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

To examine the role of the sympathetic nervous system in the development of deoxycorticosterone acetate (DOCA)/NaCl hypertension and to test the hypothesis that the responsiveness of the sympathetic nervous system to stress is enhanced during the developmental phase of hypertension in this model before resting sympathetic activity becomes increased, DOCA/NaCl-treated rats and uninephrectomized control animals were studied after 3, 7, 14, and 28 days of treatment. Basal plasma norepinephrine and epinephrine in conscious, unrestrained resting DOCA/NaCl-treated rats were the same as in controls at 3, 7, and 14 days but were significantly elevated at 28 days of treatment. Ganglionic blockade resulted in a significantly greater decrease in mean arterial pressure in DOCA/NaCl rats than in controls at 14 and 28 days of treatment. At 14 days, DOCA/NaCl rats exhibited significantly greater increments in plasma norepinephrine and epinephrine following cold stress than did H2O controls. Basal plasma prolactin levels were elevated and release of dopamine from isolated superfused mediobasal hypothalami reduced in 28-day DOCA/NaCl hypertensive rats. These results indicate that sympathetic nervous system activity increases progressively during the development of DOCA/NaCl hypertension and that the sympathoadrenal system is hyperresponsive to environmental stress even early in the course of DOCA/NaCl treatment and suggest that hypothalamo-hypophyseal function is altered in this model of hypertension.
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PMID:Hyperresponsiveness of monoaminergic mechanisms in DOCA/NaCl hypertensive rats. 401 87

The effects of oral administration of 2 mg prazosin on several metabolic and endocrine variables were evaluated in 12 patients with hypertension (6 with normal and 6 with abnormal glucose tolerance). Prazosin was followed by a rise in plasma glucose and serum free fatty acids (FFA) in both normal and diabetic subjects; there was a trend upward in serum albumin (IRI), but growth hormone (GH), prolactin (PRL), and gastrin did not change. Although these results are in general agreement with metabolic effects of other alpha adrenergic blockers already reported, the rise in plasma glucose is at variance with studies performed with phentolamine.
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PMID:Metabolic effects of prazosin. 610

The purpose of this study was to evaluate the acute hemodynamic and hormonal effects induced by short-term exposure to loud noise in man. Loud noise (95 dBA or 100 dBA) caused an increase in blood-pressure in healthy normotensive subjects as well as in patients with essential hypertension. The blood pressure elevation was caused by vasoconstriction in patients with essential hypertension and in normotensive subjects with a positive family history of hypertension, while the blood pressure response in normotensive subjects without a family history of hypertension was due mainly to an increase in cardiac output. This might indicate that there are genetically determined differences in the cardiovascular response to noise. Stimulation with noise did not increase plasma levels of catecholamines, prolactin, cortisol or growth in normotensive subjects. In patients with essential hypertension plasma noradrenalin increased, while plasma adrenalin and plasma renin activity did not change. The increase in diastolic blood pressure caused by loud noise was not affected by beta 1-selective or non-selective beta-adrenoceptor blockade, nor was it changed by alpha 1-or combined alpha 1-and non-selective beta-adrenoceptor blockade. The elevation in blood pressure induced by noise is usually mediated by vasoconstriction, i.e. an alpha 1-effect. When alpha 1-adrenoceptors are blocked, the blood pressure response to noise is mediated by an increase in cardiac output, i.e. a beta-adrenoceptor mediated effect. It thus seems as if an increased pressure is essential during exposure to loud noise. If one part of the sympathetic nervous system is blocked, other parts can be activated in order to preserve the blood pressure on an elevated level. This indicates a temporary resetting of the baroreceptors during exposure to noise, which probably is mediated from the hypothalamus.
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PMID:Cardiovascular effects of noise. 612 83

