title: Castration reduces blood pressure and autonomic venous tone in male spontaneously hypertensive rats.
abstract: OBJECTIVE
  The development of arterial hypertension is sexually dimorphic. Venous tone is elevated in the spontaneously hypertensive rat model of hypertension. This study tested the hypothesis that endogenous androgens exacerbate venous tone in the developmental stages of spontaneous hypertension.
  
  
  METHODS
  Male spontaneously hypertensive rats (SHRs) were subjected to sham operation, castration or castration + testosterone treatment. Ten-week-old SHR rats were instrumented for the measurement of arterial and venous pressure. A balloon catheter was advanced into the right atrium. Mean circulatory filling pressure (MCFP), an index of venous tone, was calculated. Mean arterial pressure (MAP) and MCFP were recorded from conscious rats. Postsynaptic adrenergic responsiveness was assessed by constructing cumulative dose-response curves to norepinephrine (NE). Baseline values and responsiveness to NE were obtained before and after autonomic blockade.
  
  
  RESULTS
  MAP and MCFP were significantly reduced in castrated (MAP, 130 +/- 4 mmHg; MCFP, 5.5 +/- 0.2 mmHg) versus sham-operated SHRs (MAP, 149 +/- 5 mmHg; MCFP, 6.7 +/- 0.3 mmHg) or castrated + testosterone-treated SHRs (MAP, 145 +/- 6 mmHg; MCFP, 7.1 +/- 0.4 mmHg). Ganglion blockade abolished these differences in MAP and MCFP. Infusion of NE caused dose-dependent increases in MAP and MCFP. The MAP responses in castrated SHRs were displaced to the right of those for sham and castrated + testosterone-treated SHRs. This was not evident in the venous circulation, where there were no marked differences in the NE dose-MCFP response curves.
  
  
  CONCLUSIONS
  Accordingly we conclude that endogenous male sex steroids contribute to the elevated arterial and venous pressures observed in the SHR.
authors.affiliation: Basic Biomedical Sciences, University of South Dakota School of Medicine, Vermillion, South Dakota, USA. dsmartin@usd.edu
authors.forename: Doug S
authors.initials: DS
authors.lastname: Martin
authors.forename: Scott
authors.initials: S
authors.lastname: Biltoft
authors.forename: Rebecca
authors.initials: R
authors.lastname: Redetzke
authors.forename: Erin
authors.initials: E
authors.lastname: Vogel
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D009919:Orchiectomy; D051381:Rats; D013737:Testis / Q000503:physiopathology*; D013739:Testosterone / Q000008:administration & dosage / Q000097:blood / Q000502:physiology; D014655:Vascular Resistance / Q000187:drug effects / Q000502:physiology
chemical_list: D013739:Testosterone; D009638:Norepinephrine