Evidence against a role for dopamine D<sub>1</sub> receptors in the myocardium of the pig

Woerkens, Leon J. van; Duncker, Dirk J.; Boer, Marinus O. den; McFalls, E.O.; Sassen, L. M. A.; Saxena, Pramod R.; Verdouw, Pieter D.

doi:10.1111/j.1476-5381.1991.tb12414.x

Cited by 23 publications

(24 citation statements)

References 12 publications

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“…The peripheral location of dopamine receptors and the significant physiological effects of dopaminergic agents on renal, adrenal, cardiovascular function, and corpus cavernosum have been of great interest [Aperia et al, 1987;Siragy et al, 1989Siragy et al, , 1990Siragy et al, , 1992Van Woerkens et al, 1991;Kujacic et al, 1995].…”

Section: Discussionmentioning

confidence: 99%

Novel identification of peripheral dopaminergic D2 receptor in male germ cells

Otth

Torres

Ramírez-Reveco

et al. 2006

J of Cellular Biochemistry

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Dopamine is a recognized modulator in the central nervous system (CNS) and peripheral organ functions. The presence of peripheral dopamine receptors outside the CNS has suggested an intriguing interaction between the nervous system and other functional systems, such as the reproductive system. In the present study we analyzed the expression of D2R receptors in rat testis, rat spermatogenic cells and spermatozoa, in different mammals. The RT-PCR analysis of rat testis mRNA showed specific bands corresponding to the two dopamine receptor D2R (L and S) isoforms previously described in the brain. Using Western blot analysis, we confirmed that the protein is present in rat testis, isolated spermatogenic cells and also in spermatozoa of a range of different mammals, such as rat, mouse, bull, and human. The immunohistochemistry analysis of rat adult testis showed that the receptor was expressed in all germ cells (pre-and postmeiotic phase) of the tubule with staining predominant in spermatogonia. Confocal analysis by indirect immunofluorescence revealed that in non-capacitated spermatozoa of rat, mouse, bull, and human, D2R is mainly localized in the flagellum, and is also observed in the acrosomal region of the sperm head (except in human spermatozoa). Our findings demonstrate that the two D2 receptor isoforms are expressed in rat testis and that the receptor protein is present in different mammalian spermatozoa. The presence of D2R receptors in male germ cells implies new and unsuspected roles for dopamine signaling in testicular and sperm physiology.

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Section: Discussionmentioning

confidence: 99%

Novel identification of peripheral dopaminergic D2 receptor in male germ cells

Otth

Torres

Ramírez-Reveco

et al. 2006

J of Cellular Biochemistry

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“…These data support earlier observations in in vitro experiments and in the intact anaesthetized animals that epinine and dopamine share similar but relatively weak P-adrenoceptor agonist activity as compared to isoprenaline and that the effects of epinine are more selectively mediated through P2-adrenoceptors, whereas dopamine is non-selective or relatively PI-selective depending on the animal species or tissue that was used (Ferrini & Miragoli, 1986;English et al, 1988;Deighton et al, 1990;Bravo et al, 1991). Furthermore, we have shown previously that DI-receptors do not play a major role in the heart, under physiological conditions (Van Woerkens et al, 1991). The lack of a pronounced positive inotropic action of epinine was recently confirmed by infusion of epinine in patients with moderate heart failure due to ischaemic heart disease (Rousseau et al, 1992).…”

Section: Discussionmentioning

confidence: 91%

Differential cardiovascular and neuroendocrine effects of epinine and dopamine in conscious pigs before and after adrenoceptor blockade

