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Dive into the research topics where Mark Gunning is active.

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Featured researches published by Mark Gunning.


Journal of Clinical Investigation | 1992

Atrial natriuretic peptide(31-67) inhibits Na+ transport in rabbit inner medullary collecting duct cells. Role of prostaglandin E2.

Mark Gunning; Hugh R. Brady; G. Otuechere; Barry M. Brenner; Mark L. Zeidel

Atrial natriuretic peptide (ANP)(31-67), a portion of the atrial peptide prohormone, circulates in humans, and its plasma level varies with atrial pressure. Like the more widely studied carboxy-terminal fragment ANP(99-126), ANP(31-67) stimulates natriuresis and diuresis. We examined the mechanism of this natriuresis by measuring the effects of ANP(31-67) on Na+ transport in cells of the rabbit inner medullary collecting duct (IMCD). ANP(31-67) (10(-8) M) caused a 26 +/- 4% inhibition of oxygen consumption (QO2); half-maximal inhibition occurred at 10(-11) M, suggesting a physiologic effect. This effect was not additive with either ouabain or amiloride, suggesting that it reflected inhibition of Na+ transport-dependent QO2. ANP(31-67) reduced the amphotericin-induced stimulation of QO2 consistent with inhibition by this peptide of the Na(+)-K(+)-ATPase. In addition, ANP(31-67) reduced ouabain-sensitive 86Rb+ uptake under Vmax conditions. Several lines of evidence indicated that PGE2, a known endogenous IMCD Na(+)-K(+)-ATPase inhibitor, mediates pump inhibition by ANP(31-67). Thus, ANP(31-67) inhibits Na+ transport by inhibiting the Na(+)-K(+)-ATPase of IMCD cells, an effect mediated by the generation of PGE2.


Circulation Research | 1989

Enkephalinase inhibition increases plasma atrial natriuretic peptide levels, glomerular filtration rate, and urinary sodium excretion in rats with reduced renal mass.

Helen M. Lafferty; Mark Gunning; Patricio Silva; Mark B. Zimmerman; Barry M. Brenner; Sharon Anderson

To investigate the in vivo effects of inhibition of endopeptidase 24.11, an enkephalinase enzyme shown to be involved in atrial natriuretic peptide (ANP) breakdown in vitro, we infused phosphoramidon, a specific inhibitor of endopeptidase 24.11, into rats with reduced renal mass (and chronic extracellular volume expansion) and into normal rats. Relative to baseline values in rats with remnant kidneys, phosphoramidon led to elevations of plasma ANP levels and concomitant increases in urinary sodium excretion, fractional excretion of sodium, glomerular filtration rate, filtration fraction, and urinary cyclic GMP excretion. Similar changes in renal function and urinary cyclic GMP excretion were obtained with thiorphan, another endopeptidase 24.11 inhibitor. These enhanced ANP levels and renal actions were not observed with phosphoramidon in normal rats. These results show that plasma ANP levels can be modulated in rats with reduced renal mass by inhibition of endopeptidase 24.11.


American Journal of Physiology-regulatory Integrative and Comparative Physiology | 1997

Role of guanylyl cyclase receptors for CNP in salt secretion by shark rectal gland

Mark Gunning; Richard J. Solomon; Franklin H. Epstein; Patricio Silva

The role of C-type natriuretic peptide (CNP) and its guanylyl cyclase-linked receptors in mediating salt secretion by the rectal gland of the spiny dogfish shark ( Squalus acanthias) was investigated using HS-142-1, a competitive inhibitor of the binding of natriuretic peptides to their guanylyl cyclase receptors. CNP binds to receptors and activates guanylyl cyclase in rectal gland membranes in a way that is inhibited by HS-142-1. Guanylyl cyclase activation in rectal gland membranes is far more sensitive to CNP than to atrial natriuretic peptide, whereas the reverse is true for membranes derived from mammalian (rabbit) renal collecting duct cells. HS-142-1 inhibited the stimulatory effect of CNP on ouabain-inhibitable oxygen consumption by rectal gland tubules. In explanted rectal glands continuously perfused with blood from intact donor sharks, HS-142-1 inhibited the increase in salt secretion normally provoked by infusing isotonic saline solutions into the donor animal. These results strongly support the view that CNP released into the systemic circulation in response to volume expansion mediates the secretion of chloride by the rectal gland via receptors linked to guanylyl cyclase.The role of C-type natriuretic peptide (CNP) and its guanylyl cyclase-linked receptors in mediating salt secretion by the rectal gland of the spiny dogfish shark (Squalus acanthias) was investigated using HS-142-1, a competitive inhibitor of the binding of natriuretic peptides to their guanylyl cyclase receptors. CNP binds to receptors and activates guanylyl cyclase in rectal gland membranes in a way that is inhibited by HS-142-1. Guanylyl cyclase activation in rectal gland membranes is far more sensitive to CNP than to atrial natriuretic peptide, whereas the reverse is true for membranes derived from mammalian (rabbit) renal collecting duct cells. HS-142-1 inhibited the stimulatory effect of CNP on ouabain-inhibitable oxygen consumption by rectal gland tubules. In explanted rectal glands continuously perfused with blood from intact donor sharks, HS-142-1 inhibited the increase in salt secretion normally provoked by infusing isotonic saline solutions into the donor animal. These results strongly support the view that CNP released into the systemic circulation in response to volume expansion mediates the secretion of chloride by the rectal gland via receptors linked to guanylyl cyclase.


Physiological Reviews | 1990

Diverse biological actions of atrial natriuretic peptide

Barry M. Brenner; B. J. Ballermann; Mark Gunning; Mark L. Zeidel


Journal of The American Society of Nephrology | 1991

Nitric oxide: a potential mediator of amino acid-induced renal hyperemia and hyperfiltration.

Andrew J. King; Julia L. Troy; Sharon Anderson; Julia R. Neuringer; Mark Gunning; Barry M. Brenner


American Journal of Physiology-renal Physiology | 1988

Characterization of ANP receptors in rabbit inner medullary collecting duct cells

Mark Gunning; B. J. Ballermann; Patricio Silva; Barry M. Brenner; Mark L. Zeidel


American Journal of Physiology-renal Physiology | 1993

C-type natriuretic peptide receptors and signaling in rectal gland of Squalus acanthias

Mark Gunning; C. Cuero; Richard J. Solomon; Patricio Silva


Kidney International | 1992

Natriuretic peptides and the kidney: current concepts.

Mark Gunning; Barry M. Brenner


American Journal of Physiology-renal Physiology | 1990

Brain natriuretic peptide: interaction with renal ANP system

Mark Gunning; B. J. Ballermann; Patricio Silva; Barry M. Brenner; Mark L. Zeidel


Current Opinion in Nephrology and Hypertension | 1993

Urodilatin: a potent natriuretic peptide of renal origin.

Mark Gunning; Barry M. Brenner

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Patricio Silva

Brigham and Women's Hospital

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Mark L. Zeidel

Beth Israel Deaconess Medical Center

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Richard J. Solomon

Beth Israel Deaconess Medical Center

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Hugh R. Brady

University College Dublin

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Franklin H. Epstein

Beth Israel Deaconess Medical Center

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