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Dopamine, hypertension and obesity

Abstract

Dopamine, a neurotransmitter, precursor of noradrenaline, is responsible for cardiovascular and renal actions, such as increase in myocardial contractility and cardiac output, without changes in heart rate, producing passive and active vasodilatation, diuresis and natriuresis. These cardiovascular and renal actions take place through the interaction with dopamine receptors, D1, D2, D3, D4, and D5. Recent findings point to the possibility of D6 and D7receptors. Dopamine is known to influence the control of arterial pressure by influencing the central and peripheral nervous system and target organs such as kidneys and adrenal glands, in some types of hypertension. Although dopamine and its derivatives have been shown to have antihypertensive effects, these are still being studied; therefore it is important to explain some physiological and pharmacological aspects of dopamine, its receptors, and the clinical uses it could have in the treatment of arterial hypertension and more recently in obesity, based on evidence proving a clear association between obesity and the decrease in the expression of D2 receptors in the brain of obese persons.

Introduction

Dopamine (DA) is one of the main catecholamines in mammals. Its major role as a brain neurotransmitter is well known as well as its contribution to the development of pathologies, mainly arterial hypertension (AHT).1,2,3 In recent years knowledge of the DA role in both renal as well as systemic physiology has been increasing, and major achievements have been made in the identification of receptors and their functioning mechanisms.2 Traditionally, DA receptors are divided into two families according to the stimulation or inhibition they may produce at the adenyl cyclase level. The D1-like receptors increase the production of cAMP through the interaction with Gs proteins (s = stimulant), stimulating adenyl cyclase. The D2-like receptors, in turn, interact with Gi proteins (i = inhibitory), inhibiting adenyl cyclase and decreasing production of cAMP.4 Two types of D1 receptors have been described: the D1A (D1 in human beings) and the D1B (D5 in human beings).5 D2s (s = short), D2l (l = long), D3, and D4 exist in the D2 family.4,6 Both D2 isoforms result from an alternative mRNA division.6 Lately two new D1-like receptors have been discovered in Gallus Domesticus and in marine anguilla: D1C and D1D.7,8 Two major theories might explain this D1/D2 differentiation mechanism: speciation and products of gene duplication mechanisms.9 The DA receptors belong to a family with seven transmembrane domains coupled to G proteins,4 sharing among them most of their structural characteristics.

Receptors localisation in kidneys

The existence of D1-like receptors in the proximal and distal cortical tubules, the juxtaglomerular apparatus, the renal vasculature and the cortical collecting duct (CCD) has been shown.10 D2-like receptors are also localised in the juxtaglomerular apparatus, the proximal and distal cortical tubules and CCD, in the renal vasculature adventitia, in the glomerulus and the terminal of the sympathetic nerves.10,11,12

Role of dopamine in kidney function

Usually an increase in renal diuresis and natriuresis is observed after release or administration of DA.13 These effects have been thoroughly analysed and characterised by two kinds of response, depending on whether it is produced by D1 or D2. Activation with selective agonists to D1 receptors results in hypotension, increase in renal flow,14 diuresis, and natriuresis, whereas stimulation of D2 produces hypotension, bradycardia, decrease in afterload and vasodilatation in certain vascular beds15 (see Table 1). These effects are Na+ dependant, ie, increases in plasma [Na+] induce higher excretion of water and Na+, and result in high dopamine levels in urine.16

Table 1 Characteristics and distribution of receptors for dopamine in humans

Proximal tubules produce DA by means of L-DOPA uptake from tubular filtrate through a Na+ dependent transportation mechanism, which is further decarboxylated into DA by AADC (L- aromatic amino acid decarboxylase).17 Since DA urine levels are much higher than levels circulating in plasma, synthesis in proximal tubules is said to be the main renal DA source, because AADC inhibition reduces DA excretion through urine.17 L-DOPA uptake through distal tubules and DA production takes place by means of α2-adrenergic receptors.18

DA capability of producing kidney natriuresis and diuresis is mainly the result of the inhibition of two water and sodium transportation complexes in proximal nephron. One of them is the Na+/ K+/ATPase pump, located in the basolateral membrane of the proximal tubules and in other places such as CCD, where it is mainly inhibited by the activation of D1 receptors.19,20,21 D2 receptors have an opposite effect on these receptors, because by means of the Gi protein activation, which inhibits adenyl cyclase, the cAMP that would block the pump is not produced.22 The other mechanism consists of the Na+/H+ exchanger, which is also located in the proximal tubules and inhibited by D1 receptors agonists. D2 receptors do not seem to act on this exchanger at the proximal tubule level.14

