Author:
Toot Jonathan D,Reho John J,Ramirez Rolando J,Novak Jacqueline,Ely Daniel L
Abstract
Abstract
Background
Testosterone (T) and the sympathetic nervous system each contribute to the pathology of hypertension. Altered blood vessel reactivity is also associated with the pathology of high blood pressure. The purpose of this study was to examine the effects of T manipulation in the regulation of resistance-sized blood vessel reactivity.
Methods
Adult spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) male rats at 8 weeks of age were used. The rats were divided into groups consisting of gonadally intact controls (CONT), castrate with sham implant (CAST) and castrate with T implant (CAST + T) (n = 6 to 12 per group). Following a short-term period of T treatment (approximately 4 weeks), plasma norepinephrine (NE) and plasma T were assessed by performing high-performance liquid chromatography and RIA, respectively. Resistance-sized mesenteric artery reactivity was assessed on a pressurized arteriograph for myogenic reactivity (MYO), phenylephrine (PE) responsiveness and passive structural mechanics.
Results
SHR and WKY males exhibited similar physiological trends in T manipulation, with castration significantly lowering plasma T and NE and T replacement significantly increasing plasma T and NE. T manipulation in general resulted in significant alterations in MYO of second-order mesenteric arteries, with T replacement decreasing MYO in SHR (P < 0.05) compared to CONT, T replacement increasing MYO, and CAST decreasing MYO in WKY rats (P < 0.001) compared to CONT rats. Additionally, PE-induced constriction was significantly altered in both strains following T treatment, with the effective concentration of PE to constrict the vessel to 50% of the total diameter significantly increased in the CAST + T SHR compared to CONT (P < 0.05). Comparisons of passive structural mechanics between SHR and WKY treatment groups indicated in SHR a significantly increased wall-to-lumen ratio and decreased circumferential wall stress compared to WKY treatment groups.
Conclusions
These data suggest that T and NE are involved in a complex interaction with both myogenic reactivity and structural alterations of resistance-sized blood vessels and that these factors likely contribute to the development and maintenance of hypertension.
Publisher
Springer Science and Business Media LLC
Subject
Endocrinology,Gender Studies
Reference59 articles.
1. Reckelhoff JF: Gender differences in the regulation of blood pressure. Hypertension 2001, 37: 1199–1208.
2. Folkow B: Physiological aspects of primary hypertension. Physiol Rev 1982, 62: 347–504.
3. Costarella CE, Stallone JN, Rutecki GW, Whittier FC: Testosterone causes direct relaxation of rat thoracic aorta. J Pharmacol Exp Ther 1996, 277: 34–39.
4. Toot JD, Reho JJ, Novak J, Dunphy G, Ely DL, Ramirez RJ: Colony social stress differentially alters blood pressure and resistance-sized mesenteric artery reactivity in SHR/y and WKY male rats. Stress 2011, 14: 33–41.
5. Jenkins C, Salisbury R, Ely D: Castration lowers and testosterone restores blood pressure in several rat strains on high sodium diets. Clin Exp Hypertens 1994, 16: 611–625. 10.3109/10641969409067965
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