Woerkens

Boomsma

Veld

et al. 1992

British J Pharmacology

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1 The effects of epinine or dopamine (both 1-10 tg kg-min-') on systemic haemodynamics and plasma concentrations of catecholamines and prolactin were studied in conscious pigs before and after combined non-selective a-and P-adrenoceptor blockade.2 The plasma concentrations of the two compounds did not differ from each other over the entire dose-range. 3 Epinine increased aortic blood flow (AoBF, 24 ± 6%), which was due to an increase in heart rate (HR) for doses less than 10 ,g kg-' min-'. At 10 fg kg-' min-', HR decreased slightly (10 ± 3%, as compared to the value obtained at 5 psg kg-' min-') and stroke volume increased up to 15% (P <0.05). Mean arterial pressure (MAP, 99 ± 3 mmHg at baseline) decreased dose-dependently (14 ± 2%, P <0.05) up to the infusion rate of 5 tLg kg-' min-, but increased by 4.0 ± 1.8 mmHg during infusion of 10 1tg kg' min-'. Systemic vascular resistance (SVR) decreased up to 23 ± 3% for doses less than 10 yg kg-I min', but did not change further during infusion of the highest dose. LVdP/dt,,,, increased during the two highest infusion rates up to 22 ± 6% (P <0.05). After the infusion was stopped there was an abrupt increase in HR (18 ± 4%, P<0.05) and a further decrease in SVR before all parameters returned to baseline. 4 Dopamine caused increases in AoBF (27 ± 3%) similar to epinine, the only difference being that HR continued to increase (32 ± 5%) and MAP (13 ± 3%) and SVR continued to decrease (31 ± 3%) over the entire dose-range. The increase in LVdP/dt,,,, at the highest dose (48 ± 4%, P <0.05) was more pronounced than with epinine. 5 Adrenoceptor blockade inhibited all epinine-induced changes, but did not affect the dopamineinduced changes in AoBF, SVR and MAP, but attenuated the increases in HR and LVdP/dtmax. 6 Noradrenaline (NA) and adrenaline (Ad) concentrations did not change during infusion of epinine or dopamine, but NA increased by 50% within 2.5 min after stopping the infusion of epinine. After adrenoceptor blockade NA and Ad concentrations did not change during infusion of dopamine, which contrasted with a decrease of 55 ± 5% (P<0.05) in NA during infusion of epinine. 7 Prolactin concentrations decreased gradually from 480 ± 40 pg ml-' to 270 ± 50 pg ml1' (P < 0.05) during infusion of epinine, but did not change significantly during dopamine infusion. 8 The differential effects of epinine and dopamine on MAP, SVR, plasma NA (before and after adrenoceptor blockade) and prolactin, leads us to conclude that in conscious pigs, epinine is a more potent a, P2 and D2-receptor agonist, but a weaker D,-receptor agonist than dopamine.

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“…Therefore, an increase in cardiac contractility by an action of dopamine on P,-adrenoceptors could in part be responsible for the beneficial renal effects [4]. In anaesthetized pigs, combined a-and ,-adrenoceptor blockade abolished the dopamine-induced increase in heart rate and contractility, but the decrease in systemic and renal vascular resistance was not significantly affected [8]. In humans, it still remains unknown whether the increase in cardiac output after low-dose dopamine is primarily caused by stimulation of cardiac PI-adrenoceptors or is merely a consequence of the vasodilating effect secondary to activation of vascular DA receptors.…”

Section: Introductionmentioning

confidence: 96%

Effects of acute beta‐adrenoceptor blockade with metoprolol on the renal response to dopamine in normal humans.

Olsen

Lang-Jensen

Hansen

et al. 1994

Brit J Clinical Pharma

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Denmark1 The present study investigated the contribution of adrenergic PI-receptor stimulation to the cardiovascular and renal effects of low-dose dopamine in eight normal, water-loaded humans. 2 Metoprolol (100 mg) or placebo was administered orally at 08.00 h in a randomized, double-blind fashion on two different days. Renal clearance studies were performed during a 1 h baseline period, two 1 h periods with dopamine infusion (3 gg kg-min-'), and a 1 h recovery period. Cardiac output was measured by an ultrasonic Doppler method, and lithium clearance (CLLd) was used to estimate proximal tubular outflow. 3 Baseline values of heart rate, systolic pressure and mean arterial pressure decreased with metoprolol compared with placebo, but cardiac output, effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) were not significantly changed. Metoprolol significantly decreased baseline CLLi and sodium clearance (CLNa) by 19% (P < 0.01) and 34% (P < 0.01), respectively. 4 Metoprolol blunted the dopamine-induced increases in heart rate and systolic pressure, but cardiac output increased to the same extent on both study days by 26% (placebo, P < 0.05) and by 31% (metoprolol, P < 0.01), respectively. With and without metoprolol, dopamine did not significantly change GFR, and the percentage increases in ERPF were similar on the two study days (40% (P < 0.001) and 42% (P < 0.001), respectively). Dopamine increased CLLi and CLNa by 31% (P < 0.01) and 114% (P < 0.01), respectively, with placebo, and by 36% (P < 0.01) and 114% (P < 0.01), respectively, with metoprolol. Values during infusion remained significantly lower with metoprolol compared with placebo.

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Evidence against a role for dopamine D₁ receptors in the myocardium of the pig

Cited by 23 publications

References 12 publications

Novel identification of peripheral dopaminergic D2 receptor in male germ cells

Novel identification of peripheral dopaminergic D2 receptor in male germ cells

Differential cardiovascular and neuroendocrine effects of epinine and dopamine in conscious pigs before and after adrenoceptor blockade

Effects of acute beta‐adrenoceptor blockade with metoprolol on the renal response to dopamine in normal humans.

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Evidence against a role for dopamine D1 receptors in the myocardium of the pig

Cited by 23 publications

References 12 publications

Novel identification of peripheral dopaminergic D2 receptor in male germ cells

Novel identification of peripheral dopaminergic D2 receptor in male germ cells

Differential cardiovascular and neuroendocrine effects of epinine and dopamine in conscious pigs before and after adrenoceptor blockade

Effects of acute beta‐adrenoceptor blockade with metoprolol on the renal response to dopamine in normal humans.

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Evidence against a role for dopamine D₁ receptors in the myocardium of the pig