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Nongenomic vasodepressor effects of testosterone (TES) infusions in conscious male rats are neuronal nitric oxide synthase (nNOS)‐dependent
Author(s) -
Sellers Minga M.,
Greenway Clayton D.,
Perkins Lisa M.,
Stallone John N.
Publication year - 2011
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.25.1_supplement.823.9
Previously we reported the hypotensive effect of androgens on mean arterial blood pressure (MAP) involves a direct vasodilatory action on the peripheral vasculature that is structurally‐specific and independent of cytosolic androgen receptor. Thus, the effect of nNOS inhibition on TES‐induced reductions in MAP was studied in conscious, unrestrained, chronic‐catheterized, ganglionic‐blocked (hexamethonium, HEX, 30 mg/kg, i.p.) male Sprague‐Dawley rats 16–20 wks age. Rats were pretreated i.v. with nNOS inhibitor (S‐methyl‐thiocitrulline, SMTC, 20 μg/kg‐min x 30 min) or saline (Cont) and then MAP and heart rate (HR) were recorded at baseline and with increasing doses of TES (0.375–6.00 μM/kg‐min, i.v.). Vehicle‐controls (VC) received 10% EtOH/saline (0.15 ml/kg‐min i.v.). Data are means ± SE (n = 5–8 rats/group). In Cont, baseline MAP and HR averaged 104 ± 4 mmHg and 353 ± 12 beats/min. TES produced dose‐dependent reductions in MAP to a low of 87 ± 4 (Δ16%), HR was unchanged. SMTC abolished the effects of TES on MAP (112 ± 9 vs. 106 ± 8) and HR (333 ± 8 vs . 326 ± 8). Neither MAP nor HR were altered by VC. A 20 μg i.v. bolus of Na‐nitroprusside reduced MAP 30–40 mmHg, but HR was unchanged, confirming blockade by HEX. These data suggest the hypotensive effect of TES involves a direct vasodilatory action on the peripheral vasculature which, like the effect observed in isolated arteries, involves activation of nNOS. (NIH HL‐080402)