title: Cardiovascular regulation in TGR(mREN2)27 rats: 24h variation in plasma catecholamines, angiotensin peptides, and telemetric heart rate variability.
abstract: Dysfunction of the sympathetic nervous system might play an important role in disturbed 24h blood pressure regulation in transgenic hypertensive TGR (mREN2)27 (TGR) rats. Our study was performed to determine possible differences in activity of the sympathetic nervous system in TGR rats in comparison to their normotensive Sprague-Dawley (SPRD) controls; we measured plasma catecholamine and angiotensin concentrations throughout 24h under synchronized light-dark 12h:12H (LD 12:12) conditions. In the TGR rat strain, rhythms of plasma catecholamines were blunted, and the concentrations were significantly decreased. In addition, TGR rats showed increased plasma angiotensin I and II concentrations without any significant rhythm. An impaired autonomic regulation was confirmed by monitoring heart rate variability in TGR rats. Data showed that the TGR rat strain is characterized by a reduction in plasma catecholamines and an increase in angiotensin peptides. At present, it is not clear whether the reduction in catecholamines represents a decrease in sympathetic tone mediated by baroreflex activation or an increased catecholamine turnover induced by elevated angiotensin II. However, the blunted, but normally phased, rhythms in plasma catecholamines in TGR rats make it unlikely that the sympathetic nervous system is mainly responsible for the inverse circadian blood pressure rhythm in the transgenic strain.
authors.affiliation: Institute of Pharmacology and Toxicology Mannheim, Ruprecht-Karls University of Heidelberg, Germany.
authors.forename: S
authors.initials: S
authors.lastname: Schiffer
authors.forename: S
authors.initials: S
authors.lastname: Pummer
authors.forename: K
authors.initials: K
authors.lastname: Witte
authors.forename: B
authors.initials: B
authors.lastname: Lemmer
mesh_terms: D000803:Angiotensin I / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000809:Angiotensins / Q000737:chemistry*; D000818:Animals; D030801:Animals, Genetically Modified; D002395:Catecholamines / Q000097:blood; D006339:Heart Rate; D006579:Heterozygote; D006973:Hypertension / Q000503:physiopathology; D008297:Male; D010455:Peptides / Q000737:chemistry*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011945:Receptors, Angiotensin / Q000235:genetics; D012083:Renin / Q000235:genetics; D013997:Time Factors
chemical_list: D000809:Angiotensins; D002395:Catecholamines; D010455:Peptides; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D000803:Angiotensin I; D012083:Renin