caa a22 4500 477072259 CHVBK 20180405111429.0 cr unu---uuuuu 170330e19960601xx s 000 0 eng 10.1007/BF00120497 doi (NATIONALLICENCE)springer-10.1007/BF00120497 Sympathetic nervous system in salt-sensitive and obese hypertension: Amelioration of multiple abnormalities by a central sympatholytic agent [Elektronische Daten] [Paul Ernsberger, Richard Koletsky, Laura Collins, David Bedol] Summary: Excess activity of the sympathetic nervous system (SNS) is linked to human obese hypertension and to salt-sensitive hypertension. Paradoxically, reduced SNS activity has been implicated as a contributor to obesity, particularly in animal models, and salt loading usually inhibits SNS activity. We have investigated the relationship between SNS activity, diet, and hypertension in the obese spontaneously hypertensive rat (SHROB), a model with a recessive obesity trait superimposed on a hypertensive background with multiple metabolic abnormalities resembling human syndrome X. We examined the role of SNS overactivity in the adverse impact of excess dietary salt and the possible beneficial effects of sympatholytic therapy. Mean blood pressure (MBP) was increased in SHROB and SHR fed a 4% NaCl diet. The pressor effect of dietary salt was abolished by ganglionic blockade, suggesting that increased SNS activity contributed to the pressor effect of the high-salt diet. Moxonidine, a second-generation central antihypertensive, controlled hypertension in both SHROB and SHR. Kidney damage in SHROB was accelerated by dietary salt and was reduced by moxonidine. Moxonidine elicited progressive weight loss in SHROB but not in SHR. Food intake in SHROB was reduced to the level of lean SHR. SHROB and SHR treated with moxonidine showed improved glucose tolerance. Additionally, SHROB showed reduced levels of triglycerides, cholesterol, and insulin following moxonidine therapy. Inhibition of the SNS, as with moxonidine therapy, may ameliorate multiple abnormalities and have therapeutic advantages in obese hypertensive syndromes. Kluwer Academic Publishers, 1996 glomerulosclerosis nationallicence hyperlipidemia nationallicence imidazoline receptors nationallicence insulin resistance nationallicence moxonidine nationallicence SHROB nationallicence obese spontaneously hypertensive rats nationallicence Ernsberger Paul Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut Koletsky Richard Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut Collins Laura Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut Bedol David Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut Cardiovascular Drugs and Therapy Kluwer Academic Publishers 10(1996-06-01), 275-282 0920-3206 10<275 1996 10 10557 https://doi.org/10.1007/BF00120497 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00120497 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Ernsberger Paul Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut NATIONALLICENCE 700 1- Koletsky Richard Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut NATIONALLICENCE 700 1- Collins Laura Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut NATIONALLICENCE 700 1- Bedol David Department of Medicine, Case Western Reserve School of Medicine, Cleveland, Ohio aut NATIONALLICENCE 773 0- Cardiovascular Drugs and Therapy Kluwer Academic Publishers 10(1996-06-01), 275-282 0920-3206 10<275 1996 10 10557 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer