Key result
In conscious rats, ganglionic blockade after molsidomine administration significantly decreased hindquarter vascular resistance (p<0.025) but not superior mesenteric resistance, indicating a compensatory sympathetic vasoconstriction in the hindquarters.
Why the study?
Does molsidomine-induced hypotension trigger a compensatory increase in hindquarter vascular resistance in conscious rats?
Does molsidomine-induced hypotension trigger a compensatory increase in hindquarter vascular resistance in conscious rats?
p-value: p=<0.025
In conscious rats, molsidomine-induced hypotension elicits a compensatory sympathetic vasoconstriction specifically in the hindquarter vascular bed, acting as a primary defense mechanism against hypotension.
Highlights bed-specific sympathetic compensation in rat vasodilator responses; hypothesis-generating for human regional vascular regulation.
The purpose of this study was to test whether hindquarter (terminal aortic) vascular resistance uniquely increases in order to compensate for interventions which result in a lowering of arterial pressure. Changes in hindquarter resistance were compared to changes in superior mesenteric resistance after the administration of the nitrovasodilator drug, molsidomine. Hindquarter blood flow or superior mesenteric flow was measured in conscious rats using an electromagnetic flow probe implanted around the terminal aorta or the superior mesenteric artery, respectively. Twenty minutes after an intravenous bolus injection of molsidomine (1 mg/kg), ganglionic blockade with hexamethonium bromide (25 mg/kg, i.v.) significantly decreased hindquarter resistance, but not superior mesenteric resistance. In the absence of molsidomine, ganglionic blockade has no effect on resistance in either vascular bed. These findings suggest that excitation of sympathetic vasoconstrictor fibers supplying the hindquarters but not those supplying the superior mesenteric area occurred in response to the hypotensive effect of molsidomine. This is consistent with the hypothesis that augmenting-hindquarter resistance is the first line of defense against hypotensive interventions.
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Teranishi et al. (1994) studied Hypotension (experimental) (n=10). Molsidomine followed by hexamethonium bromide vs. Superior mesenteric vascular bed / Baseline was evaluated on Change in hindquarter vascular resistance after ganglionic blockade (p=<0.025). In conscious rats, ganglionic blockade after molsidomine administration significantly decreased hindquarter vascular resistance (p<0.025) but not superior mesenteric resistance, indicating a compensatory sympathetic vasoconstriction in the hindquarters.
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