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      Enhanced Dendroaspis Natriuretic Peptide Immunoreactivity in Experimental Ureteral Obstruction

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          Whether the postobstructive diuresis can in part be related to an altered regulation of Dendroaspis natriuretic peptide (DNP) was investigated. Male Sprague-Dawley rats were bilaterally obstructed of their ureters. Control group was with sham ureteral obstruction. Forty-eight h later, tissue levels of DNP immunoreactivity were determined in the plasma, heart, and kidneys. Urine samples were collected in some rats under anesthesia. The plasma DNP immunoreactivity was significantly increased by 45% in the experimental group. The tissue levels of DNP immunoreactivity in the atrium, ventricle, or kidneys did not significantly differ between the experimental and control groups. The urinary flow and sodium excretion rate were 3- to 4-fold increased in the experimental group. The urinary DNP excretion was also increased in the experimental group, which was positively correlated with the urinary volume and sodium excretion. The urinary excretion of cGMP was 2- to 3-fold increased in the experimental group. These results indicate that an enhanced DNP activity may in part be causally related to the postobstructive diuresis.

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          Mechanism of relaxations to dendroaspis natriuretic peptide in canine coronary arteries.

          Experiments were designed to determine mechanisms by which Dendroaspis natriuretic peptide (DNP) causes relaxations in coronary arteries. Rings of canine left circumflex artery with and without endothelium were suspended in organ chambers filled with Krebs-Ringer bicarbonate solution (37 degrees C, bubbled with 95% O2/5% CO2). Concentration-response curves to DNP (10(-10) to 3 x 10(-7) M) were obtained in arteries contracted with prostaglandin (PGF(2alpha), 2 x 10(-6) M), either in the absence or the presence of C-ANP (10(-6) M) to inhibit natriuretic clearance receptors; indomethacin to inhibit cyclooxygenase (INDO, 10(-5) M), N(G)-monomethyl-L-arginine to inhibit production of nitric oxide (L-NMMA; 10(-4) M), HS-142-1 to inhibit particulate guanylate cyclase (10(-5) M); 1H-[1,2,4]oxadiazolo-[4,3-alpha]quinoxalin-1-one to inhibit soluble guanylate cyclase (ODQ; 10(-5) M), or tetraethylammonium to inhibit potassium channels (TEA; 10(-3) or 10(-2) M). Relaxations to DNP were greater in rings with than in those without endothelium. C-ANP significantly attenuated relaxations to DNP only in rings with endothelium. HS-146-1 but not INDO, L-NMMA, ODQ, and TEA significantly reduced relaxations to DNP in rings with and without endothelium contracted with PGF(2alpha). These results suggest that the endothelium augments inhibitory effects of DNP and that natriuretic clearance receptors mediate this component of the response to DNP in canine coronary arteries. In addition, relaxations to DNP in canine arterial smooth muscle involve activation of particulate guanylate cyclase but not hyperpolarization.

            Author and article information

            S. Karger AG
            October 2002
            02 September 2002
            : 92
            : 2
            : 369-372
            aDepartment of Physiology and Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju; bDepartment of Physiology, Chonbuk University School of Medicine, Jeonju, Korea
            63302 Nephron 2002;92:369–372
            © 2002 S. Karger AG, Basel

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            Figures: 1, Tables: 2, References: 16, Pages: 4
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