Pathophysiological role of dopamine on the development of hypertension in rats.

Yoshimura, Manabu; Kambara, Seiichi; Okabayashi, Hideoki; Ikegaiki, Iwao; Matsuzawa, Makoto; Suga, Kunihiko; Takahashi, Hakuo; Ijichi, Hamao

doi:10.1253/jcj.51.1226

Cited by 9 publications

(8 citation statements)

References 18 publications

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“…This would be in line with previous studies which, by showing increased activity of the enzyme responsible for the production of DA, increased production of DA and attenuated natriuresis during DA inhibition, have indicated that DA is an intrarenal natriuretic hormone which contributes to the natriuretic response to high salt diet (see reviews by Aperia et al 1991, Jose et al 1992, Lee 1993, Hubbard & Henderson 1995, Jose et al 1998. It would also be in line with a study by Yoshimura et al (1987) that inhibition of DA synthesis during salt loading in SHR increased NA excretion. This observation is consistent with previous ®ndings that hypertensive subjects fail to increase urine DA in response to dietary sodium loading (Gordon et al 1989).…”

Section: Discussionsupporting

confidence: 89%

“…The higher DA excretion in SHR is in line with previous observations (Stier et al 1986, Kuchel et al 1987) although one study reports a similar excretion between SHR and WKY (Stier et al 1993). No conclusions can be drawn, however, as to whether renal sympathetic nerves or plasma are major contributors to urinary NA during the present conditions, but the observation con®rms the higher sympatho-adrenal activity in SHR which has been implicated as a major factor underlying the development of hypertension in this strain (Yoshimura et al 1987, Wyss et al 1992. As for the higher NA excretion in SHR as compared with WKY, the sympathetic nervous system activity is increased overall in SHR ( Judy et al 1976) and Thore Ân & Ricksten (1979) have demonstrated that SHR have a higher renal sympathetic nerve activity, which may explain the ®nding.…”

Section: Discussionsupporting

confidence: 86%

“…This ®ts well with the ®nding in the present study that NA excretion during CNSinduced natriuresis increased most in SHR after a high sodium diet. It would also be in line with a study by Yoshimura et al (1987) that inhibition of DA synthesis during salt loading in SHR increased NA excretion.…”

Section: Discussionsupporting

confidence: 85%

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Renal dopamine and noradrenaline excretion during CNS‐induced natriuresis in spontaneously hypertensive rats: influence of dietary sodium

Hansell

Isaksson

Sjöquist

2000

Acta Physiologica Scandinavica

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Abnormalities in dopamine (DA) and noradrenaline (NA) activities and sodium handling may be involved in the pathogenesis of hypertension. The present study was designed to investigate whether any differences exist between normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) in urinary excretion of DA, NA and sodium after 15 weeks on a low, medium or high sodium diet and during a subsequent elevation of the cerebroventricular fluid sodium concentration (CNS-induced natriuresis). Seven features were noted: (1) Basal sodium and DA excretion after the diet regimen was correlated to the dietary sodium content in both strains, except that sodium and DA excretion in SHR showed no further increase after the high sodium diet over and above that after medium sodium diet. (2) For any given sodium diet, SHR excreted more DA and NA as compared with WKY. (3) Blood pressure in SHR, as opposed to that in WKY, was higher after medium and high sodium diet than after low sodium diet. (4) During CNS-induced natriuresis NA excretion decreased or remained unchanged in WKY, but increased in SHR. (5) The DA/NA excretion ratio during CNS-induced natriuresis increased in WKY while decreased in SHR, which would not favour a natriuretic/vasodilatory response in the latter. (6) The ability of SHR to respond with CNS-induced natriuresis was attenuated after high sodium diet. (7) The magnitude of CNS-induced natriuresis was in both strains correlated to the sodium diet; the higher the dietary sodium content, the greater the natriuretic response. In conclusion, the study shows some clear differences in the catecholamine and sodium handling between WKY and SHR which may be involved in the pathogenesis of hypertension in SHR. Furthermore, increased sodium in the diet sensitizes the brain and kidney to increase the ability to respond with natriuresis for a given sodium stimulus.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 86%

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Renal dopamine and noradrenaline excretion during CNS‐induced natriuresis in spontaneously hypertensive rats: influence of dietary sodium

Hansell

Isaksson

Sjöquist

2000

Acta Physiologica Scandinavica

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“…10 n It was also reported that inhibition of peripheral dopamine production by carbidopa reduced renal sodium excretion and accelerated the development of hypertension in the SHR. 12 It has been demonstrated that the major renal action of kidney dopamine, which is to increase renal sodium excretion, is mediated via a tubular dopamine-1 (DA-1) receptor 47 coupled to both adenylate cyclase 13 ' 14 and phospholipase C. 14~16 Therefore, it is reasonable to speculate that a defect in either one or both of the cellular signaling processes may contribute to the abnormal renal response to DA-1 receptor activation. Indeed, a defect in DA-1 receptor adenylate cyclase coupling in the proximal convoluted tubules from the SHR has recently been reported.…”

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confidence: 99%

Diminished phospholipase C activation by dopamine in spontaneously hypertensive rats.