The endogenous catecholamine dopamine lowers blood pressure by acting on two receptor subtypes: dopamine 1 and dopamine 2. Dopamine 1 receptors subserve vasodilation, especially in the renal, coronary, mesenteric, and cerebral vascular beds. Dopamine 2 receptors have been located at the endings of postganglionic sympathetic nerves and, when activated, inhibit norepinephrine release. Inhibition of emesis and inhibition of prolactin release also appear to be dopamine 2-mediated phenomena. The receptor subtypes have been classified by differences in chemical structure of agonists and by specific antagonists. Dopamine also acts on beta 1 receptors to stimulate the heart and alpha 1 and alpha 2 receptors to cause vasoconstriction. Alpha adrenergic activity and lack of oral availability limit the use of dopamine in the treatment of hypertension. However, studies with the selective dopamine 1 agonist, fenoldopam, and dopamine 2 agonists such as LY 141865 and bromocriptine, indicate that agonists of both receptor subtypes can lower blood pressure in experimental animals and in hypertensive patients. Initial use of dopamine agonists in the treatment of hypertension and its possible involvement in the etiology and maintenance of hypertension are discussed.
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PMID:Dopamine receptors and hypertension. Physiologic and pharmacologic implications. 614 92

Hormonal and mean arterial pressure (MAP) responses to posture, isometric handgrip, angiotensin II (AII), adrenocorticotrophic hormone (ACTH), and metoclopramide (MCP), a dopamine (DA) antagonist, were examined in nine men with essential hypertension and nine age- and weight-matched normotensive men on a constant 100 mEq sodium and 80 mEq potassium intake before and after 4 days of administration of the DA agonist, bromocriptine (BEC; 2.5 mg three times a day). BEC depressed supine basal MAP in the hypertensives, and decreased MAP response to posture and isometric exercise in both groups. Hypertensives displayed greater (p less than 0.01) NE responses to posture and exercise than the normotensives. BEC decreased the NE response to 10 minutes of upright posture and exercise more in hypertensives (p less than 0.01) than in normotensives, but following BEC, the responses were similar. BEC did not affect basal PRA or PRA responses to posture and exercise in the two groups. PA responses to ACTH and MCP were similar in both groups, but the hypertensives displayed greater (p less than 0.01) PA responses to AII. BEC suppressed PA responses to AII (p less than 0.01) and to high dose ACTH (p less than 0.05) to a similar extent in both groups. The prolactin as well as the PA response to DA antagonism with MCP was similar in the two groups. These results suggest that dopaminergic control of NE secretion may be altered in essential hypertension. Blood pressure lowering effects of BEC in patients with essential hypertension may be related, in part, to depression of sympathetic nervous system activity.
Hypertension
PMID:Dopaminergic modulation of pressor and hormonal responses in essential hypertension. 627 98

Endocrine function was studied in a 24 year old female with lipoatrophic diabetes (LD). Baseline endocrine studies (serum triglycerides: 2600 mg/dl) demonstrated hyperprolactinemia (serum prolactin 51 ng/ml), increased ACTH levels, absence of suppression of ACTH to a high dose of dexamethasone which suppressed serum cortisol normally and, hyperresponsiveness of TSH to stimulation with TRH. Thyroid hormone levels (total and free fraction) were essentially normal. Major metabolites of thyroid hormone (T3, rT3, 3, 3'-T2, and 3', 5'-T2) were also normal and exhibited a normal response to the administration of L-thyroxine and propylthiouracil. Exchange of 84% of the patient's plasma resulted in a decrease in serum triglycerides (700 mg/dl) which was followed by a rebound to the original level in seven days. After the sixth plasmapheresis serum triglycerides stabilized at less than 1000 mg/dl. Plasmapheresis was associated with the appearance of amenorrhea and galactorrhea; also hypertension and proliferative retinopathy developed during this therapy. Repeat endocrine function studies (serum triglycerides: 700 mg/dl) showed a further rise in serum prolactin (greater than 160 ng/ml), persistence of abnormal ACTH secretion and normalization of TSH responsiveness. Lipoatrophic diabetes is associated with abnormal central endocrine function but appropriate peripheral target gland secretion. A course of plasmapheresis improves the hypertriglyceridemia but not the endocrine dysfunction. In this patient with LD the most important side effect of plasmapheresis was the development of cardiovascular complications.
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PMID:Lipoatrophic diabetes: endocrine dysfunction and the response to control hypertriglyceridemia. 628 8

