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

In 40 patients (pts) with essential hypertension (EH) the plasma levels of insulin, glucagon, gastrin and prolactin during 2 week therapy with nifedipine were evaluated. In pts with EH there were higher levels of hormones than in control subjects. During nifedipine therapy there was no elevation of the plasma hormone levels although the blood pressure was lowered. This study shows that there are other than hypertension factors in the pathogenesis of elevated hormone levels in EH.
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PMID:[Essential hypertension. Treatment with nifedipine and levels of insulin, glucagon, gastrin and prolactin]. 194 46

The effects of the angiotensin-converting enzyme inhibitor captopril on blood pressure, heart rate, plasma prolactin, and renin activity were examined in a single-blind, placebo-controlled trial on 30 patients with essential hypertension (15 given drug, 15 placebo). Captopril, 25 mg administered orally, reduced the blood pressure and increased the plasma renin activity. Captopril decreased mean plasma prolactin from 17.5 +/- 1.4 ng/mL to 9.1 +/- 1.0 ng/mL (p less than 0.001). Significant correlation was found between captopril-induced change from control values of plasma prolactin (delta plasma prolactin) vs delta plasma renin activity (r = -0.688, p less than 0.001). These results suggest that acute administration of captopril was accompanied by a reduction in plasma prolactin and that this reduction may be of clinical significance during therapy of hypertension.
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PMID:Effect of captopril on plasma prolactin in patients with essential hypertension. 219 85

To assess the dopaminergic regulation of blood pressure and the renin-angiotensin-aldosterone system in fourteen essential hypertension (EHT) and six normotensives (NT), intravenous injections of 10 mg of the dopamine antagonist, metoclopramide (MCP), were given. Essential hypertension patients were divided into two subgroups according to the basal values of plasma renin activity (PRA). Plasma prolactin (PRL), aldosterone (ALDO), norepinephrine (NE) and epinephrine (E) in seven high-renin EHT revealed significantly higher basal values than normal- and low-renin EHT. Intravenous injections of MCP caused significant increases in PRL and ALDO but not in NE, E and PRA in all subjects. However, in high-renin EHT the responses of PRL and ALDO were significantly marked compared to other subjects. In spite of these hormonal changes after MCP, blood pressure was unaltered. The present data suggest that "tonic inhibition" of PRL and ALDO by the dopaminergic system is partially regulated by the renin-angiotensin system regardless of the levels of blood pressure.
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PMID:Pressor and hormonal responses to intravenous injection of metoclopramide in normotensive and hypertensive patients. 223 66

Both dopamine and atrial natriuretic factor (ANF) are known to suppress aldosterone secretion. Since it is possible that dopaminergic mechanisms facilitate ANF release, we investigated the relationship between these two inhibitory systems by comparing the increases in aldosterone induced by metoclopramide, a dopaminergic antagonist, with decreases in ANF. Aldosterone, ANF, prolactin, plasma renin activity, cortisol and potassium were measured before and after the intravenous injection of 10 mg metoclopramide, blood samples being collected at 15-min intervals up to 2 h after the injection. These studies were performed in patients with essential hypertension who were maintained on a constant sodium intake (100 mmol/day), before and after 5 days of treatment with ibopamine, an orally active dopamine analogue. Before ibopamine metoclopramide induced the expected, marked increases in aldosterone and in prolactin, but only minimal, non-significant decreases in ANF. All other humoral parameters, as well as blood pressure and heart rate, were unaffected by metoclopramide. After ibopamine treatment, which caused a transient natriuretic effect, the responses of aldosterone and of ANF to metoclopramide were similar to those observed in control studies, whereas that of prolactin was enhanced. Thus, it appears that the suppressive effect exerted by the dopaminergic tone on aldosterone secretion is independent of ANF both before and after dopaminergic stimulation.
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PMID:Dopaminergic control of aldosterone secretion is not mediated by atrial natriuretic factor in patients with essential hypertension. 297 75

