Stimulation of renin by blockade of α2-adrenoceptors in man

Leeuw, Peter W. de; Es, P. N. Van; Tchang, Pau T.; Bos, R. De; Birkenhäger, W. H.

doi:10.1097/00004872-198812040-00130

Cited by 6 publications

(3 citation statements)

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“…In patients with low renin hypertension, however, the same clonidine treatment increased plasma renin activity (Golub et al, 1983). Overall it appears that clonidine treatment lowers plasma renin activity in most patients which may be due to presynaptic inhibition of noradrenaline release in nerve endings close to the juxtaglomerular cells (de Leeuw et al, 1988); however, enhanced renin activity may be possible in some groups of patients.…”

Section: Renal Function A-adrenergic Drugs On Humanmentioning

confidence: 94%

“…Similar to the renal blood flow studies it was found that renin release can be enhanced by the nonselective antagonist, phentolamine, and by the q-adrenoceptor antagonist, yohimbine, but not by the a,adrenoceptor antagonist, doxazosin. Interestingly, the renin release enhancements by yohimbine infusion were markedly attenuated by simultaneous intrarenal infusion of the Padrenoceptor antagonist, atenolol (de Leeuw et al, 1988). Thus, the effect of q-adrenoceptor antagonists on renin release depends on intact padrenoceptors.…”

Section: Effects Of Renal A-adrenoceptor Stimulationmentioning

confidence: 95%

“…These studies are based on the direct infusion of drugs into the renal artery of hypertensive patients undergoing diagnostic arteriography to exclude a stenosis of the renal artery. In their initial study these authors demonstrated that intrarenal infusion of vehicle did not affect renal blood flow or renovascular resistance, while infusion of the a-adrenoceptor antagonist, phentolamine (6 pg/kg/min), enhanced renal blood flow from 320 * 16 to 400 f 38 mUmird100 g kidney weight and reduced renovascular resistance from 0.38 * 0.10 to 0.29 0.14 units (n = 5 , P c 0.05); intrarenal infusion of the a, -adrenoceptor antagonist, doxazosin ( 1 pg/ kg/min), however, caused only very small alterations which barely reached statistical significance in some (de Leeuw et al, 1986;de Leeuw and Birkenhager, 1988) but not other studies (de Leeuw et al, 1985). In other studies these authors compared the effects of intrarenal infusion of the vehicle, doxazosin, and the %-adrenoceptor antagonist, yohimbine (1-10 pg/kg/min); in these studies yohimbine infusion significantly enhanced renal blood flow and this enhancement was always greater than those achieved by the a, -adrenoceptor antagonist, doxazosin (de Leeuw and Birkenhager, 1988;de Leeuw et al, 1987).…”

Section: Effects Of Renal A-adrenoceptor Stimulationmentioning

confidence: 99%

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α‐Adrenergic regulation of human renal function

Michel

1996

Fundamemntal Clinical Pharma

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Pharmacological and molecular cloning techniques have identified six human subtypes of alpha-adrenoceptors which are designated alpha 1A, alpha 1D, alpha 2A, and alpha 2C. At the protein level human kidney expresses predominantly alpha 2A-adrenoceptors while other alpha 2-adrenoceptor subtypes or alpha 1-adrenoceptors have not been detected consistently in radioligand binding studies. However, the presynaptic receptors, which inhibit noradrenaline release in the human kidney, appear to belong to the alpha 2C-subtype. Intrarenal infusion of the nonselective alpha-adrenoceptor antagonist, phentolamine, and of the selective alpha 2-adrenoceptor antagonist, yohimbine, but not of the selective alpha 1-adrenoceptor antagonist, doxazosin, increase renal blood flow and renin release in hypertensive patients undergoing diagnostic renal angiography. Thus, alpha 2- but not alpha 1-adrenoceptors appear to mediate a tonic renal vasoconstriction and inhibition of renin release. Effects of systemically given alpha 1-adrenoceptor agonists and antagonists are difficult to interpret on a mechanistic level since direct effects in the kidney and indirect effects due to baroreflex activation and peripheral presynaptic and central sympatholytic actions may at least partially offset each other. Moreover, some of these drugs may additionally act independent of alpha-adrenoceptors, for example, via imidazoline recognition sits. The net result in a given subject may depend on the endogenous sympatho-adrenal tone. Thus, for each target population of interest, effects have to be described empirically for each drug.

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Section: Renal Function A-adrenergic Drugs On Humanmentioning

confidence: 94%

Section: Effects Of Renal A-adrenoceptor Stimulationmentioning

confidence: 95%

Section: Effects Of Renal A-adrenoceptor Stimulationmentioning

confidence: 99%

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α‐Adrenergic regulation of human renal function

Michel

1996

Fundamemntal Clinical Pharma

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Neural Control of Renal Function

Moss

Colindres

Gottschalk

1992

Comprehensive Physiology

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The sections in this article are: Current Research Historical Perspective Neuroanatomy and Neurophysiology Efferent Renal Innervation Afferent Renal Innervation Renal Adrenergic Receptors General Concepts Prejunctional Renal Receptors Post‐ and Extrajunctional Adrenoceptors Renal Tubular and Vascular Dopamine Receptors Renal Cholinergic Receptors Cellular Transduction of Neurotransmitter Effects Sympathetic Nervous System and Renal Hemodynamics Vasoconstrictor Responses Vasodilatory Responses Sympathetic Nervous System and Renal Tubular Function Studies in Anesthetized Animals Studies in Conscious Animals Effects of Neurotransmitters on Renal Tubular Function Cellular Mechanisms in the Renal Tubular Responses to Catecholamines Sympathetic Nervous System and Renin Secretion by the Kidney General Concepts Effects of Direct and Reflex Stimulation of the Renal Nerves Effects of Renal Denervation on Renin Release Renal Adrenoceptors Involved in Renin Secretion Interactions Between Nerves and Prostaglandins in Renin Release

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Modulation der renalen Transmitter-Freisetzung durch präsynaptische Rezeptoren

Rump

Schollmeyer

1989

Klin Wochenschr

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Renal sympathetic nerve varicosities possess a variety of receptors which when activated by appropriate agonists can modulate noradrenaline release at the local level of the kidney. Thus, activation of prejunctional alpha 1- and alpha 2-adrenoceptors, prostaglandin (PG), dopamine, adenosine and serotonin receptors inhibits, whereas activation of prejunctional beta 2-adrenoceptors and angiotensin (A) II receptors enhances renal noradrenaline release. Moreover, neuronally released noradrenaline itself activates prejunctional inhibitory alpha 1- and alpha 2-adrenoceptors forming a "negative feedback loop" of its own release (autoinhibition). PGE2 and adenosine locally formed in the kidney by renal nerve stimulation inhibits noradrenaline release through activation of their specific prejunctional receptor system (transjunctional inhibition).

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Stimulation of renin by blockade of α2-adrenoceptors in man

Cited by 6 publications

References 0 publications

α‐Adrenergic regulation of human renal function

α‐Adrenergic regulation of human renal function

Neural Control of Renal Function

Modulation der renalen Transmitter-Freisetzung durch präsynaptische Rezeptoren

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