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Research Article Free access | 10.1172/JCI105560
Cardiovascular Research Laboratories, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
†Address requests for reprints to Dr. John W. Eckstein, Dept. of Internal Medicine, University of Iowa, University Hospitals, Iowa City, Iowa 52240.
*Submitted for publication July 15, 1966; accepted December 22, 1966.
Supported by research grants HE-02644 and HE-09835, Research Career Program Awards HE-K6-4626 and HE-K3-17013, and postdoctoral fellowship HE-28-749 from the National Heart Institute.
Presented in part at the Fiftieth Annual Meeting of the Federation of American Societies for Experimental Biology, Atlantic City, N. J., April 15, 1966.
Find articles by Schmid, P. in: JCI | PubMed | Google Scholar
Cardiovascular Research Laboratories, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
†Address requests for reprints to Dr. John W. Eckstein, Dept. of Internal Medicine, University of Iowa, University Hospitals, Iowa City, Iowa 52240.
*Submitted for publication July 15, 1966; accepted December 22, 1966.
Supported by research grants HE-02644 and HE-09835, Research Career Program Awards HE-K6-4626 and HE-K3-17013, and postdoctoral fellowship HE-28-749 from the National Heart Institute.
Presented in part at the Fiftieth Annual Meeting of the Federation of American Societies for Experimental Biology, Atlantic City, N. J., April 15, 1966.
Find articles by Eckstein, J. in: JCI | PubMed | Google Scholar
Cardiovascular Research Laboratories, Department of Internal Medicine, University of Iowa College of Medicine, Iowa City, Iowa
†Address requests for reprints to Dr. John W. Eckstein, Dept. of Internal Medicine, University of Iowa, University Hospitals, Iowa City, Iowa 52240.
*Submitted for publication July 15, 1966; accepted December 22, 1966.
Supported by research grants HE-02644 and HE-09835, Research Career Program Awards HE-K6-4626 and HE-K3-17013, and postdoctoral fellowship HE-28-749 from the National Heart Institute.
Presented in part at the Fiftieth Annual Meeting of the Federation of American Societies for Experimental Biology, Atlantic City, N. J., April 15, 1966.
Find articles by Abboud, F. in: JCI | PubMed | Google Scholar
Published April 1, 1967 - More info
Cardiovascular responses to graded iv infusions of norepinephrine were observed in 24 dogs that had been treated for 1 week with either placebo, dexamethasone, or deoxycorticosterone. Eight dogs served as control and received daily iv injections of placebo; eight dogs received the mineralocorticoid, deoxycorticosterone; and eight received the glucocorticoid, dexamethasone. The three groups did not differ with respect to base-line hemodynamic variables either before administration of norepinephrine or after autonomic reflexes had been inhibited by ganglionic blockade. Comparisons of the three groups' hemodynamic responses to norepinephrine were made both before and after ganglionic blockade with the parallel line bioassay as a statistical test.
Dogs given deoxycorticosterone had much greater increases in mean arterial pressure and peripheral resistance with norepinephrine than did dogs given dexamethasone or placebo. Dogs given dexamethasone had slightly greater increases in mean arterial pressure than did dogs given placebo; changes in peripheral resistance were similar in the two groups. The augmented response of mean arterial pressure was apparent only after ganglionic blockade in the dexamethasone group. The vascular effects of norepinephrine, therefore, were markedly augmented by treatment with doxycorticosterone and only slightly augmented by treatment with dexamethasone.
The effect of norepinephrine on mean right atrial pressure was augmented in both groups treated with steroid before hexamethonium but only in the group treated with dexamethasone after hexamethonium.
The results indicate that deoxycorticosterone and dexamethasone have different qualitative and quantitative effects on circulatory responses to norepinephrine.