68, P less than 0.01), LV mass (r = 0.525, P less than 0.001), LV posterior wall thickness (r = 0.39, P less than 0.05), Sokolow-Lyon index (r = 0.721, P less than 0.001) and end-diastolic diameter of the left atrium (r = 0.334, P less than 0.05). The results suggest a contribution of LV and left atrial abnormalities to ANP secretion in essential hypertension.
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PMID:Relationship between plasma atrial natriuretic peptide and left atrial and left ventricular involvement in essential hypertension. 297 14

An exaggerated natriuretic response to volume expansion (VE) is observed in many essential hypertensive patients. The plasma levels of atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (EH) during VE (1 800 ml isotonic saline IV over 3 hours). NT and EH groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in EH, mean +/- sem). In response to VE, ANP increased to the same extent in both groups (a change of + 19.3 +/- 5.2 in NT and 22.2 +/- 7.1 pg/ml in EH) despite the marked difference in observed natriuresis (36 +/- 3.5 in NT and 54.9 +/- 6.3 mmol/3 in EH, p less than 0.02). The change in ANP induced by VE was inversely correlated with the fall in hematocrit and the variation in fractional excretion of sodium in both groups. These results suggest that atrial natriuretic peptide may participate in the control of the renal response to isotonic volume expansion, but they do not support a predominant role of atrial natriuretic peptide in the exaggerated natriuretic responses to volume expansion of patients with essential hypertension.
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PMID:[Role of atrial natriuretic peptide in the renal response to acute volume expansion in the normal and essential hypertensive patient]. 297 95

To further investigate the mechanism(s) of the exaggerated natriuretic response of hypertensives to volume expansion (VE; 1,800 ml iv isotonic saline over 3 h), the plasma levels of immunoreactive atrial natriuretic peptide (ANP) were measured in 11 normal subjects (NT) and 12 patients with mild essential hypertension (HT). NT and HT groups were similar with respect to age and basal levels of renin, aldosterone and ANP (34.5 +/- 5.5 in NT and 32.5 +/- 6.3 pg/ml in HT, mean +/- SE). In response to VE, ANP increased to the same extent in both groups (a change of 19.3 +/- 5.2 in NT and of 22.2 +/- 7.1 pg/ml in HT) despite the finding of an exaggerated natriuretic response to VE in essential hypertension (36 +/- 3.5 in NT and 54.9 +/- 6.3 nmol/3 h in HT, P less than 0.02). In addition, the fall in hematocrit and serum protein associated with saline infusion was less marked in HT than NT. The change in ANP induced by VE was inversely correlated with the percent fall in hematocrit and the increment in the fractional excretion of sodium in both groups. These observations suggest that ANPs may participate in the control of the renal response to isotonic VE; however they do not support an unequivocal influence of ANP in the exaggerated natriuretic response to VE of patients with essential hypertension.
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PMID:Response of atrial natriuretic peptide to acute saline loading in essential hypertension. 297 45

In this study plasma levels of atrial natriuretic peptide and of the catecholamines epinephrine and norepinephrine were investigated in hypertensive patients (HT) (n = 30). 22 normotensive patients (NT) served as controls. Hypertensives showed an elevated ANP-level in comparison with controls (46.8 +/- 3.3 vs. 36.8 +/- 3.3 pg/ml, M +/- SEM, p less than 0.01). When patients with myocardial infarction or with reduced ejection fraction were excluded, the same relation was demonstrated (49.3 +/- 3.2 vs. 33.6 +/- 2.0 pg/ml, p less than 0.01). Plasma norepinephrine was 230.8 +/- 52.3 pg/ml in HT compared with 138.0 +/- 19.6 pg/ml in NT (p less than 0.05). Epinephrine was 70.8 +/- 10.5 vs. 54.8 +/- 9.7 pg/ml in HT and NT. To exclude an increased left ventricular enddiastolic - and hence left atrial - pressure as the cause for the elevation of ANP and norepinephrine, HT and NT were matched for the same levels of enddiastolic pressure (LVEDP) (n = 18). For each level of LVEDP ANP was higher in HT than in NT (p less than 0.01). The same held true for norepinephrine (p less than 0.05) and to a lesser extent for epinephrine (p = 0.09). Our results demonstrate that patients with essential hypertension exhibit markedly elevated levels for ANP and catecholamines which is not due to myocardial failure. We propose that the increased secretion of the vasodilatory hormone ANP serves as counterregulation against the vasoconstrictor norepinephrine. The endocrine function of the heart may play a pivotal role in the modulation of sympathetic activity.
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PMID:[Elevated levels of atrial natriuretic peptide and plasma catecholamines in arterial hypertension--indications for an interaction]. 297 96

The effects of acute exercise on plasma concentrations of atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and plasma renin activity (PRA) were studied in 13 patients with previously untreated essential hypertension, and 8 matched normotensive control subjects. Resting levels of ANP and PRA were similar in the two groups, while resting AVP concentrations were 1.4 times higher in hypertensive subjects. Graded exercise was performed on a bicycle ergometer with workload increased each minute until exhaustion (Wmax). Wmax was higher in normal subjects than in hypertensive patients. Blood pressure and heart rate rose more steeply in hypertensive patients. Plasma ANP increased during acute exercise in both groups, but the average increase in hypertensives was substantially greater than in normal subjects (P less than 0.05). The increase in ANP during exercise was greater in hypertensives with left ventricular (LV) hypertrophy, and there was a positive correlation between LV mass and the percentage rise in ANP during exercise (r = 0.56, P less than 0.005). Plasma AVP did not alter during exercise. Plasma renin concentrations showed a small rise during exercise in both groups, which was 16% less in hypertensive subjects (P less than 0.05). The enhancement of ANP release during exercise in hypertensive subjects may reflect both cardiac structural changes and increased redistribution of blood to the cardiopulmonary compartment.
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PMID:Exaggerated atrial natriuretic peptide release during acute exercise in essential hypertension. 297 6

