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Effect of Castration on Mesenteric Arterial and Portal Venous Responses to Splanchnic Nerve Stimulation
Author(s) -
Martin Doug Stuart,
Kjellsen Barton
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.611.3
Subject(s) - splanchnic , medicine , splanchnic nerves , endocrinology , stimulation , castration , blood pressure , mean arterial pressure , vascular resistance , blood flow , anesthesia , heart rate , hormone
Androgens exacerbate hypertension development. Our previous work suggested that androgens also amplify adrenergic constriction (Journal of Hypertension 23:2229). This study tested the hypothesis that male sex steroids modulate neural control of splanchnic resistance and capacitance function. Five week old male spontaneously hypertensive rats (SHR) underwent sham operation or castration and were studied at 12‐16 weeks of age. Mean arterial blood pressure (MAP) and heart rate (HR) were recorded in conscious rats. The rats were then anesthetized and instrumented for splanchnic nerve stimulation and mesenteric arterial and portal venous blood flow recording. Frequency response curves (1‐12 Hz) were constructed before and after inhibition of N type calcium channels with omega conotoxin. MAP was elevated in sham operated (151±6 mm Hg) compared to castrated SHR (135±3 mm Hg). Splanchnic nerve stimulation caused frequency dependent changes in mesenteric arterial and portal venous blood flow in both groups. However, the responses were greater in sham operated SHR compared castrated SHR. Treatment with omega conotoxin markedly attenuated the differences between groups. Collectively, these data show that castration modulates neurally mediated splanchnic resistance and capacitance vascular responses. This effect may be mediated in part via the N type calcium channel. Supported by NIH #63053 and AHA #0515443Z.