Atrial Natriuretic Peptide (ANP) is a Negative Modulator of Adrenocortical Cell Function in Sceloporus undulatus (Eastern Fence Lizard)

CARSIA, R.V.; JOHN-ALDER, H.B.*; UMDNJ School of Osteopathic Medicince, Stratford; Rutgers Univ., New Brunswick: Atrial Natriuretic Peptide (ANP) is a Negative Modulator of Adrenocortical Cell Function in Sceloporus undulatus (Eastern Fence Lizard)

In mammals, ANP is a consistent suppressor of aldosterone secretion, but its effects on adrenal steroidogenic function in non-mammalian vertebrates are both stimulatory and inhibitory in a species-specific manner (Kocsis et al., 1995). Limited studies suggest that ANP is inhibitory for chelonian adrenocortical function, but no other class of reptiles has been examined. In the present study, the action of ANP (rat analogue) and its interaction with adrenocorticotropin (ACTH) and angiotensin II (ANG II) were investigated using freshly isolated adrenocortical cells from eastern fence lizards. ANP inhibited basal and maximal ANG II-stimulated rates of ALDO and B production in a concentration-dependent manner. Similar efficacies (inhibition of 70-90%) and potencies (ED50 ~1 nM) were observed. ANP had no effect on ALDO and B production rates in response to a maximal steroidogenic concentration of ACTH (1 nM). ANP inhibited ALDO and B production rates in response to a low and more physiological concentration of ACTH (10 pM; ~50 pg/ml), albeit it was decidedly less efficacious (inhibition of ~50%) and potent (~10 nM) viz. its effect on ANG II action. Other ANP analogues (chicken ANP, eel ANP) shared similar potencies and efficacies of inhibition with rat ANP on maximal ALDO rates in response to ANG II. A brain natriuretic peptide (rat BNP) was equally efficacious but was less potent (~10 nM). However, an ANP clearance receptor analogue was without effect. This study indicates that ANP is a potent and efficacious inhibitor of ANG II-regulated ALDO and B production by lizard adrenocortical cells. Supported by USDA 00-35206-9330 to R.V.C. and NSF IBN0135167 to H. J.-A.

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