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Active Myogenic Tone: A Requisite for Hemoglobin Mediated Vascular Contraction?

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Pages 339-351 | Published online: 11 Jul 2009

Figures & data

Figure 1. Typical isometric tension responses of a pair of isolated rat thoracic aortic rings to hemoglobin (Hb). In a vessel ring with 30 nM norepinephrine-induced tone enhancement, 2 µM Hb elicited a notable additional contraction (upper tracing). In contrast, in a tone matched vessel ring with a passively induced tension by mechanical stretching, the same dose of Hb did not elicit a notable contraction (lower tracing).

Figure 1. Typical isometric tension responses of a pair of isolated rat thoracic aortic rings to hemoglobin (Hb). In a vessel ring with 30 nM norepinephrine-induced tone enhancement, 2 µM Hb elicited a notable additional contraction (upper tracing). In contrast, in a tone matched vessel ring with a passively induced tension by mechanical stretching, the same dose of Hb did not elicit a notable contraction (lower tracing).

Figure 2. Responses of rat aortic rings with different passive tension (PT) levels to Hb. The vessel rings were mechanically stretched to different tension levels. After stabilized at a desired tension level, the vessel rings were treated with 2 µM Hb and resultant total developed tension (DT) were recorded. When adjusted for the imposed tension (DT–PT), Hb treatment did not elicit any additional tension increase at all the PT values tested (0.2–2.5 g).

Figure 2. Responses of rat aortic rings with different passive tension (PT) levels to Hb. The vessel rings were mechanically stretched to different tension levels. After stabilized at a desired tension level, the vessel rings were treated with 2 µM Hb and resultant total developed tension (DT) were recorded. When adjusted for the imposed tension (DT–PT), Hb treatment did not elicit any additional tension increase at all the PT values tested (0.2–2.5 g).

Figure 3. Responses of agonist or passively tone enhanced aortic rings to 2 µM Hb. In norepinephrine (NE) tone induced vessel rings, the Hb mediated additional tension increase was significantly higher in 10 nM NE (NE-High) compared with 1 nM NE (NE-Low) (P < 0.01, N = 4–6). In vessel rings passively tone enhanced to 1 nM (PT-High) or 10 nM NE (PT-Low) levels, Hb did not elicit additional tension increases (P > 0.05, N = 4–6).

Figure 3. Responses of agonist or passively tone enhanced aortic rings to 2 µM Hb. In norepinephrine (NE) tone induced vessel rings, the Hb mediated additional tension increase was significantly higher in 10 nM NE (NE-High) compared with 1 nM NE (NE-Low) (P < 0.01, N = 4–6). In vessel rings passively tone enhanced to 1 nM (PT-High) or 10 nM NE (PT-Low) levels, Hb did not elicit additional tension increases (P > 0.05, N = 4–6).

Figure 4. Pretreatment NE doses and 2 µM Hb mediated additional contraction. Hb elicited vascular tension increases were calculated (vascular tension developed after Hb + NE − tension after NE alone) and plotted against NE dose. A notable Hb mediated contraction occurred only at NE doses greater than 1 nM. The dotted line represents a regression line fitted with a variable slope sigmoidal curve.

Figure 4. Pretreatment NE doses and 2 µM Hb mediated additional contraction. Hb elicited vascular tension increases were calculated (vascular tension developed after Hb + NE − tension after NE alone) and plotted against NE dose. A notable Hb mediated contraction occurred only at NE doses greater than 1 nM. The dotted line represents a regression line fitted with a variable slope sigmoidal curve.

Figure 5. Hb mediated additional tension responses in 30 nM NE, 65 µM actylcholine (Ach) or 18 µM 8-brom-cyclic guanosine 3,5-mono-phosphate (Br-cGMP) pretreated rat aortic rings. As shown previously, in 30 nM NE pretreated vessel rings, 2 µM Hb elicited a significant additional tension increase (P < 0.05, N = 5). When Ach as high as 1 mM were treated to vessel rings at basal state without prior tone enhancement, no additional contraction occurred with subsequent Hb treatment. Similarly, treatment with Br-cGMP as high as 20 µM did not allow Hb mediated additional contraction.

Figure 5. Hb mediated additional tension responses in 30 nM NE, 65 µM actylcholine (Ach) or 18 µM 8-brom-cyclic guanosine 3,5-mono-phosphate (Br-cGMP) pretreated rat aortic rings. As shown previously, in 30 nM NE pretreated vessel rings, 2 µM Hb elicited a significant additional tension increase (P < 0.05, N = 5). When Ach as high as 1 mM were treated to vessel rings at basal state without prior tone enhancement, no additional contraction occurred with subsequent Hb treatment. Similarly, treatment with Br-cGMP as high as 20 µM did not allow Hb mediated additional contraction.

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