Radioautographic Localization of Atrial Natriuretic Factor Receptors in the Rat Testis

Pelletier, Georges

doi:10.1002/j.1939-4640.1988.tb01063.x

Cited by 17 publications

(7 citation statements)

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“…Evidence of specific ANP binding in isolated adult rat Leydig cells suggested that these hormones activate specific receptors (8). Further studies, using the 125I-ANP radioreceptor methods, confirmed this hypothesis (9,10). Experimental results on cultured murine and rat Leydig cells demonstrated that ANP increases cyclic GMP levels, inducing a selective activation of particulate guanylate cyclase (6,11,12).…”

mentioning

confidence: 80%

“…In isolated rat Leydig cells this stimulatory effect is still debated. Although ANP receptors have been identified in rat Leydig cells (8)(9)(10) and in spite of the ability of ANP to stimulate cGMP production in these cells, Mukhopadhyay and co-workers (13) did not observe any effect on testosterone secretion. The absence of steroidogenic response to rAP-II has been justified as due to a low guanylate cyclase activity in these cells (13).…”

Section: Discussionmentioning

confidence: 99%

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The role of calcium ions in rat Leydig cell steroidogenesis induced by atrial natriuretic peptide

Mioni¹

1993

Acta Endocrinologica

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Foresta C, Mioni R. The role of calcium ions in rat Leydig cell steroidogenesis induced by atrial natriuretic peptide. Acta Endocrinol 1993:128:274-80. ISSN 0001-5598 The aim of this study was to clarify whether calcium ions play a role in the mechanisms by which rat atriopeptin II exerts its stimulatory effects on rat Leydig cell steroidogenesis. The absence of calcium in the medium and the calcium channel-blocker drug, verapamil, both significantly inhibited testosterone production in rat atriopeptin Il-treated rat Leydig cells. Similar effects were observed on human chorionic gonadotropin-stimulated Leydig cells. Furthermore, 8-Bromoguanosine 3\m=' \:5\m=' \cyclic mono\x=req-\ phosphate, the putative second messenger of atrial natriuretic peptide, significantly increased rat Leydig cell steroidogenesis, determining a stimulatory effect comparable to that obtained with rat atriopeptin II. Calcium-free medium and verapamil inhibited this stimulatory effect. The addition of a calcium ionophore, A-23187, significantly counteracted the inhibitory effect of verapamil on rat atriopeptin I I \ x=r eq-\ induced and 8-Bromoguanosine 3\ m=' \ : 5\ m=' \ monophosphate-induced testosterone production. Furthermore, rat atriopeptin II significantly stimulated the calcium flux through the plasma membrane, as evaluated by the 45Ca2+ uptake method. This effect was strongly inhibited by the addition of verapamil. These data underline that calcium ions may play a role in the mechanisms by which atriopeptin II stimulates rat Leydig steroidogenesis, although other post-receptor systems cannot be excluded.

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confidence: 80%

Section: Discussionmentioning

confidence: 99%

The role of calcium ions in rat Leydig cell steroidogenesis induced by atrial natriuretic peptide

Mioni¹

1993

Acta Endocrinologica

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“…Interestingly, the vasodilatory effects of circulating ANP and BNP are partly mediated by local endothelial CNP secretion (Nazario et al, 1995). As Leydig cells have receptors for ANP and BNP (Pelletier 1988;Khurana & Padney 1993) it is tempting to speculate that Leydig cell CNP secretion could be regulated in the same way as in endothelial cells. Interestingly, all natriuretic peptides are known to inhibit endothelial ET-1 secretion (Inagami et al, 1995).…”

Section: Effects Of Natriuretic Peptides On the Testis 57mentioning

confidence: 99%

Atrial natriuretic peptide, brain natriuretic peptide and c‐type natriuretic peptide: effects on testicular microcirculation and immunohistochemical localization

1997

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SummaryThe effect of local injection of atrial (ANP), brain (BNP) and C-type (CNP) natriuretic peptides and an ANP antagonist (HS-142±1) on testicular microcirculation and vasomotion was studied using laser Doppler¯owmetry. The natriuretic peptides were also localized immunohistochemically within the testis.ANP, BNP-32, CNP-22 and CNP-53 all caused a dose-related increase in testicular blood¯ow. The effect of ANP was blocked by concomitant injection of the ANP antagonist. Immunoreactive (ir) CNP and ir BNP were found in Leydig cells whereas ir ANP was observed in the seminiferous tubules. It is suggested that the natriuretic peptides could play a role in local regulation of the testicular microcirculation.

