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

Dopamine may exert a tonic inhibitory effect on aldosterone secretion and enhance renal sodium excretion. Nonmodulating hypertension in part is characterized by decreased aldosterone secretion in response to angiotensin II (AII) as well as a decreased natriuretic response to a saline load. This study assesses whether an abnormally increased dopaminergic inhibition of aldosterone secretion underlies the adrenal defect in nonmodulating hypertension and whether abnormalities of renal dopamine formation contribute to sodium retention. We measured the plasma dopamine concentration in 39 patients with nonmodulating hypertension and in 32 patients with normal modulation on a 10-meq sodium intake. Dopamine levels were significantly higher (P less than 0.05) in nonmodulators. The aldosterone response to AII (3 ng/kg.min) was assessed before and during administration of the dopamine antagonist metoclopramide in 13 patients. Metoclopramide did not change the adrenal response to AII in either hypertensive subgroup. In 12 normal subjects mean urinary dopamine levels were higher in a sodium-replete state (200-mmol intake) than in a low sodium state (10-mmol intake; 1.68 +/- 0.28 vs. 0.92 +/- 0.22 mumol/day; P less than 0.01) as expected. Modulators demonstrated this same effect, while nonmodulators did not [modulators, 3.66 +/- 0.82 and 1.37 +/- 0.14 mumol/day; nonmodulators, 1.33 +/- 0.28 and 1.68 +/- 0.90 mumol/day; P less than 0.02]. The sodium-retaining tendency of nonmodulators may reflect, at least in part, reduced intrarenal dopamine production in the sodium-replete state, but the adrenal defect in aldosterone release in nonmodulators is not mediated by excess dopaminergic inhibition of aldosterone secretion.
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PMID:The role of dopamine in nonmodulating hypertension. 275 83

1. Dopamine (DA) binding sites in the left and right ventricle of hypertensive rats were assessed after two weeks of induction of hypertension by left renal artery occlusion. 2. The ratio of left ventricular (LV) weight to total body weight was significantly increased in hypertensive rats from 2.046 +/- 0.120 mg g-1 to 3.125 +/- 0.090 mg g-1 (P less than 0.01) while no significant difference was noted in the right ventricle (RV). 3. The hypertrophied LV was associated with a 78% increase in its protein content, however, the ratio of protein content to ventricular wet weight was not significantly different from controls. No change in RV protein content and concentration was observed. 4. Dopamine affinity of sarcolemmal protein was not significantly different in control and experimental LV and RV and the ratio of DA affinity in LV:RV was 10:1. 5. Saturation of LV with DA was reached at around 7 min whereas RV was saturated at approximately 15 min.
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PMID:Dopamine receptors in the hypertrophied rat heart. 295 87

Dopamine (DA) receptors have been divided into two subtypes: DA1 receptors which subserve vasodilation in renal, mesenteric, coronary, and cerebral vascular beds, and DA2 receptors which when activated cause inhibition of release of norepinephrine in sympathetic nerve endings. The subdivisions were made on the basis of differences in chemical structure and potency series of agonists and antagonists for the two receptor subtypes. Agonists and antagonists are now available which selectively act on DA1 or DA2 receptors. The clinical use of DA, DA pro-drugs, and selective DA agonists is discussed with particular emphasis on the treatment of congestive heart failure and hypertension. Finally, data are presented concerning possible relationships between peripheral DA1 and DA2 receptors and DA receptors classified in the central nervous system.
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PMID:Dopamine: receptors and clinical applications. 315 32

Dopamine is a natriuretic hormone and is synthesized in the kidney in response to a sodium load. This relationship results in a positive correlation between urinary sodium and dopamine outputs. Uncoupling of the renal sodium-dopamine relationship is reflected in a loss of this correlation and will result in the sluggish excretion of a sodium load. We measured 24-h urinary sodium and dopamine outputs in Thais and Iranians, who traditionally have very different dietary salt environments (salt-rich and salt-scarce, respectively). There was a highly significant positive correlation between sodium and dopamine in the Thais (r = 0.53, P less than 0.001) but no suggestion of such a correlation in the Iranians (r = 0.03). We hypothesize that in some races the uncoupling of the renal sodium-dopamine relationship, possibly as a mechanism to help conserve dietary sodium, predisposes the race to the development of hypertension when the individuals encounter a salt-rich diet.
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PMID:Further ethnic differences in the renal sodium-dopamine relationship: its uncoupling in Iranian but not in Thai normotensive subjects. 324 Dec 69

Spontaneously hypertensive rats (SHR) received a highly magnesium enriched diet during the development of hypertension, which caused plasma Mg concentrations to be markedly increased. Arterial blood pressure was reduced in supplemented animals. Levels of noradrenaline, 3-dihydroxyphenylacetic acid and homovanillic acid in cortex, hypothalamus, striatum and brain stem remained unchanged. Dopamine levels in the cortex, hypothalamus and striatum were also unchanged. Dopamine levels in brain stem increased. However the correlation between treatment with magnesium, dopamine-related variables in the brain and decrease in blood pressure in SHR remains hypothetical.
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PMID:Effects of high magnesium intake on central catecholamines in spontaneously hypertensive rat. 327 3