Given the significance of kidneys for the control of the haemodynamic balance, and vis-à-vis the effects of DA on them, the relationship between DA and AHT development has been studied.23 It has been shown that the absence of DA codifying alleles is related to increases in systolic and diastolic pressure, thus suggesting a causal relation between the gene for the D1A receptor and AHT.24,25 Also, defects of coupling or activation of second messengers by this receptor (without affecting their distribution or quantity) are also related to the AHT appearance.21 In this regard, the presence of polymorphic forms of the D1 codifying gene has been described in patients with essential AHT.26 The D5/D1 ratio in nephron is insignificant, therefore DA actions related to the D1 (D1-like) family are normally attributed to D1.24,27

As far as D2-like receptors are concerned, D3 is expressed in proximal tubules and juxtaglomerular cells. It inhibits renin release by decreasing cAMP, as opposite to D1 activation, which results in renin release. Disruption of these receptors brings about sodium retention and the increase of renin-dependent AHT.12,28 Besides this particular effect on natriuresis, activation of these receptors influences renal haemodynamics thus producing postglomerular vasoconstriction,11 which increases glomerular filtration rate (GFR). D4 receptor, like D1A, is located in the cortical collecting tubule, and its activation inhibits the vasopressin-dependent reaction of water and Na+ in CCD by means of an interaction of Gi proteins.20,29,30

Modulation mechanisms of the response to DA

Na+/H+ exchanger

It is inhibited by the paracrine effect of DA on the proximal tube resulting from D1 receptors activation, which stimulates adenyl cyclase.31 However, it can be also inhibited by a mechanism independent of the cAMP generation, directly through the G protein interaction.32 Another inhibiting mechanism independent of cAMP is that taking place through PLC activation.33 Inhibition of this exchanger due to DA is predominantly observed under sodium reload conditions that sensitise kidneys and thus increase their capability to have a natriuresis-inducing response to this stimulus.16 In spontaneously hypertensive rats (SHR)—a model of genetic hypertension—a decrease in DA capability to inhibit this type of hypertension has been demonstrated; this has been attributed to a lower expression and activity of Gs protein and a higher expression and activity of G protein.34 This is the result of a failure in the post-transductional mechanism of the receptors, since there is no decrease in the number of D1 receptors or demonstrable alterations in its structure.34

Na+/K+/ATPase pump

The Na+/K+/ATPase pump, after using ATP, introduces two K+ molecules and expels three Na+ molecules; this electric gradient is further used for water and Na+ resorption. DA reversibly inhibits this pump, mainly through type 1 receptors, which results in an increase in natriuresis.4,15 The second messengers responsible for the enzyme phosphorylation are apparently phospholipase A2 (PLA2), with the subsequent release of arachidonic acid and its metabolites, and phospholipase C (PLC). Their actual distribution and mediation seem to be of dependent nature.14

The existence of this pump in the gastrointestinal tract has been demonstrated, specifically in the jejunum, where it also influences the Na+ balance, particularly in young animals, whose renal system is not fully developed. A recent study showed that a high Na+-content diet inhibits this pump by increasing DA synthesis, which would aid hydroelectrolitic tolerance of the body during a sodium overload.35 The inhibition of the jejunum Na+/K+/ATPase pump, under sodium overload conditions, is also observed in adult animals after ablation of one of their kidneys, which would mean a possible DA-induced connection between kidney and intestine.36

PKC (protein kinase C)

DA also activates PCK, both in its novel as well as classic forms, through it D1 receptors. DA translocates the enzyme so that it acts as a integral membrane protein and this, in turn, can activate pumps and/or transporting channels, as demonstrated in an experiment in proximal tubule cells.37 In this experiment, Nowicki and Cols demonstrated that dopamine interacts with PKC, in Ca+-dependent and independent mechanisms. PKC stimulation by DA would be induced by D1A receptors that would increase cAMP levels, thus activating PKA which, in turn, would further activate PKC.33

PCK is also activated in kidneys by noradrenaline and angiotensin II (Ang II). Once this protein is activated, both a Na+ transportation stimulation through the membrane (if it is stimulated by noradrenaline and Ang II) or an inhibition (if it is stimulated by DA) can take place. This contradictory behaviour can be explained based on the existence of PCK isoforms, which would respond to different stimuli.38 D1 receptors were found to have no influence on PKC-α and λ variants, but do decrease PKC-ζ and σ expression; the opposite occurs with noradrenaline and Ang II.38

Angiotensin II

Angiotensin II stimulates Na+ and water resorption in the proximal tubule. This effect is opposite to that produced by DA, which inhibits said resorption through the activation of Gs proteins. The receptors for Angiontensin II are located in the apical and basolateral membrane of the proximal tubules.17 DA, through D1 receptors, diminishes the expression of AT1 receptors in the proximal tubule; this effect is mediated by an increase in the intracellular cAMP concentration.17