et al. 1992

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It is reported that a defect in dopamine-1 (DA-1) receptor adenylate cyclase coupling in the proximal convoluted tubule in the spontaneously hypertensive rat may contribute to the diminished natriuretic response to DA-1 receptor agonists. Since the tubular DA-1 receptor is also coupled to phospholipase C, and both of these cellular signaling processes are involved in DA-1 receptor-mediated diuresis and natriuresis, it is important to know whether a similar defect is also present in DA-1 receptor-coupled phospholipase C pathway. The present study was therefore designed to determine the functional status of DA-1 receptor-phospholipase C coupling system of adult spontaneously hypertensive rats using a renal cortical slice preparation. In addition, the renal response to exogenously administered dopamine (1 /ig/kg/min i.v.) was also determined. We found that basal phospholipase C activity was significantly higher in hypertensive rats than in age-matched Wistar-Kyoto rats (7J6±0J2% versus 5.61±0.27%, p<0.05). However, compared with the normotensive controls, dopamine-induced increases in phospholipase C activity were significantly attenuated in the preparations of hypertensive rats in a concentration-dependent manner (13±6% versus 38±6% for 1 mM dopamine, p<0.05; 49±6% versus 71±9% for 3 mM dopamine, p<0.05; 50±16% versus 106±22%, p<0.05 for 10 mM dopamine). The diminished dopamine-induced phospholipase C activation was due to a deficiency in dopamine receptor-phospholipase coupling since the DA-1 receptor antagonist SCH 23390 (30 /iM), which blocked 50% of dopamine-induced inositol phosphate production in the Wistar-Kyoto rats, did not exert such an effect in the spontaneously hypertensive rats. The in vivo functional study showed that the diuretic and natriuretic responses to intravenous administration of dopamine were significantly diminished in spontaneously hypertensive rats compared with Wistar-Kyoto rats (urine output, 34± 1 versus 63±10 fil/30 min,p<0.05; urinary sodium excretion, 1.8±0.1 versus 3.2±0.2 ^teq/30 min,/x0.05). These results suggest that there is a defect in the tubular DA-1 receptor-phospholipase C coupling process in spontaneously hypertensive rats that may contribute to a diminished natiiuretic response to DA-1 receptor activation. (Hypertension 1992;19:102-108) I t is generally accepted that an abnormality in renal handling of sodium is one of the factors in the pathogenesis and/or maintenance of high blood pressure in genetic hypertension. Central to this assumption are the observations that spontaneously hypertensive rats (SHR), as opposed to their normotensive Wistar-Kyoto (WKY) counterparts, retain sodium avidly before the development of hypertension 1 and that urinary sodium excretion (U Na V) in SHR is normal or subnormal despite the presence of elevated blood pressure.2 Furthermore, dietary sodium restriction retards the development of hypertension in SHR.

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“…The increase in urinary dopamine excretion was blunted in group 2, and disappeared in group 3. Such a defect in dopamine mobilization in AHT has been already described (20)(21)(22)(23), but mainly in genetic models of AHT. Our results suggest that in this experimental model of acquired AHT, dopamine impairment can appear during the evolution of AHT.…”

Section: Discussionmentioning

confidence: 76%

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Sanchez

Damase‐Michel²,

Tran

et al. 1995

Hypertens Res

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The effect of chronic salt loading (10 g of NaCI for a period of 7 days) on urinary dopamine release has been investigated in 3 groups of beagle dogs: normotensive dogs (group 1: n = 7), and 2 groups of dogs made hypertensive by chronic sinoaortic denervation [group 2: (n = 6) during the first 4 months after sinoaortic denervation i.e. a model of arterial hypertension with high levels of plasma catecholamines and group 3: (n = 6) one year after denervation i. e. a model of arterial hypertension with normal sympathetic tone]. In normal dogs (group 1), salt loading induced an increase in urinary dopamine excretion during the two first days after salt loading. The rise in urinary dopamine was blunted in group 2. It was not observed in group 3. Salt loading failed to change arterial pressure and heart rate in the three groups of animals. These data show an alteration of the renal dopaminergic system in hypertensive sinoaortic denervated dogs suggesting that a dopaminergic impairment can appear during the development of arterial neurogenic hypertension.(Hypertens Res 1995; 18 Suppl. I: 5187-5190)Key Words: dopamine, hypertension, sinoaortic denervation, kidneyAlthough its physiological relevance is still unclear, it is now admitted that endogenous renal dopamine (ERD) plays a role in the regulation of sodium excretion (1) through activation of specific receptors (2). Moreover, as alteration of sodium handling is one of the factors involved in pathophysiology of arterial hypertension (AHT), a great interest focuses on the potential role of ERD in this pathology. Indeed, several studies showed impairment of renal dopamine mobilization during salt loading in hypertensive models (3). Most of the time, these studies concerned models of genetic AHT. The aim of our work was to investigate whether ERD could be altered during the development of acquired AHT elicited by sinoaortic denervation in dogs. Material and MethodsNineteen beagle dogs weighting from 13 to 16 kg were studies: seven normal normotensive dogs (group 1) were compared to 12 animals made hypertensive by sinoaortic denervation (SAD) as previously described (4). Briefly, carotid and aortic nerves were cut under chloralose anesthesia (80 mg/kg iv.) during 2 successive procedures, 1 at time 0, and the second 7 weeks later. During surgery, care was taken to keep both vagal and sympathic fibers in the vagus intact. The effectiveness of baroreceptor denervation was checked by the failure of norepinephrine (2 mg/kg) to induce bradycardia and nitroglycerine (1, 3, 10 and 30 mg/kg) to induce tachycardia. During the 4 first months, AHT elicited by SAD is associated with a high level in plasma catecholamines. One year after SAD, plasma catecholamine levels return to basal values (4). Furthermore, functional (5) and histological (6) renal alterations are similar to those observed in human AHT.

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Pathophysiological role of dopamine on the development of hypertension in rats.

Cited by 9 publications

References 18 publications

Renal dopamine and noradrenaline excretion during CNS‐induced natriuresis in spontaneously hypertensive rats: influence of dietary sodium

Renal dopamine and noradrenaline excretion during CNS‐induced natriuresis in spontaneously hypertensive rats: influence of dietary sodium

Diminished phospholipase C activation by dopamine in spontaneously hypertensive rats.

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

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