Central dopaminergic mechanisms involved in the regulation of plasma aldosterone concentration were investigated in 16 conscious sheep following Na depletion with intramuscularly administered furosemide. Intracerebroventricular infusion of dopamine (20 micrograms/min) decreased plasma aldosterone significantly to 52 +/- 8% of basal level and increased plasma renin activity (PRA) significantly to 172 +/- 25% of basal level in this animal model. In addition, intracerebroventricular infusion of the dopamine antagonist metoclopramide (20 micrograms/min) in artificial cerebrospinal fluid vehicle significantly increased aldosterone levels to 144 +/- 14% of basal level and decreased PRA to 62 +/- 5% of basal value. Neither intracerebroventricular infusion of the vehicle nor intravenous infusions of metoclopramide or dopamine at the same doses changed aldosterone or PRA levels. Intracerebroventricular bolus injections of metoclopramide (20 micrograms/kg in 0.4 ml of vehicle) were also effective, increasing aldosterone levels to 266 +/- 22% of basal level and decreasing PRA to 70 +/- 12% of basal level. Intravenous bolus injections of the same dose of metoclopramide were ineffective. Dopamine was infused intracerebroventricularly into two uniadrenalectomized sheep with the remaining adrenal transplanted to the neck. Aldosterone levels were decreased to 49 +/- 10% of basal level, and PRA was increased to 157 +/- 10% of basal value. None of the infusions or injections changed arterial or intracranial pressure, or plasma K, Na, and cortisol levels. These data indicate that endogenous or exogenous dopamine may act on central dopamine receptors to decrease plasma aldosterone concentration by an unknown humoral mechanism. The known aldosterone regulators, plasma Na, K, angiotensin II, and adrenocorticotropic hormone, are not involved in the regulation.
Hypertension 1987 Aug
PMID:Central dopaminergic regulation of aldosterone secretion in sheep. 330 64

The purpose of the present study was to analyze the influence of dopamine on norepinephrine release in resistance vessels in spontaneously hypertensive rats (SHR). Perfused mesenteric vasculature preparations from spontaneously hypertensive rats (7-10 weeks old) and age-matched normotensive Wistar Kyoto rats (WKY) were used to compare the effects of dopamine on both pressor responses and norepinephrine release. Both responses to electrical nerve stimulation were significantly greater in SHR than in WKY rats. Dopamine reduced these responses in a dose-dependent manner in WKY. However, this suppression of responses to electrical stimulation was attenuated in SHR. These results suggest that the enhanced adrenergic transmission in SHR may partly reflect impaired dopamine-mediated inhibition of nerve terminals, which would contribute to the pathogenesis of hypertension.
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PMID:The role of dopamine in the regulation of neurotransmitter release in spontaneously hypertensive rats. 339 55

The purpose of the present study was to analyse the regulatory mechanisms of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in the resistance vessels in hypertension. The perfused mesenteric arteries were used for the experiment in spontaneously hypertensive rats (SHR; 7-10 weeks old) and age-matched normotensive Wistar-Kyoto (WKY) rats. Norepinephrine overflow during electrical nerve stimulation was significantly greater in SHR than in WKY rats. A low concentration of epinephrine (5.5 X 10(-9) mol/l) potentiated norepinephrine overflow from the nerve endings in SHR, and this was antagonized by propranolol, while this overflow was reduced by the same concentration of epinephrine in WKY rats. Higher concentrations of epinephrine decreased the norepinephrine overflow both in SHR and WKY rats, and this was antagonized by yohimbine. Dopamine reduced the norepinephrine overflow during electrical nerve stimulation, suppression being significantly less in SHR than in WKY rats. These results suggest that in SHR the increased norepinephrine overflow from sympathetic nerve endings may be partly caused by the facilitatory effect of epinephrine (through presynaptic beta-adrenoceptors) and impaired dopamine-mediated inhibition on the nerve terminals, which might contribute to the enhanced adrenergic activity in hypertension.
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PMID:Effects of epinephrine and dopamine on norepinephrine release from the sympathetic nerve endings in hypertension. 347 13

In order to assess the neurohormonal responses to oral administration of two drugs with different antihypertensive mechanisms, and their implications for long-term efficacy, we studied the changes in plasma renin activity, aldosterone, catecholamines and blood pressure after two cross-over periods of treatment with captopril and hydrochlorothiazide for three months in 14 patients with moderate essential hypertension. Similar levels of plasma renin activity were achieved with both but plasma levels of noradrenaline and aldosterone rose with hydrochlorothiazide (P less than 0.005 and P less than 0.05). Dopamine levels decreased with captopril. Six patients on hydrochlorothiazide had potassium levels under 3.5 mmol/l. Captopril and hydrochlorothiazide were effective in controlling blood pressure in 78% and 50% of the patients respectively, but in cases where noradrenaline was significantly increased after treatment, the effect on diastolic blood pressure was less (P less than 0.05). These data suggest that captopril is highly effective for blood pressure control and that the neurohormonal responses to the drug probably provide additional benefits for long-term therapy in hypertension.
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PMID:Neurohormonal responses to antihypertensive treatment with captopril or hydrochlorothiazide. 353 50

To clarify role of dopamine in the development of hypertension, the effect of a dopamine synthesis inhibitor on blood pressure and urinary output of catecholamines was investigated in spontaneously hypertensive rats (SHR) fed with high sodium diet. Rats were orally given carbidopa, an inhibitor of peripheral DOPA decarboxylase, or the vehicle for 4 weeks. Carbidopa administration accelerated significantly the development of hypertension as compared to the control SHRs with the vehicle. Carbidopa administration resulted in a significant decrease of urinary excreted sodium, urinary dopamine and renal content of dopamine. Conversely, carbidopa administration resulted in a significant increase of urinary excreted norepinephrine, urinary epinephrine and renal content of norepinephrine as compared with control SHRs. These results suggest that decreased dopamine synthesis in kidneys and probably other peripheral tissue accelerates the development of hypertension, mediated by a decrease of natriuresis and an enhancement of sympatho-adrenomedullary activity. Dopamine plays an important role in its protective action against the development of hypertension enhanced by salt loading, and decreased dopaminergic mechanisms accelerated hypertension in SHR.
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PMID:Effect of decreased dopamine synthesis on the development of hypertension induced by salt loading in spontaneously hypertensive rats. 362 32


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