In 40 male patients with essential hypertension less than the age of 36 years, the plasma prolactin (PRL), plasma renin activity (PRA) and plasma catecholamines (noradrenaline (NA) and adrenaline (A)) were determined simultaneously. Those levels were significantly increased compared to the levels in 14 age-matched healthy male control subjects. Furthermore, there were significant correlations between the PRL and plasma NA or PRA (p less than 0.05 in each case), and between the PRA and plasma NA (p less than 0.05). However, no significant relationships were observed between systolic or diastolic blood pressure and PRL, plasma NA or PRA. These findings indicate that the central dopaminergic activity is reduced in a number of young adults with essential hypertension, and that in the patients with the reduced central dopaminergic activity, the peripheral sympathetic activity is stimulated and PRA is also increased probably due to the increased peripheral sympathetic activity, and the possibility exists that such changes are related to the development of hypertension.
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PMID:Prolactin, renin and catecholamines in essential hypertension. 634 64

The effects of direct administration of TRH, TSH, LHRH, LH, ACTH, GH, FSH and prolactin into cerebral ventricle system on metabolic, respiratory, cardiovascular and behavioral responses were assessed in unanesthetized rats, Intraventricular administration of TRH, TSH, LHRH or LH caused hypothermia, decreased metabolism and/or cutaneous vasodilation at room temperature (22 degrees C). Intraventricular administration of FSH, ACTH or prolactin caused hyperthermia, increased metabolism and/or cutaneous vasoconstriction. Intraventricular administration of GH caused an insignificant change in thermoregulatory responses. There was no change in respiratory evaporative heat loss in response to either of the drugs tested. In addition, intraventricular administration of TRH, LHRH or LH caused tachycardia, hypertension and a reduction in the epinephrine-induced reflex bradycardia. In contrast, intraventricular administration of prolactin caused bradycardia, hypotension and an enhancement in the epinephrine-induced reflex bradycardia in conscious rats. There was no change in cardiovascular function in response to intraventricular administration of TSH, FSH, ACTH or GH. Furthermore, following intraventricular administration of TRH, but not TSH, LHRH, LH, FSH, GH, ACTH or prolactin three main categories of behavior were provoked: activity of normal type--forward locomotion stimulation, head and body rearing; stereotype activity--increased grooming and head swaying; and abnormal type behavior--tail elevation and piloerection in rats. The data indicate that most of the anterior pituitary hormones and their releasing hormones act through a central mechanism to influence physiological and/or behavioral functions.
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PMID:Effects of anterior pituitary hormones and their releasing hormones on physiological and behavioral functions in rats. 635 Jul 20

In the present studies, the content and the in vitro production of prolactin by decidua as well as the concentrations of prolactin in amniotic fluid, maternal and fetal serum in normal term pregnancies, induced abortions at various gestational ages, and in pregnancies complicated by diabetes mellitus, preeclampsia, chronic hypertension, and polyhydramnios were measured. Maternal and fetal prolactin levels varied considerably throughout gestation, but at term did not differ significantly between normal and abnormal pregnancies. Prolactin levels in amniotic fluid as well as decidual prolactin content and production were significantly lower only in pregnancies complicated by either hypertension or polyhydramnios. In both normal and abnormal pregnancies, decidual prolactin production correlated strongly with amniotic fluid concentrations. The present data suggest that 1) maternal and fetal prolactin levels do not differ significantly between normal and abnormal pregnancies, 2) the decidua is the principal source of amniotic fluid prolactin, and 3) the significantly lower levels of prolactin in amniotic fluid of pregnancies complicated by hypertension or polyhydramnios are probably due to adverse effects of these conditions on the synthesis and release of prolactin by decidua.
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PMID:Decidual, amniotic fluid, maternal and fetal prolactin in normal and abnormal pregnancies. 636 59

Ten patients with acromegaly, six with active acromegaly and four with inactive acromegaly were studied with regard to the possible relationship between aldosterone metabolism and hypertension. It was noted that tetrahydroaldosterone-3-glucuronide levels were highest in those cases which exhibited the highest prolactin levels. It was in these cases that hypertension was present and they were active as judged by clinical and biochemical parameters. On administration of bromocryptine there was a reduction of tetrahydroaldosterone-3-glucuronide, prolactin and also a significant reduction of blood pressure. The significance of these results is discussed.
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PMID:Aldosterone in acromegaly. 637 68


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