The possibility that some of the cardiovascular, sedative or neurohormonal effects of clonidine are mediated by opiate receptors was investigated in normotensive and hypertensive subjects. In normal subjects intravenous (i.v.) clonidine lowered blood pressure, increased sedation and raised levels of plasma renin activity and growth hormone. Levels of other anterior pituitary hormones (prolactin, luteinizing hormone and follicle stimulating hormone) and of arginine vasopressin were unchanged. The effects of clonidine were similar after the administration of naloxone. In patients with essential hypertension clonidine lowered blood pressure, increased sedation and reduced plasma noradrenaline levels. There was an insignificant fall in levels of plasma renin activity. Prior administration of naloxone did not influence the effects of clonidine. It is concluded that the cardiovascular, sedative and neurohormonal effects of acutely administered clonidine are not dependent on opiate receptor activation in either normal or hypertensive man.
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PMID:Naloxone does not affect the cardiovascular, sedative or neurohormonal effects of clonidine in normal and hypertensive man. 300 7

The effect of chronic converting enzyme inhibition with enalapril on the PRA, PRL and plasma aldosterone responses to metoclopramide was studied in 10 patients with mild to moderate essential hypertension. Enalapril reduced supine blood pressure and increased heart rate significantly. PRA and urinary sodium excretion rose significantly. PRA levels did not change after metoclopramide neither during placebo nor during enalapril. The aldosterone response to metoclopramide was not altered by enalapril, indicating that this response is independent of the renin-angiotensin system. The PRL response to metoclopramide was considerably enhanced after 4 weeks of treatment with enalapril. It is proposed that enalapril, by decreasing the formation of angiotensin II, increases the prolactin reserve.
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PMID:Enhanced response of plasma prolactin to metoclopramide during chronic converting enzyme inhibition. 303 57

To investigate the effects of dietary sodium on the peripheral dopaminergic mechanism, changes of unconjugated plasma dopamine(DA) and its related humoral factors were studied in 8 patients with essential hypertension(EH) and 8 age-matched normal controls(N) while they were receiving ordinary meals (Na, 130-180 mEq daily) followed by higher sodium (250-300 mEq daily) diets for a week. Plasma and urinary DA, norepinephrine(NE) and epinephrine(E) were measured by the highly sensitive COMT-mediated radioenzymatic procedure, which permits an accurate estimation of plasma DA as low as 5-6 pg/ml. Under high sodium diets, blood pressure and heart rate were not changed significantly in N and EH subjects. Urinary NE and E tended to decrease, while urinary DA increased significantly in both groups of subjects (p less than 0.05). There was a significant correlation between urinary sodium and DA (r = 0.590, p less than 0.001), but plasma DA failed to correlate significantly to urinary sodium or DA in all subjects. Plasma NE and E tended to decrease in both N and EH subjects, while plasma DA increased significantly (p less than 0.05) in EH from 7.2 +/- 0.8 pg/ml [mean +/- SEM] to 9.3 +/- 1.0 and slightly in N from 9.1 +/- 1.8 to 11.2 +/- 1.3. Plasma renin activity(PRA) and plasma aldosterone(PAC) were invariably decreased in all subjects, while plasma prolactin(PRL) remained unchanged. A significant correlation was observed between plasma DA and NE under ordinary meals (r = 0.733, p less than 0.01), but this correlation disappeared under high sodium diets. Plasma DA showed an inverse correlation to PAC (r = 0.351, p less than 0.05) under both dietary conditions. Upright posture induced a significant rise (p less than 0.05) in NE, E, DA, PRA and PAC with ordinary meals, but the responses of NE and PAC were apparently attenuated with high sodium diets. An intravenous injection of metoclopramide (MCP, 10 mg), a DA receptor antagonist, provoked a slight rise in plasma NE and DA with ordinary meals, of which responses were further enhanced with high sodium diets. MCP induced a definite rise in PAC and PRL in all subjects under both dietary conditions (p less than 0.01), while plasma E and PRA remained unchanged after MCP challenge. The results lend support to the view that unconjugated plasma DA could be a useful marker of peripheral dopaminergic activity, which might be a physiological regulator responsible for the suppression of aldosterone secretion and sympathetic nerve activity observed during high sodium intake.
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PMID:[Effects of high sodium diet on dopaminergic mechanism in normal and hypertensive subjects]. 306 95

