The significance of duration of salt loading on cardiovascular response and urinary excretion of catecholamine in rats.

Yoshimura, Manabu; Yamazaki, Hideaki; Takashina, Ryosaku; Kambara, Seichi; Iyoda, Isao; Sasaki, Susumu; Takahashi, Hakuo; Takeda, Kazuo; Ijichi, Hamao

doi:10.1507/endocrj1954.33.169

Cited by 14 publications

(6 citation statements)

References 12 publications

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“…These results are not surprising since conflicting results have been reported concerning dopamine values in essential AHT: similar (10, 11) as well as increased (12,13) or decreased levels (14,15) have been observed. Our data are in agreement with the fact that the involvement of ERD in resting eunatremic conditions seems to be unlikely (16,18) asking the question of the reality of a dopaminergic basal tone (17).…”

Section: Discussionsupporting

confidence: 90%

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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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Section: Discussionsupporting

confidence: 90%

“…Salt loading is associated in normotensive dogs with a rise in urinary DA excretion, as it could be expected from previous studies with rats (18,19) or humans (3,20). The increase is of short term duration (2 days) since the third day of experiment, urinary dopamine values returned to basal levels.…”

Section: Discussionsupporting

confidence: 67%

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Sanchez

Damase‐Michel²,

Tran

et al. 1995

Hypertens Res

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“…We speculate this may be related to a decrease in the number of D 1 -like receptors 62,63 in the proximal tubule available for receptor-receptor interactions between the D 1 -like receptor and the AT 1 receptor after 5 days on a HS diet, which we will study in the future.…”

Section: Discussionmentioning

confidence: 95%

The Renin-Angiotensin and Renal Dopaminergic Systems Interact in Normotensive Humans

Natarajan¹,

Eisner

Armando³

et al. 2016

Journal of the American Society of Nephrology

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The renin-angiotensin-aldosterone (RAAS) and renal dopaminergic systems interact to maintain sodium balance. High NaCl intake increases renal synthesis of dopamine and dopaminergic receptor activity, decreasing epithelial sodium transport, whereas sodium deficit activates the RAAS, increasing epithelial sodium transport. We tested the hypothesis that attenuation of the natriuretic effect of dopamine D 1 -like receptors during salt restriction results in part from increased RAAS activity in seven salt-resistant normotensive adults using a double-blind placebo-controlled balanced crossover design. All subjects attained sodium balance on low (50 mmol Na + /day) and high (300 mmol Na + /day) NaCl diets, administered 4 weeks apart. Sodium, potassium, lithium, para-aminohippurate, and creatinine clearances were measured before, during, and after a 3-hour infusion of fenoldopam, a D 1 -like receptor agonist, with and without pretreatment with enalapril, an angiotensin converting enzyme inhibitor. On the high NaCl diet, fenoldopam-induced natriuresis was associated with the inhibition of renal proximal and distal tubule sodium transport. On the low NaCl diet, fenoldopam decreased renal distal tubule sodium transport but did not cause natriuresis. The addition of enalapril to fenoldopam restored the natriuretic effect of fenoldopam and its inhibitory effect on proximal tubule sodium transport. Thus, on a high NaCl diet fenoldopam causes natriuresis by inhibiting renal proximal and distal tubule transport, but on a low NaCl diet the increased RAAS activity prevents the D 1 -like receptor from inhibiting renal proximal tubule sodium transport, neutralizing the natriuretic effect of fenoldopam. These results demonstrate an interaction between the renin-angiotensin and renal dopaminergic systems in humans and highlight the influence of dietary NaCl on these interactions. During salt depletion, sodium balance is maintained by increased activity of several systems, including the renin-angiotensin-aldosterone (RAAS) and sympathetic nervous systems.

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“…Sodium retention caused by excess sodium intake is one of the possible factors influencing expression of nNOS gene in the adrenal, because sodium retention is thought to occur on day 10 during high sodium load; that blood pressure was greater than normal and values of pulse rate and urinary excretion of norepinephrine were lower than normal on day 10 of application of high sodium load to rats implies that sodium retention and reflex suppression of the sympathetic nervous activity had occurred [29,30]. If nNOS in the adrenal were involved in maintaining blood pressure, an increase in blood pressure due to sodium retention would be expected to cause the down-regulation of nNOS gene.…”

Section: Discussionmentioning

confidence: 99%

Down-regulation of adrenal neuronal nitric oxide synthase mRNAs and proteins after deoxycorticosterone acetate-salt treatment in rats

Lai

Hsin

Huang

et al. 2006

The Journal of Steroid Biochemistry and Molecular Biology

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The significance of duration of salt loading on cardiovascular response and urinary excretion of catecholamine in rats.

Cited by 14 publications

References 12 publications

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

The Renin-Angiotensin and Renal Dopaminergic Systems Interact in Normotensive Humans

Down-regulation of adrenal neuronal nitric oxide synthase mRNAs and proteins after deoxycorticosterone acetate-salt treatment in rats

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