Effects of EDTA and verapamil on renin release in dogs.

Abe, Youichi; Yukimura, Tokihito; Itoh, Hiroshi; Mori, Nobuhito; Okahara, Takeshi; Yamamoto, Kenjiro

doi:10.1254/jjp.33.627

Cited by 22 publications

(11 citation statements)

References 14 publications

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“…Reference Abe et al 34 Roy et al 48 Bell and Lindner 49 Bell and Lindner 49 Yamaguchi et al 50 Abe et al 51 Dietz et al 52 Dietz et al All studies were performed on anesthetized dogs, except for the study by DiBona and Sawin, 54 which was performed on anesthetized rats. GFR = glomerular filtration rate; NS = not significant; RBF = renal blood flow; SBP = systemic blood pressure; U N l = urinary sodium excretion.…”

Section: Reported Effects Of Calcium Blockers On Renal Hemodynamicsmentioning

confidence: 99%

Multiple effects of calcium entry blockers on renal function in hypertension.

Romero

Raij²,

Granger

et al. 1987

Hypertension

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SUMMARY Characterization of the renal effects of calcium entry blockers has not been easy because the inhibition of Ca 2+ cellular influx alters several regulatory functions. The ability of calcium blockers to dilate renal vasculature and to increase glomerular filtration rate is largely determined by the preexisting vascular tone. However, the increments in sodium excretion could occur without alterations in renal hemodynamics. Calcium blockers could increase sodium excretion by inducing a redistribution of renal blood flow toward juxtamedullary nephrons, by inhibiting tubuloglomerular feedback responses, or by a direct action on the tubular transport of sodium. These effects are poorly understood at present. In vitro studies show that the blockade of calcium entry enhances renin secretion and decreases prostaglandin synthesis. This dissociation has not been found during longterm administration, which has been proved to be effective for the treatment of essential hypertension with normal maintenance of renal function. In this respect, there are reports indicating that calcium blockers are particularly effective in a subgroup of patients with essential hypertension who exhibit subtle but detectable alterations in calcium metabolism. Further studies are needed to determine whether this significant response to calcium blockers is due to correction of an early defect of calcium cellular kinetics that initiated the increase in blood pressure. (Hypertension 10: 140-151, 1987) KEY WORDS • glomerular filtration rate blood flow • glomerular mesangium renin-angiotensin-prostaglandin system * renal C ALCIUM entry blockers are relatively new drugs that are gaining rapid acceptance for the treatment of hypertension. '" 3 In fact, their potent properties for relaxing smooth muscle 4 could well account for their efficacy in lowering the increase of total peripheral resistance in patients with hypertension. 5 However, a fundamental concept implicit in the evaluation of any antihypertensive drug is related to its effect on renal function 6 because a decrease in renal perfusion pressure induces several compensatory reac-

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Section: Reported Effects Of Calcium Blockers On Renal Hemodynamicsmentioning

confidence: 99%

Multiple effects of calcium entry blockers on renal function in hypertension.

Romero

Raij²,

Granger

et al. 1987

Hypertension

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“…Moreover, it has been found that spontaneous renin release from whole kidneys, kidney slices, glomeruli and isolated juxtaglomerular cells is en- hanced by calcium entry blockers [1,24] and inhibited by facilitation of calcium entry [20,21,27,51]. In addition, hormones known to mobilize calcium in several tissues such as angiotensin II, vasopressin and norepinephrine have been found to inhibit renin release by a calcium dependent process [10,16,77,79].…”

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

confidence: 99%

Intracellular control of renin release — An overview

Kurtz

1986

Klin Wochenschr

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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 ...

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“…C. Churchill 1982a,b, 1987;Matsumara et al 1984;Raguki et al 1988), and is enhanced by calcium entry blockers (P.C. Churchill et al 1981;Abe et al 1983;Kurtz et al 1984;Antonipillai and Horton 1985). Inhibition of calcium release from intracellular stores has also been reported to enhance renin release (Fray and Lush 1984).…”

Section: Calciummentioning

confidence: 99%

Cellular control of renin secretion

Kurtz

Wagner

Reviews of Physiology, Biochemistry and Pharmacology

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Effects of EDTA and verapamil on renin release in dogs.

Cited by 22 publications

References 14 publications

Multiple effects of calcium entry blockers on renal function in hypertension.

Multiple effects of calcium entry blockers on renal function in hypertension.

Intracellular control of renin release — An overview

Cellular control of renin secretion

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