Dopaminergic modulation of pressor and hormonal responses in essential hypertension.

Sowers, James R.; Golub, Michael S.; Berger, Morris E.; Whitfield, L.

doi:10.1161/01.hyp.4.3.424

Cited by 36 publications

(14 citation statements)

References 28 publications

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“…38 Studies in sodium-and potassium-equilibrated hypertensive and normotensive whites reported that treatment with the dopamine D2 agonist bromocriptine significantly reduced mean arterial pressure and prolactin levels in the hypertensive subjects but not in the normotensive subjects. 39,40 The greater effect of bromocriptine on the plasma norepinephrine response to posture and of bromocriptine on prolactin levels in the hypertensives suggested decreased central dopaminergic activity in the maintenance of hypertension. 40 In hypertension, the sympathetic nervous system is often hyperactive.…”

Section: Discussionmentioning

confidence: 99%

“…39,40 The greater effect of bromocriptine on the plasma norepinephrine response to posture and of bromocriptine on prolactin levels in the hypertensives suggested decreased central dopaminergic activity in the maintenance of hypertension. 40 In hypertension, the sympathetic nervous system is often hyperactive. 41 Bromocriptine has been shown to reduce plasma norepinephrine levels in whites, which suggests the involvement of the dopaminergic system.…”

Section: Discussionmentioning

confidence: 99%

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Modulation of Blood Pressure and Obesity With the Dopamine D2 Receptor Gene Taq I Polymorphism

2000

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Abstract-Pharmacological data suggest that obesity and blood pressure (BP) may be modulated through the dopamine D2 receptor (DD2R), which may represent an underlying mechanism that links these conditions. A TaqI polymorphism near the DD2R gene has been associated with indices of obesity in white populations. We compared anthropometric and fasting plasma biochemical parameters between 209 nondiabetic hypertensive and 174 gender-matched normotensive Chinese subjects. The hypertensives had increased dyslipidemia, increased fasting plasma glucose concentrations, and a greater degree of obesity. The A1 and A2 alleles of the DD2R gene TaqI polymorphism were identified with a polymerase chain reaction-based restriction fragment length polymorphism protocol. The A1 allele frequency was decreased in the hypertensives (42.0%) compared with the control subjects (52.0%, Pϭ0.006), and genotype frequencies were different (Pϭ0.05) between the 2 groups. In the combined population (nϭ383), systolic, diastolic, and mean arterial BPs were 6, 5, and 6 mm Hg lower, respectively, in subjects with the A1A1 genotype relative to the A2A2 genotype (all PϽ0.05), whereas skinfold thickness was increased at the iliac (PϽ0.001) and triceps (PϽ0.03) sites but not at the biceps or subscapular sites. Furthermore, this DD2R gene polymorphism was shown to be a significant independent predictor of diastolic BP and iliac and triceps skinfold thicknesses (all PϽ0.03). These contrasting associations of the DD2R TaqI polymorphism A1 allele with lower BP but increased markers of "gynoidal" or peripheral subcutaneous obesity (iliac and triceps skinfold thicknesses) in our Chinese population may provide some insight into the underlying relationship between BP and body fat distribution, but the exact nature of this link remains to be determined. (Hypertension. 2000;36:177-182.)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Modulation of Blood Pressure and Obesity With the Dopamine D2 Receptor Gene Taq I Polymorphism

2000

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“…In line with these data demonstrating decreased urinary excretion of DA with salt loading is the observation that hypertensive whites appear to be more sensitive to the natriuretic and hypotensive effects of DA and DA agonists than normotensive subjects. 46 - 47 Thus, hypertensive blacks appear to differ from whites in that they have low urinary DA excretion under low dietary salt conditions but have urinary DA responses to salt similar to those of normotensive blacks. The diminished urinary DA response to dietary salt loading in normotensive blacks as compared with normotensive whites 17 -19 probably reflects the greater prevalence of salt sensitivity in the normotensive black population.…”

Section: Discussionmentioning

confidence: 99%

Salt sensitivity in blacks. Salt intake and natriuretic substances.