Vasopressin (AVP)

AVP induces Ang II release, and its secretion is controlled from the hypothalamus and directly influenced by DA through D1 receptors. It produces, by means of the AT1 receptors, an increase in the Ang II secretion. This latter, in turn, produces antidiuresis at the renal level and AVP plasma levels are increased.39

Nitric oxide

There exist similarities between DA and the nitric oxide (NO) system in kidneys. Both are vasodilators, inhibit resorption by blocking the Na+/K+/ATPase pump and the Na+/H+ exchanger, and both are synthesised in the proximal tubules. Recent experiments showed that the NO system positively influences the D1A expression, by increasing the receptor synthesis, either under hypoxia conditions or not.40 In addition, acute inhibition of NO synthesis is related to a decrease in the DA excretion in urine,27 which showed a positive relation between these two systems.

Joint D1/D2 interaction

A brief description of the mechanism underlying the DA action has been presented and it is evident that there exist inconsistencies among some of them to carry out a final effector response, thus suggesting that there are more complex modulations which have not been fully understood. The inconsistencies observed in the effects of DA on kidney regarding D1/D2 activation could also be the result of differences in the laboratory techniques, in the use of different animal species or in the insufficient pharmacological selectivity in the tools employed.11

In any case, synergic actions in both types of receptors have been demonstrated. For instance, both enhance ATP-induced arachidonic acid release, which, together with the synergism in the cAMP and phosphatidylinositol production, could explain the synergism in the Na+/K+/ATPase pump.41 Both types of receptors have opposite functions that could serve as a regulating or balancing system in stress situations, such as an acute sodium reload, in which case D2-like receptors would favour the Na+/K+/ATPase inhibiting action of the D1-like receptors and even enhance diuretic response by these receptors.41,42,43

Obesity and hypertension

The relationship between obesity and hypertension is well known, obesity being one of the major risk factors for the development of AHT.44 A recent study45 found an evident association between obesity and a decrease in the expression of D2 receptors in the brain of obese individuals (BMI >40 k/m2). Since DA regulates the brain reward circuits producing an agreeable feeling as a response to certain stimuli,46,47 deficiency in DA action in these patients could perpetuate pathological intake as a means to compensate a decrease in these circuits, the so-called Reward Deficiency Syndrome.45 A higher prevalence of the Taq1 allele for D2 receptors has been observed in obese individuals, which is related to a decrease in this receptor expression in these patients. Another study in obese patients with polymorphism for this allele (Taq1) showed a gynecoid distribution of body fat, without a considerable deviation in arterial tension values.48 Although this is not a conclusive study, the development of obesity-coexisting AHT is not discarded, because these are relatively young patients which would not have developed AHT yet.

In addition, it has been already explained that defects in D1A can lead to AHT development, hence the importance of establishing a relationship between this defect and obesity. In obese, hyperinsulinaemic and hypertensive rats (obese Zucker rats) a decrease in the number of junction sites (D1A receptors) has been observed as well as a decrease in the G protein stimulation by DA in the proximal tubules, specifically in basocellular membranes,49,50 when compared with normal rats. Alteration in effectiveness of dopamine action on D1A receptors, observed in these rats, would lead to a lower inhibition of Na+/K+/ATPase pump, which, in turn, would result in a decrease in diuresis and an increase in AHT. We have demonstrated in our laboratory that DA increases plasma insulin concentration when dopamine receptors are stimulated, whereas metoclopramide blocks this effect; meaning that there is also a relationship between the insulin-glucose balance and DA.2

In summary, alterations in D2 receptors do not lead to obesity development; however there are not conclusive studies showing a clear association between defective D2 receptors and AHT. D1A receptors are closely related to AHT appearance and experiments with obese rats have shown defects in them. It would be necessary to elucidate whether defects in this receptors are also a cause for obesity. The reward effect at the central level is also observed for this receptor.51 Since it has been postulated that food can trigger the reward system, it would be interesting to study if the defect at the renal level is accompanied by a deficiency at the central nervous system level and if this defect itself can produce obesity by means of the mechanism postulated for D2. In any case, D1/D2 receptors have synergic effects on diuresis and natriuresis;41 therefore a proven defect in any of them does not exclude the possibility of joint alterations both at the renal level as well as in the development of obesity.

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Correspondence to M Velasco.

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Contreras, F., Fouillioux, C., Bolívar, A. et al. Dopamine, hypertension and obesity. J Hum Hypertens 16, S13–S17 (2002). https://doi.org/10.1038/sj.jhh.1001334

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Keywords

  • dopamine
  • dopamine receptor
  • kidney
  • obesity
  • dopamine agonist

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