Rat Juxtaglomerular Cells are Endowed with DA-1 Dopamine Receptors Mediating Renin Release

Kurtz, Armin; Bruna, Roberto Della; Pratz, J.; Cavero, Icilio

doi:10.1097/00005344-198812000-00006

Cited by 43 publications

(29 citation statements)

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“…Rat juxtaglomerular cells are innervated by dopaminergic nerves and express the D 1A and D 3 receptor subtypes (8,14,29,30). D 1 -like receptors, probably via the D 1A receptor subtype in the rat, are responsible for the dopamine-mediated increase in renin secretion (6)(7)(8). The other D 1 -like receptor, the D 1B receptor, is not expressed in rat juxtaglomerular cells (8).…”

Section: Discussionmentioning

confidence: 99%

“…More recently, a multicenter sib-pair analysis study failed to support a linkage or association between the human angiotensinogen locus and essential hypertension (5). Stimulation of a D 1 -like receptor is associated with decreased renal sodium reabsorption, stimulation of renin release, and angiotensinogen gene expression (6)(7)(8)(9)(10). Thus, an abnormality resulting in inhibition of a D 1 -like receptor function may lead to sodium retention and simultaneously produce a low renin state (10).…”

Section: Introductionmentioning

confidence: 99%

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Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension.

Asico¹,

Ladines²,

Fuchs³

et al. 1998

J. Clin. Invest.

156

175

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Since dopamine receptors are important in the regulation of renal and cardiovascular function, we studied the cardiovascular consequences of the disruption of the D 3 receptor, a member of the family of D 2 -like receptors, expressed in renal proximal tubules and juxtaglomerular cells. Systolic and diastolic blood pressures were higher ( ‫ف‬ 20 mmHg) in heterozygous and homozygous than in wild-type mice. An acute saline load increased urine flow rate and sodium excretion to a similar extent in wild-type and heterozygous mice but the increase was attenuated in homozygous mice. Renal renin activity was much greater in homozygous than in wild-type mice; values for heterozygous mice were intermediate. Blockade of angiotensin II subtype-1 receptors decreased systolic blood pressure for a longer duration in mutant than in wild-type mice. Thus, disruption of the D 3 receptor increases renal renin production and produces renal sodium retention and renin-dependent hypertension. ( J .

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension.

Asico¹,

Ladines²,

Fuchs³

et al. 1998

J. Clin. Invest.

156

175

View full text Add to dashboard Cite

show abstract

“…Plasma renin activity (PRA) is measured as the generation of ANG I without the addition of exogenous renin substrate.] In addition to catecholamines, other hormones, such as the prostaglandins E 2 and I 2 (prostacyclin) (402), dopamine (476), calcitonin gene-related peptide (482), pituitary adenylyl cyclase activating polypeptide (PACAP) (322), and adrenomedullin (397), stimulate the renin release from isolated JG cells and increase the intracellular cAMP concentrations.…”

Section: Campmentioning

confidence: 99%

Physiology of Kidney Renin

Castrop

Höcherl

Kurtz

et al. 2010

Physiological Reviews

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234

277

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The protease renin is the key enzyme of the renin-angiotensin-aldosterone cascade, which is relevant under both physiological and pathophysiological settings. The kidney is the only organ capable of releasing enzymatically active renin. Although the characteristic juxtaglomerular position is the best known site of renin generation, renin-producing cells in the kidney can vary in number and localization. (Pro)renin gene transcription in these cells is controlled by a number of transcription factors, among which CREB is the best characterized. Pro-renin is stored in vesicles, activated to renin, and then released upon demand. The release of renin is under the control of the cAMP (stimulatory) and Ca2+(inhibitory) signaling pathways. Meanwhile, a great number of intrarenally generated or systemically acting factors have been identified that control the renin secretion directly at the level of renin-producing cells, by activating either of the signaling pathways mentioned above. The broad spectrum of biological actions of (pro)renin is mediated by receptors for (pro)renin, angiotensin II and angiotensin-( 1 – 7 ).

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“…These observations thus complete a series of previous studies demonstrating that all maneuvers that increase cellular cAMP levels, such as activation of adenylate cyclase, inhibition of cAMP-phosphodiesterases, and addition of membrane-permeable cAMP analogs, stimulate renin secretion. Thus activators of ␤-adrenoreceptors (27,40) and other hormones stimulating adenylate cyclase activity, such as prostaglandins E2 and I2 (24,32), adrenomedullin (34), dopamine (43), and the neurohormones CGRP (44) and PACAP (30), are known to enhance renin release, as does direct activation of AC activity by forskolin. Similarly, nonselective inhibition of cAMP phosphodiesterases by IBMX (iso-butyl-methyl-xanthine) is a well established way to stimulate renin secretion (13,16,48,97).…”

Section: Intracellular Signals Controlling Renin Secretionmentioning

confidence: 99%

Renin Release

et al. 2007

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The aspartyl-protease renin is the key regulator of the renin-angiotensin-aldosterone system, which is critically involved in salt, volume, and blood pressure homeostasis of the body. Renin is mainly produced and released into circulation by the so-called juxtaglomerular epithelioid cells, located in the walls of renal afferent arterioles at the entrance of the glomerular capillary network. It has been known for a long time that renin synthesis and secretion are stimulated by the sympathetic nerves and the prostaglandins and are inhibited in negative feedback loops by angiotensin II, high blood pressure, salt, and volume overload. In contrast, the events controlling the function of renin-secreting cells at the organ and cellular level are markedly less clear and remain mysterious in certain aspects. The unravelling of these mysteries has led to new and interesting insights into the process of renin release.

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Rat Juxtaglomerular Cells are Endowed with DA-1 Dopamine Receptors Mediating Renin Release

Cited by 43 publications

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Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension.

Disruption of the dopamine D3 receptor gene produces renin-dependent hypertension.

Physiology of Kidney Renin

Renin Release

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