title: Blood pressure maintenance in hypertensive sympathectomized rats. II. Renin-angiotensin system and vasopressin.
abstract: This study examined the contribution of the main pressor systems to the residual hypertension exhibited by genetically hypertensive (LH) rats of the Lyon strain after early chronic sympathectomy with guanethidine. Blood pressure (BP) was recorded in conscious LH and normotensive control (LN) rats, either intact or sympathectomized, during sequential blockade of the renin-angiotensin system, vasopressin receptors, the autonomic nervous system, and finally after maximal vasodilation with hydralazine. In sympathectomized rats 1) renin-angiotensin system blockade equally reduced BP in both strains, whether it was realized before (-20%) or after (-30%) vasopressin antagonism; 2) isolated vasopressin antagonism decreased BP in LH (-8%) but not in LN rats; 3) autonomic blockade and hydralazine induced additional decreases in BP that were similar in both strains; and 4) intermediate and final levels of BP remained always higher in LH than in LN rats. It is concluded that, after sympathectomy, BP is maintained primarily by the renin-angiotensin system. In sympathectomized LH rats, the maintenance of hypertension does not depend on hyperactivity of the main pressor systems but rather on an increase in the intrinsic vascular resistance that develops in the absence of the sympathetic innervation of the vessels.
authors.affiliation: Département de Physiologie et Pharmacologie Clinique, Centre National de la Recherche Scientifique, Unité de Recherche Associée 606, Faculté de Pharmacie, Lyon, France.
authors.forename: M
authors.initials: M
authors.lastname: Lo
authors.forename: C
authors.initials: C
authors.lastname: Julien
authors.forename: C
authors.initials: C
authors.lastname: Barres
authors.forename: I
authors.initials: I
authors.lastname: Medeiros
authors.forename: A M
authors.initials: AM
authors.lastname: Allevard
authors.forename: M
authors.initials: M
authors.lastname: Vincent
authors.forename: J
authors.initials: J
authors.lastname: Sassard
mesh_terms: D000803:Angiotensin I / Q000494:pharmacology; D057911:Angiotensin Receptor Antagonists; D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D006145:Guanethidine; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011922:Rats, Mutant Strains; D017483:Receptors, Vasopressin; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System / Q000502:physiology*; D013563:Sympathectomy, Chemical; D014667:Vasopressins / Q000097:blood / Q000494:pharmacology / Q000502:physiology*
chemical_list: D057911:Angiotensin Receptor Antagonists; D017483:Receptors, Vasopressin; D014667:Vasopressins; D000803:Angiotensin I; D012083:Renin; D006145:Guanethidine