Sowers

Zemel

et al. 1988

Hypertension

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SUMMARY Accumulating evidence suggests that hypertension hi blacks is manifested hi part by impaired renal excretion of salt. Consequently, this study was performed to determine if hypertensive and normotensive black subjects differ hi their ability to generate known natriuretic substances. Fourteen normotensive and 11 hypertensive blacks were maintained on constant metabolic diets containing either 40 or 180 mmol of salt per day for 14 days each. During the last 4 days of each salt intake period, urine was collected for measurement of sodium, dopamine, and norepinephrine. On the last day of each 14-day dietary period, blood pressures were measured, blood was collected for measurement of plasma atrial natriuretic factor (ANF) and aldosterone, and urine was collected over 2 hours for measurement of prostaglandin E 2 (PGE 2 ). Both the normotensive and the hypertensive groups manifested salt sensitivity; then-mean arterial pressure rose by 7 ± 0.2 and 6 ± 0.2%, respectively, when salt intake was increased from 40 to 180 mmoJ/day. The hypertensive group exhibited decreased (p < 0.05) dopamme excretion as compared with the normotensive group for both dietary salt intakes. Plasma ANF levels increased (p < 0.05) in the hypertensive group, but not in the normotensive group, with increasing dietary salt. Plasma aldosterone and urinary norepinephrine and PGE 2 were comparable in the two groups for both dietary salt Intakes. These data suggest that salt sensitivity is not unique to hypertensive blacks but occurs hi normotensive blacks as well. Decreased renal production of dopamme may be a pathogenic factor hi the development and maintenance of hypertension in blacks. compared with hypertension in whites, is characterized by a higher incidence of salt sensitivity '-4 in spite of the apparent lack of differences in sodium and salt intakes between the two populations. 5 The mechanisms involved in the relatively high incidence of salt-sensitive hypertension in blacks are poorly understood. However, an impaired natriuretic response to a salt load in hypertensive blacks could result from a reduced ability to generate natriuretic substances such as dopamine (DA), prostaglandin E? (PGE2), and atrial natriuretic factor (ANF).There is a considerable body of evidence suggesting a relationship between renal production of DA and the ability of the kidney to excrete a salt load. 6 -21 Enhanced dietary salt intake or infusion of saline results in an increase in urinary DA excretion and a decrease in norepinephrine excretion. 13 -22 That the dietary salt or saline-mediated natriuresis is causally linked to renal DA excretion is supported by the observation that administration of carbidopa, the peripheral inhibitor of the enzyme dopa decarboxylase, prevents the increases in urinary sodium in response to dietary salt 23 and saline infusion. 14 -15 However, there is evidence that salt loading does not appropriately increase urinary DA excretion in hypertensive patients, 24 -M suggesting that decreased renal DA production in response to...

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“…1,2 Decreased D 2 -like dopaminergic activity in the central nervous system has been reported in essential hypertension. 1,4 Several studies in animal models of genetic hypertension also support the notion of altered central D 2 -like dopaminergic activity in hypertension. 5,6 However, 3 D 2 -like dopamine receptors, D 2 , D 3 , and D 4 , exist, and which of the 3 cloned D 2 -like receptors participate in the D 2 -like regulation of BP is unclear.…”

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confidence: 93%

Adrenergic and Endothelin B Receptor-Dependent Hypertension in Dopamine Receptor Type-2 Knockout Mice

Bek

Asico

et al. 2001

Hypertension

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Abstract-Polymorphism of the dopamine receptor type-2 (D 2 ) gene is associated with essential hypertension. To assess whether D 2 receptors participate in regulation of blood pressure (BP), we studied mice in which the D 2 receptor was disrupted. In anesthetized mice, systolic and diastolic BPs (in millimeters of mercury) were higher in D 2 homozygous and heterozygous mutant mice than in D 2 ϩ/ϩ littermates. BP after ␣-adrenergic blockade decreased to a greater extent in D 2 Ϫ/Ϫ mice than in D 2 ϩ/ϩ mice. Epinephrine excretion was greater in D 2 Ϫ/Ϫ mice than in D 2 ϩ/ϩ mice, and acute adrenalectomy decreased BP to a similar level in D Disruption of D 3 receptors in mice produces hypertension mediated, at least in part, by activation of the renin-angiotensin system. 7 The D 2 receptor could be involved in D 2 -likemediated hypertension because it is the major D 2 -like dopamine receptor. 3,8 -11 Moreover, BP decreased when a segment of chromosome 8 that contained the D 2 receptor gene was transferred from a normotensive Brown Norway rat to a spontaneously hypertensive rat background. 12 Several variants of the human D 2 dopamine receptor have been reported. 13 Abnormalities of D 2 receptor genes could play a role in the pathogenesis of essential hypertension, because the association of a D 2 dopamine receptor polymorphism with obesity and hypertension has been reported. 14 To determine whether D 2 receptors play a role in the regulation of BP, we measured arterial pressure in congenic B6 mice mutants for the D 2 receptor. 8,9 Because D 2 -like receptors have been shown to interact with vasopressor systems, 1,6,15,16 interactions between D 2 receptors and other vasopressor systems were also studied. Methods D 2 Receptor-Deficient MiceThe original F 2 hybrid strain (129/SvXC57BL/6J, Oregon Health Sciences University, Portland) that contained the mutated D 2 recep-

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Dopaminergic modulation of pressor and hormonal responses in essential hypertension.

Cited by 36 publications

References 28 publications

Modulation of Blood Pressure and Obesity With the Dopamine D2 Receptor Gene Taq I Polymorphism

Modulation of Blood Pressure and Obesity With the Dopamine D2 Receptor Gene Taq I Polymorphism

Salt sensitivity in blacks. Salt intake and natriuretic substances.

Adrenergic and Endothelin B Receptor-Dependent Hypertension in Dopamine Receptor Type-2 Knockout Mice

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