Calcium in the control of renin secretion: Ca2+ influx as an inhibitory signal

Park, C. S.; Han, Dan; Fray, J. C. S.

doi:10.1152/ajprenal.1981.240.1.f70

Cited by 34 publications

(33 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1). We and others have shown that the inhibitory effect of these agents could be attenuated or even be abolished by calcium channel blockers such as verapamil [15,45,59]. Taken together, all of the findings mentioned above are supportive of the idea that the rate of renin release from the juxtaglomerular cells is inversely related to the calcium concentration in the juxtaglomerular cells.…”

Section: Role Of Calcium In the Intracellular Control Of Renin Releasesupporting

confidence: 61%

“…Therefore ouabain leads to an accumulation of calcium within the cell and in consequence to a rise in the intracellular calcium concentration. Ouabain has been found to inhibit renin release [14,29,49,58,59] and additional evidence was obtained to show that this inhibition is a calcium dependent process [14,25,58]. Inhibition of the calcium ATPase by vanadate also inhibits part of the extrusion of calcium and therefore leads to a rise in the intracellular calcium concentration [56].…”

Section: Role Of Calcium In the Intracellular Control Of Renin Releasementioning

confidence: 98%

See 1 more Smart Citation

Intracellular control of renin release — An overview

Kurtz

1986

Klin Wochenschr

View full text Add to dashboard Cite

The renin angiotensin aldosterone system is an important regulator of the extracellular volume and of the control of blood pressure. It is mainly controlled in its activity by the rate of renin release from the kidney. Within the kidney renin is produced, stored and released from the so-called granular juxtaglomerular cells. These cells are modified smooth muscle cells and are found in the tunica media of the afferent arteriole, just adjacent to the glomerulus. They resemble morphologically vascular smooth muscle cells but have also characteristic features of secretory cells with respect to a welldeveloped endoplasmic reticulum, a prominent Golgi-apparatus and membrane bound granules containing renin [6,73].Since the rate of renin release from juxtaglomerular cells has a direct effect on blood pressure and because an enhanced rate of renin release is known to be a major reason of hypertension, the mechanisms controlling renal renin release have attracted considerable interest among physiologists, pharmacologists and clinicians.So far four basic mechanisms controlling renin release from the kidney have been described [26]. These comprise 1. The intra-renal blood pressure, which influences renin release by an as yet undefined baroreceptor.2. The amount of NaCl-load sensed by the macula densa segment of the distal tubule (macula densa sensor).3. The sympathetic nervous system 4. A large number of humoral factors like catecholamines, angiotensin II, vasopressin, atrial natriuretic peptide as well as metabolites as for example adenosine.In spite of the large body of findings about the modulation and alteration of renal renin release, the intracellular mechanisms by which renin release is controlled within the juxtaglomerular cells are not clearly understood.During the last years the mechanisms of physiological and pharmacological alterations of renin release have been reviewed [26, 36, 39]. The present contribution wants to concentrate on the intracellular processes that influence renin release from juxtaglomerular cells. The available information will be discussed in front of the background of the present knowledge about the general mechanisms of secretion.For a variety of secretory cells including adrenal medulla and cortex, pituitary, exocrine and endocrine pancreas, neutrophils and platelets it has been found that the secretory process is triggered by the intracellular levels of calcium and cyclic nucleotides and further by the activity of protein kinase C [12,33,64,68,[70][71][72]. I shall therefore discuss in special the role of intracellular calcium, intracellular cyclic AMP and cyclic GMP and protein kinase C activity in the control of renin release from juxtaglomerular cells. In this context I will also present our own results obtained from studies on the intracellular control of renin release from isolated juxtaglomerular cells. Role of Calcium in the Intracellular Control of Renin ReleaseThe typical secretory process in a large number of secreting cells has been found to be biphasic. The secretory process ...

show abstract

Section: Role Of Calcium In the Intracellular Control Of Renin Releasesupporting

confidence: 61%

Section: Role Of Calcium In the Intracellular Control Of Renin Releasementioning

confidence: 98%

Intracellular control of renin release — An overview

Kurtz

1986

Klin Wochenschr

View full text Add to dashboard Cite

show abstract

“…30 Verapamil does not increase catecholamine synthesis, but reduces the postganglionar synthesis of noradrenaline 31 with a beneficial effect on LVH development. Moreover, some other mechanisms may be involved in the reduction of LVH by V, as its effect on the renin-angiotensinaldosterone axis by interfering with the calcium metabolism in the distal convoluted tubule [32][33][34] or decreasing the collagen content was seen in hypertensive rats. 35 Systolic function was not substantially modified by either treatment.…”

Section: Discussionmentioning

confidence: 99%

Treatment of diastolic dysfunction in hypertensive patients without left ventricular hypertrophy

Molinero

Murga

et al. 1998

J Hum Hypertens

View full text Add to dashboard Cite

The aim of this study was to evaluate the influence of verapamil SR 240 mg (V) and the combination amiloride 5 mg + hydrochlorothiazide 50 mg (AH) on diastolic dysfunction of hypertensive patients without left ventricular hypertrophy (LVH). Twenty-six hypertensive patients with diastolic dysfunction, normal systolic function and without LVH were included into a 2-week washout period and then randomised to a 6-month V or AH treatment. One blinded-to-treatment echocardiographist at

show abstract

“…Churchill and M.C. Churchill 1982a), and this inhibition has been shown to be a calcium-dependent process (Park and Malvin 1978;P. C. Churchill 1979;Cruz-Soto et al 1984).…”

Section: Calciummentioning

confidence: 99%

“…Therefore, ouabain leads to an accumulation of calcium within the cell and consequently to a rise in the intracellular calcium concentration. Ouabain has been found to inhibit renin release (Lyons and Churchill 1974;Park and Malvin 1978;P.C. Churchill 1979;Part et al 1981; P.C.…”

Section: Calciummentioning

confidence: 99%

Cellular control of renin secretion

Kurtz

Wagner

Reviews of Physiology, Biochemistry and Pharmacology

View full text Add to dashboard Cite

Calcium in the control of renin secretion: Ca2+ influx as an inhibitory signal

Cited by 34 publications

References 0 publications

Intracellular control of renin release — An overview

Intracellular control of renin release — An overview

Treatment of diastolic dysfunction in hypertensive patients without left ventricular hypertrophy

Cellular control of renin secretion

Contact Info

Product

Resources

About