title: Sympathoadrenal system is critical for structural changes in genetic hypertension.
abstract: In spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, we examined tissue and adrenal norepinephrine concentrations, left ventricular (LV) weight, LV weight/body weight ratio (LV/BW), hindquarter resistance properties, ie, perfusion pressures at maximum dilatation and constriction (PPmax, PPmin), and the slope of the methoxamine log dose-PP curve. In series 1, we studied 4-week-old controls (SHRc, WKYc), sympathectomized rats (SX; SHRsx, WKYsx), and SX rats also given prazosin (SXP; SHRsxp, WKYsxp). With SX and SXP, adrenal norepinephrine concentrations increased in both strains, but tissue (LV, muscle, kidney) norepinephrine was depleted. At 4 weeks, LV/BW, PPmin, and PPmax were all greater in SHRc than in WKYc. With SX, these differences between strains remained unchanged, but SXP abolished them completely, indicating the importance of blockade of alpha-adrenergic receptor stimuli of adrenal origin. In SHRc (but not in WKYc), there was evidence of reinnervation after 4 weeks of SX. Hence, in series 2, the SXP period was extended to 8 weeks, and we studied SHRc, WKYc, SHRsxp, and WKYsxp. Systolic blood pressure was already elevated at 4 weeks in SHRc, and by 35 weeks it was 64 mm Hg greater than in WKYc. At 21 and 35 weeks, LV/BW, PPmax, PPmin, and slopes were all greater in SHRc than in WKYc, and the findings suggested greater LV and vascular hypertrophy than at 4 weeks. In SHRsxp hypertension, LV hypertrophy and the vascular changes were completely prevented over the entire 35-week observation period. SXP mainly affected SHR and had few effects on WKY rats. The sympathetic nerves and adrenals are probably the sources of alpha-adrenergic receptor stimulation in young SHR. They account for the development of hypertension and for most of the cardiovascular structural differences between SHR and WKY rats.
authors.affiliation: Baker Medical Research Institute, Melbourne, Australia.
authors.forename: P
authors.initials: P
authors.lastname: Korner
authors.forename: A
authors.initials: A
authors.lastname: Bobik
authors.forename: C
authors.initials: C
authors.lastname: Oddie
authors.forename: P
authors.initials: P
authors.lastname: Friberg
mesh_terms: D000311:Adrenal Glands / Q000503:physiopathology*; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D006352:Heart Ventricles; D006614:Hindlimb / Q000098:blood supply; D006973:Hypertension / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000473:pathology; D009638:Norepinephrine / Q000378:metabolism; D009929:Organ Size; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D013562:Sympathectomy; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014655:Vascular Resistance
chemical_list: D009638:Norepinephrine