Why the study?
Does coarctation of the abdominal aorta reduce microvascular density in the cremaster muscle of rats?
Does coarctation of the abdominal aorta reduce microvascular density in the cremaster muscle of rats?
Arteriolar rarefaction in hypertension involves pressure-independent mechanisms, as demonstrated by reduced microvascular density in vascular beds exposed to lower pressures downstream of aortic coarctation.
May indicate pressure-independent arteriolar rarefaction; leaves open relevance to human hypertension.
To assess the role of pressure in the arteriolar rarefaction associated with hypertension, we studied microvascular density in a hindquarters muscle (cremaster) of rats, 8 wk after coarctation (n = 8) or sham-coarctation (n = 10) of the abdominal aorta. To document the level of arterial pressure in hindquarters vascular beds of similar rats 8-9 wk after initial surgery, we implanted femoral arterial catheters under anesthesia and, 2-5 days later, we measured conscious femoral arterial pressures in coarcted [93 +/- 4 (SE) mmHg; n = 7] and sham-coarcted (110 +/- 3 mmHg; n = 4) rats. The cremaster muscle microcirculation was examined after fixation and Microfil infusion at in vivo pressures. The density of distal third- to fourth-order arterioles was lower by 19% (P = 0.03) in coarcted (1.37 +/- 0.06 mm/mm2) than in sham-coarcted (1.69 +/- 0.11 mm/mm2) rats. We conclude that pressure-independent mechanisms are involved in the arteriolar rarefaction accompanying hypertension.
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Boegehold et al. (1991) studied this question.
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