We determined concentrations of atrial natriuretic peptide (ANP), angiotensin (Ang), norepinephrine (NE) and electrolyte in plasma and cerebrospinal fluid (CSF) to study possible roles of these substances within the brain in human hypertension. Blood and CSF samples were obtained from 10 patients with mild to moderate essential hypertension (EHT) aged 40-65 y and 10 age-matched normotensive subjects (NT) on a regular salt diet (8 g/day). Levels of ANP, NE, Na, K, Ca and Cl in CSF and plasma were comparable between EHT and NT. Plasma renin activity, plasma and CSF Ang II were lower in EHT than NT. CSF Ang III tended to be lower in EHT. There was no correlation between CSF and plasma ANP, or between CSF and plasma Ang II. Our results indicate that CSF levels of ANP may not be altered in middle aged patients with mild to moderate hypertension. It is also suggested that Ang II, NE and sodium in the central nervous system may not have important roles in hypertension of those patients.
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PMID:Atrial natriuretic peptide, angiotensin, norepinephrine and electrolyte in cerebrospinal fluid of essential hypertension. 297 5

Acute volume expansion, an increase in sodium intake and a restraint on sodium excretion endow the plasma with the capacity to cause a natriuresis, to inhibit sodium transport and to stimulate vascular reactivity. One natriuretic substance, the atrial natriuretic peptide, has been identified. Cytochemical techniques can detect the presence of a Na-K ATPase inhibitor in the plasma of normal man and the rat, the concentration of which is controlled by salt intake. The substance responsible appears to originate in the hypothalamus. The plasma concentration of the cytochemically detectable Na-K ATPase inhibitor is substantially raised in the plasma of patients with essential hypertension, of the spontaneously hypertensive rat and of the Milan hypertensive rat. An hypothesis is put forward that links salt intake, a genetic renal lesion, the endogenous Na-K ATPase inhibitor, the atrial natriuretic peptide, and the substance responsible for vascular reactivity, with the rise in arterial pressure in hereditary forms of hypertension.
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PMID:[Cytochemical demonstration of an endogenous inhibitor of Na-K ATPase and its relationship to familial arterial hypertension]. 303 98

Plasma levels of atrial natriuretic peptide (ANP) were measured in 32 untreated subjects with essential hypertension and in 31 patients undergoing long-term treatment with beta-blockers. Patients receiving beta-blockers had significantly higher mean plasma ANP levels (72.0 +/- 36.0 [SD] pg/ml) than did untreated hypertensive subjects (39.8 +/- 15.8 pg/ml; p less than 0.01) and healthy normotensive controls (33.9 +/- 16.6 pg/ml; n = 61, p less than 0.01), while the mean plasma ANP concentration in untreated hypertensive subjects was not statistically different from that in control subjects. Administration of atenolol, 50 mg/day, for 4 weeks to 10 untreated subjects resulted in a significant (p less than 0.001) rise in plasma ANP levels (from 38.8 +/- 9.5 to 68.7 +/- 20.6 pg/ml). In 31 patients undergoing long-term treatment with beta-blockers, multivariate regression analysis revealed that age, pretreatment mean blood pressure, and plasma concentration of cyclic 3',5'-guanosine monophosphate (cGMP) were significant predictors of plasma ANP levels. These results suggest that beta-adrenergic receptor blockade in patients with essential hypertension elevates plasma ANP levels with a concomitant rise in cGMP concentrations, and that increased ANP in plasma may play a role in the compensatory mechanism that operates in response to beta-adrenergic receptor blockade.
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PMID:Effect of beta-adrenergic receptor blockade on atrial natriuretic peptide in essential hypertension. 303 46

A disturbed adrenergic dependent blood pressure regulation may represent a familial component in the pathogenesis of essential hypertension; its possible relation to sodium metabolism is presently unknown. Body sodium, the cardiovascular pressor reactivity to infused noradrenaline or angiotensin II, plasma levels of noradrenaline, adrenalin, renin, angiotensin II, aldosterone and atrial natriuretic peptide were measured on a low or high sodium diet in 10 normotensive young subjects without and 13 normotensive subjects with familial predisposition to hypertension. On the low sodium diet, the two groups did not differ significantly in the considered parameters, while blood pressure was slightly higher in predisposed subjects (+7/+7 mmHg). The change from the low to the high sodium diet was associated with a significant increase in supine systolic blood pressure in predisposed but not in non-predisposed subjects (P less than 0.05). Exchangeable sodium, body weight atrial natriuretic peptide and the pressor reactivity to infused adrenalin or angiotensin II increased significantly while plasma catecholamines, renin, angiotensin II and aldosterone levels were suppressed to a comparable extent in the two groups. The findings of this investigation confirm that sodium has an important regulatory effect on cardiovascular pressor responsiveness. The disturbed noradrenergic-dependent regulation of predisposed subjects is not explained by an abnormal adaptation of sympathetic dependent mechanisms or of other pressor factors to variations in dietary sodium intake.
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PMID:Sodium and responses to infused noradrenaline and angiotensin II in subjects predisposed to hypertension. 306 5


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