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“…Pelletier, 1988;Mukhopadhyay et al, 1986), adrenocorticotrophin, but not j3-endorphiq dynorphine or a-melanocyte stimulating hormone (Juniewicz et al 1988;Margioris et al, 1989), histamine (Mayerhofer et al, 1989), P-adrenergic agents (Moger & Anakwe, 1986;Tolszczuk et al, 1988), fibroblast growth factor (Sordoillet et al, 1988). transforming growth factor-j3 , activin (Lin e f al., 1989), corticotrophin-releasing factor (Ulisse et al, 1989), renin/ angiotensin I1 (Naruse et al, 1984;Millan & Aguilera, 1988;in man, Okuyama et al, 1988) and calcitonin (Chausmer et nl.. 1982).…”

Section: Potential P a R A C R I N E Mechanisms F O R R E G U L A T Imentioning

confidence: 99%

Intratesticular Control Of Steroidogenesis

Sharpe

1990

Clinical Endocrinology

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Men are men because of testosterone, and the effects of this hormone are evident in virtually every organ or tissue in a normal adult man. Because testosterone is a classical endocrine hormone with effects throughout the body, many endocrinologists will have failed to realize that, in terms of its effects on fertility, the primary role of testosterone is not endocrine but paracrine, as it is the local action of testosterone on spermatogenesis which determines fertility. When looked at from this perspective it is logical to question the traditional endocrine teaching which states that testosterone secretion is controlled solely by pituitary luteinizing hormone (LH). Certainly, the levels of testosterone and LH in peripheral blood show a close relationship, but it is not the level of testosterone in peripheral blood which determines fertility. If the primary role of testosterone is within the testis, then it is not unreasonable to expect that local mechanisms may exist to regulate the intratesticular levels of this steroid. The object of this review is to examinecritically the evidence for such mechanisms, their possible nature and their physiological and clinical significance (if any).Before reviewing the data on intratesticular control of steroidogenesis it is essential to place it in perspective. To do this, three principal questions need to be answered: ( I ) Why might intratesticular mechanisms for local control of testosterone production be required? (2) What is the role (or roles) of testosterone within the testis? A proper understanding of how testosterone controls spermatogenesis is essential if the local regulation of testosterone production is to be evaluated from a physiological perspective. ( 3 ) What are the constraints or problems relating to studies on the intratesticular control of steroidogenesis? It is essential to understand the potential limitations of studies on this subject so that a reasoned interpretation of the results can be made. Most relevant data is derived from studies in uitro, and the relationship of such data to the situation in uivo is often difficult to establish. W H Y M I G H T INTRATESTICULAR M E C H A N I S M S F O R T H E C O N T R O L OF TESTOSTERONE P R O D U C T I O N BE REQUIRED?It can be argued that paracrine control of testicular testosterone production is irrelevant, because (a) the serum levels of LH and testosterone clearly change together (i.e. they control each other) and (b) the removal of LH in animals by hypophysectomy or immunoneutralization lowers intratesticular testosterone levels so drastically that 787

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Radioautographic Localization of Atrial Natriuretic Factor Receptors in the Rat Testis

Cited by 17 publications

References 10 publications

The role of calcium ions in rat Leydig cell steroidogenesis induced by atrial natriuretic peptide

The role of calcium ions in rat Leydig cell steroidogenesis induced by atrial natriuretic peptide

Atrial natriuretic peptide, brain natriuretic peptide and c‐type natriuretic peptide: effects on testicular microcirculation and immunohistochemical localization

Intratesticular Control Of Steroidogenesis

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