The pathophysiological role of the central dopaminergic mechanism in human essential hypertension (EH) is still unknown. We studied on the relationship between the dopaminergic activity and the salt-sensitivity. Twenty three hospitalized patients with EH were divided into the salt-sensitive group (SS, n = 12) or non salt-sensitive group (NSS, n = 11) by their responses whether they caused more than 8% increase in mean blood pressure (MBP) when the dietary salt was increased from 2g/day to 20g/day for 7 days of each. The change of central dopaminergic activity by the salt load was evaluated by the decrement of plasma prolactin (PRL) response to small dosage (25 micrograms) of thyrotropin releasing hormone. The mean percent change of PRL response by the salt load in the SS group was -6.5 +/- 8.3% (mean +/- SEM), which was significantly lower than 26.8 +/- 5.5% in the NSS group (p less than 0.01). There was a significant negative correlation between the percent changes of PRL response and the percent changes of MBP by the salt load (r = -0.448, p less than 0.05). These results suggested that the rise in blood pressure by salt load in SS patients with EH might be due to a reduced activity of the central dopaminergic mechanism.
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PMID:[Salt sensitivity and central dopaminergic activity in patients with essential hypertension]. 314 15

In 51 patients with pregnancy hypertension (H) and 51 normotensive gravid women (N), matched for age of gestation, plasma prolactin was measured at 8.30 am (PRL1) and 9.30 am (PRL2) in basal conditions and after 10 minutes of upright posture (PRL3). While in N there was a fall from PRL1 to PRL2 which was nonsignificant, in H there was a significant fall from PRL1 to PRL2. With upright posture there was a further decrease in prolactin in N and a significant increase in H. With multiple regression analysis, systolic and diastolic blood pressure did not show any independent relations with PRL1, PRL2 and PRL3, while serum proteins and proteinuria showed a significant relation with PRL1, as did serum proteins, serum potassium and serum urate with PRL2 and serum urate with PRL3. As has been suggested in primary hypertension, a certain increase in peripheral sympathetic tone, dependent on a decreased central dopaminergic activity, may be present in patients who develop pregnancy hypertension compared to normotensive pregnant controls and may be involved in the pathogenesis of pregnancy hypertension.
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PMID:Role of prolactin in pregnancy hypertension. 330 30

We studied natriuresis during central hypervolaemia by immersing eight normal subjects and eight patients with uncomplicated essential hypertension up to the neck in water, either in the absence (study 1) or presence (study 2) of dopamine blockade by metoclopramide. Water immersion without metoclopramide induced an exaggerated natriuresis in hypertensives compared with normotensives (P less than 0.001). This occurred in the presence of identical hormonal (plasma renin activity, plasma aldosterone and prolactin), renal (creatinine clearance) and pressor responses in both groups (study 1). The marked natriuresis seen during water immersion alone in normotensives was significantly blunted (P less than 0.02) but not abolished during water immersion with addition of metoclopramide. On the other hand, the exaggerated natriuresis found in hypertensives during water immersion alone was completely abolished during water immersion plus dopamine blockade by metoclopramide (study 2). Similar hormonal, renal and pressor changes were detected in both normotensive and hypertensive subjects during water immersion plus metoclopramide administration. Our data demonstrate that metoclopramide abolishes the exaggerated natriuretic response seen in hypertensives during volume expansion produced by water immersion, and suggest that dopamine may play a critical role in mediating the hypernatriuresis of essential hypertension.
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PMID:Dopamine blockade abolishes the exaggerated natriuresis of essential hypertension. 332 13


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